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BALKAN JOURNAL OF STOMATOLOGY ISSN 1107 - 1141 TUPNB

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ALBANIARuzhdie QAFMOLLA - Editor Address:Emil KUVARATI Dental University Clinic Besnik GAVAZI Tirana, Albania BOSNIA AND HERZEGOVINA Maida GANIBEGOVIĆ - Editor Address:Naida HADŽIABDIĆ Faculty of DentistryMihael STANOJEVIĆ Bolnička 4a 71000 Sarajevo, BIHBULGARIANikolai POPOV - Editor Address:Nikola ATANASSOV Faculty of DentistryNikolai SHARKOV G. Sofiiski str. 1 1431 Sofia, BulgariaFYROMJulijana GJORGOVA - Editor Address:Ana STAVREVSKA Faculty of DentistryLjuben GUGUČEVSKI Vodnjanska 17, Skopje Republika MakedonijaGREECEAnastasios MARKOPOULOS - Editor Address:Haralambos PETRIDIS Aristotle University Grigoris VENETIS Dental School Thessaloniki, Greece

ROMANIAAndrei ILIESCU - Editor Address:Victor NAMIGEAN Faculty of Dentistry Cinel MALITA Calea Plevnei 19, sect. 1 70754 Bucuresti, Romania

SERBIAVojislav LEKOVIĆ - Editor Address:Slavoljub ŽIVKOVIĆ Faculty of Dentistry Zoran STAJČIĆ Dr Subotića 8 11000 Beograd, Serbia

TURKEYEnder KAZAZOGLU - Editor Address:Pinar KURSOGLU Yeditepe University Arzu CIVELEK Faculty of Dentistry Bagdat Cad. No 238 Göztepe 81006 Istanbul, TurkeyCYPRUSGeorge PANTELAS - Editor Address:Huseyn BIÇAK Gen. Hospital NicosiaAikaterine KOSTEA No 10 Pallados St. Nicosia, Cyprus

Editorial board

Editor-in-Chief Ljubomir TODOROVIĆ, DDS, MSc, PhD Faculty of Dentistry University of Belgrade Dr Subotića 8 11000 Belgrade Serbia

Council:President: Prof. M. VulovićPast President: Prof. A. IliescuPresident Elect: Prof. P. KoidisVice President: Prof. H. BostanciSecretary General: Prof. L. ZouloumisTreasurer: Dr. E. HassapisEditor-in-Chief: Prof. Lj.Todorović

Members: R. Qafmolla P. Kongo M. Ganibegović S. Kostadinović N. Sharkov V. Mihovska M. Carčev A. Minovska A. Pissiotis S. Dalambiras

A. Adžić B. Rašović A. Vucur A. Creanga D. Stamenković M. Barjaktarević E. Kazazoglu M. Akkaya G. Pantelas S. Solyali

BALKAN STOMATOLOGICAL SOCIETYTUPNB

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The whole issue is available on-line at he web address of the BaSS (www.e-bass.org)

International Editorial (Advisory) Board Christoph HÄMMERLE - Switzerland George SANDOR - Canada Barrie Kenney - USA Ario SANTINI - Great Britain Predrag Charles LEKIC - Canada Riita SUURONEN - Finland Kyösti OIKARINEN - Finland Michael WEINLAENDER - Austria

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6 P. Papadopoulos, A. Kolokotronis Balk J Stom, Vol 13, 2009

Clinical Uses

Biphosphonates appear to play a multifactorial role in many kinds of clinical cases. One of the early clinical uses of biphosphonates was as bone scan imaging agent3. They are also used in the treatment of Paget’s disease, hypercalcemia (the result of excessive bone resorption and release of Ca into circulation) related to malignancy, in the management of bone metastases by reducing skeletal tumour burden in patients with multiple myeloma and prostate cancer20. They play an extinguished role - reduce the incidence of new fractures in the management of osteoporosis characterized by abnormal rarefaction of bone, especially the third generation biphosphonates (riserdronate) in postmenopausal women21. They have an anti-osteolytic effect by inhibition of osteoclastic action22. They can be applied to counteract bone loss in chronic periodontitis23. Besides all these, they play an anti-neoplastic role by interacting with osteoclasts, osteoblasts, tumour cells, cytokine and growth factor production, leading to the interruption of bone destruction; by immunomodulating properties on γδ T cells (activate them), they have pre-apoptotic and anti-angiogenic potentials - their use as radiation sensitizers.

Properties

The first is inhibition of calcification when given at high doses and bone resorption24,25. Biphosphonates impair the mineralization of normal calcified tissues, such as bone and cartilage and dentine, enamel and cementum2. In the latter case, their administration can lead to a reduction of the extraction force. In addition to it, they decrease bone loss or actually increase bone mineral density. At the cellular level, biphosphonates increase proliferation of osteoblasts and cartilage cells, biosynthesis of collagen and osteocalcin by bone cells, and proteoglycans by cartilage cells. The effect on collagen may be due to impaired intracellular collagenolysis. It is very interesting to mention that bone that has been treated with biphosphonates is still able to show an anabolic response to intermittent parathyroid hormone although the effect is blunted2. They also exhibit anti-angiogenic properties by depriving tumour cells of adequate nutrient and blood supply. Biphosphonates alter the bone microenvironment making it less favourable for tumour cell proliferation20.

Side-Effects

Biphosphonate therapy is presented by many scientists and case reports observations to be related

with important adverse effects including renal toxicity, fever, bone pain, hypocalcemia and mild gastrointestinal complains26-30. In particular, the biphosphonate associated osteonecrosis of the jaws is a subject that draws the intense interest of the dental community. Osteonecrosis is characterized by the death of bone that results as a natural consequence of a wide variety of systemic and local factors compromising the blood flow of bone, such as haemoglobinopathies, anticardiolipin antibodies, defects of thrombotic and fibrinolytic systems, fat emboli, alcoholism, systemic lupus erythematosus (SLE) 31-34, corticosteroid administration and recently, as proven, biphosphonate therapy. Bone exposure caused by osteonecrosis has particular sites of establishment on the jaws: the posterior mandible in the molar area along the mylohyoid ridge is the most common one, followed by the posterior maxilla.

The complication of exposed bone jaws associated with biphosphonate therapy (osteonecrosis/osteopetrosis) is explained by 2 theories. The leading theory suggests that it is caused by cessation of bone remodelling and bone turnover by the basic osteoclast inhibiting effect of the drugs when given to reduce loss of bone density in osteoporosis, or to prevent cancer spread in bone. Since the jaws have a greater blood supply than other bones, and a faster turnover rate related both to their daily activity and the presence of teeth (which mandates daily bone remodelling around the periodontal ligament), biphosphonates are highly concentrated in the jaws. Coupled with chronic invasive dental diseases and treatments and the thin mucosa over bone, this anatomic concentration of biphosphonates causes this condition to be manifested exclusively in the jaws. Thus the exposed bone in the jaws is the direct result of the action of the drugs on the daily remodelling and replenishment of bone. Osteoblasts and osteocytes live for only about 150 days. If upon their death the mineral matrix is not resorbed by osteoclasts which release the cytokines of bone morphogenetic protein and insulin-like growth factors to induce new osteoblasts from the stem cell population, the osteon becomes acellular and necrotic. The small capillaries within the bone become involuted and the bone avascular. A spontaneous breakdown of the overlying mucosa, injury or invasive surgery in the jaws, usually cause this necrotic bone to expose. It then fails to heal.

According to the competing theory (based only on experimental evidence) biphosphonates, pamidronate and zoledronate, inhibit endothelial cell proliferation in the jaws thus leading to loss of blood vessels and avascular necrosis35,36. We must underline that osteonecrosis is actually a chemically induced form of osteopetrosis, an inherited autosomal dominant trait characterized by the loss of osteoclast development with 7 subtypes. In osteopetrosis, as in biphosphonate induced exposed bone, angiogenesis in the soft tissues is normal.

Balk J Stom, Vol 13, 2009 Dental Concern of the Use of Biphosphonates 7

Moreover, the comparison between osteonecrosis and osteoradionecrosis is useful for the differential diagnosis of the first. Unlike osteoradionecrosis (ORN), biphosphonate associated osteonecrosis (BAO) doesn’t appear to be amenable to hyperbaric oxygen therapy. In ORN, radiation induced tissue damage is characterized by hypoxia, hypocellularity and hypovascularity which are reversible or preventable to some degree with revascularization of bone. By contrast, in BAO the alteration in bone metabolism is such that revascularization alone is insufficient to alter the course of the lesions because biphosphonates are not metabolized appreciably and have the potential to remain in the bone indefinitely37,38. It has been reported that BAO is refractory to hyperbaric oxygen therapy and advised against using hyperbaric oxygen in the treatment of these patients.

A distinguished feature between the 2 situations is coming out from the observation that the maxilla is commonly involved in BAO, whereas this is sighted rarely in cases of ORN. It is critical to mention that BAO has substantial clinical implications because many patients fail to heal after dental surgical procedures, e.g. extraction.

Osteonecrosis is often related to a site of previous dental treatment but can also occur in regions without it. Jaw pain is present, as well as an infection secondary to bone exposure26. Extractions make the conditions worse with a non-healing socket sequestration, pain, offensive smell, soft tissue infections and deformity3. The class of biphosphonates that is mostly related with osteonecrosis is the nitrogen-containing (zolendronate, pamidronate).

Besides osteonecrosis and exposed bone lesions, biphosphonate therapy is being associated with avascular necrosis although our current knowledge of the related process is limited, showing that these drugs are a direct factor in a multifactorial aetiology leading to avascular necrosis in the jaws. They are suggested to produce ischemic changes in the maxilla and mandible3.

Finally dental implant failure attributable to oral biphosphonate therapy has been reported in patients with osteoporosis39.

Preventive Measures and Recommendation

The whole description of the implications of the biphosphonate therapy reflects the critical value of several preventive measures and recommendations in order to avoid them. Generally, impacted teeth that are completely covered by bone or soft tissue should be left undisturbed, but those with an oral communication are recommended to be removed and given a month healing period. Prophylactic antibiotic coverage for invasive dental procedures is necessary and thus penicillin remains the

drug of choice19. In case of penicillin allergy, combination of guinolones and metronidazole would be appropriate.

Before initiating biphosphonate therapy and for non invasive dental care, biphosphonate therapy need not to be delayed. In case of invasive procedures, such as extractions, commencement of biphosphonate therapy should be delayed for a month to allow sufficient time for home recovery and healing. Once the regimen of biphosphonate therapy has begun, surveillance schedule of once every 4 months is recommended40.

While receiving biphosphonate therapy, tooth extractions should be avoided as well as selective surgery within the jaws, replaced by alternatives including root canal treatment and amputation of the crown. Patients with dentures should have well maintained soft liners to minimise trauma of the oral mucosa, or leave their dentures out. Pain control is important Fluoride and possibly 0.12% chlorhexidine may be considered to decrease the possibility of tooth extraction26. Placing implants should be strictly avoided41.

Treatment of Patients with Osteonecrosis/ Established Avascular Necrosis of the Jaws

Attempts to accomplish debridement, cover the exposed bone with flaps, or bone contouring procedures are being considered only in cases refractory to non-surgical management, and in the face of continuing symptoms19. This model of therapy is suitable for avascular necrosis of the jaws being shown by table 1.

Bone grafting either as a free graft or by microvascular transfer involves affected bone. There is a risk that there could be 2 problem areas, the donor graft site as well as the recipient jaw site. Major resection surgery should be avoided5.

In osteonecrosis, treatment should be directed towards eliminating or controlling pain, preventing progression of the exposed bone .The necrotic exposed bone itself is not painful and will remain structurally sound to support normal jaw function. Once secondarily infected, it will become painful and may lead to cellulitis and fistula formation42, 43. Pathologic fractures do not usually occur unless debridement surgeries have reduced the structural integrity of the mandible.

Therefore, aside from rounding off sharp bony projections that produce soft tissue inflammation, and a long term course of penicillin V-K 500 mg, 4 times a day, and 0.12% chlorhexidine44 is prescribed. Occasionally, severe cellulitis will warrant hospital care using IV antibiotics (ampicillin).


Conclusions

Summarising the main points concerning biphosphonates, on the basis of dental interest, we should mention that they are used in the treatment of Paget’s disease, multiple myeloma and in chronic periodontitis by counteracting bone loss. However, it is critical to notice that biphosphonate therapy needs to be stopped 6 months before the attempt of any surgical or invasive method in the mouth, including tooth extraction, thus minimising the danger of osteonecrosis.

There are many unknown facts regarding the process of biphosphonate related osteonecrosis of the jaws. The incidence is currently low, 0.1-1% of all patients on biphosphonates, and may differ among different bone

pathologies, biphosphonates and dosage regiments. The most important question, however, is whether this is a cumulative problem.

Moreover, biphosphonate therapy has become a standard of care for patients with malignant bone disease. Preclinical and preliminary clinical data suggest that biphosphonates may prevent cancer-treatment induced bone loss in patients with breast or prostate cancer receiving oestrogen/androgen therapies. In addition to it, biphosphonates have demonstrated anti-tumour activity in preclinical models and clinical evidence supports the fact that biphosphonates may slow the progression of bone lesions or prevent bone metastases45. Therefore, trials to determine the anti-tumour effects of these drugs in patients with early stage breast and prostate cancer, non-small

Ensure correct diagnosis

Cease biphosphonate if possible minimum 3 months before surgical intervention (it is possible that this time span is too short)

Antibiotics if secondary infection (penicillin, cephalosporin, clindamycin) Antiseptic mouth wash (e.g. Chlorhexidine gluconate)

Cover with periodontal pack.

Localised surgical debridement without primary reconstruction

Minimal mucoperiosteal flap reflection to preserve the blood supply to underlying bone should be used

Resolution Non-Resolution

Surgical resection without primary therapy reconstruction

Alternatives to biphosphonate

Table 1: Therapeutic management of the established avascular necrosis of the jaws

Balk J Stom, Vol 13, 2009 Dental Concern of the Use of Biphosphonates 9

cell lung cancer and renal cell carcinoma will provide important insight into the optimal timing and modality of biphosphonate therapy in those patient populations. The clinical applications of these medicines are likely to expand further in oncology as these trials mature. This whole concept reveals a part of the new horizons in biphosphonate therapy research45.

References

1. Menschutkin M. Ueber die Einwirkung des Chloracetyls auf phosphorige Saüre. Annals of Chemical Pharmaracology, 1865; 133:317-320.

2. Von Baeyer H, Hofmann KA. Acetodiphosphorige Saure. Berichte der Deutschen Chemischen Gesellschaft, 1897; 30:973-1978.

3. Cheng A, Marrokokki A, Carter G, Stein B. The dental implications of biphosphonates and bone disease. Australian Dental Journal - Medications Supplement, 2005; 50:4.

4. Sparidans RW, Twiss IM, Talbot S. Biphosphonates in bone diseases. Pharmacology World Science, 1998; 20:206-213.

5. Rogers MJ, Gordon S, Benford HL, Coxon FP, Luckman SP, Monkkonen J, Frith JC. Cellular and molecular mechanisms of action of biphosphonates. Journal of Cancer, 2000; 88:2961-2978.

6. Martin TJ, Grin V. Biphosphonates-mechanisms of action. Australian Prescriber, 2000; 23:130-132.

7. Carter GD, Goss AN. Letter to the editor. Biphosphonates and avascular necrosis of the jaws. Aus Dent J, 2003; 48:268.

8. Francis MD, Russel RGG, Fleisch H. Biphosphonates inhibit formation of calcium phosphate crystals in vitro and pathological calcification in vivo. Journal of Science, 1969; 165:1264-1266.

9. Hansen NM, Felix R, Bisaz S, Fleisch H. Aggregation of hydroxyapatite crystals. Biochimica et Biophysica Acta, 1976; 451:549-559.

10. Francis MD. The inhibition of calcium hydroxyapatite crystal growth by polyphosphonates and polyphosphates. Calcified Tissue Research, 1969; 3:151-162.

11. Boulenc X, Marti E, Joyeux H, Roques C, Berger Y, Fabre G. Importance of the paracellular pathway for the transport of a new biphosphonate using the human CACO-2 monolayers model. Biochemical Pharmacology, 1993; 46:1591-1600.

12. Boulenc X, Roques C, Joyeux, Berger Y, Fabre G. Biphosphonates increase tight junction permeability in the human intestinal epithelial (Caco-2) model. Int J Pharmacol, 1995; 123:13-24.

13. Fleisch H. Bisphosphonates: Mechanisms of action. Endocrine Reviews, 2006; 19:80-100.

14. Bisaz S, Jung A, Fleisch H. Uptake by bone of pyrophosphate, biphosphonates and their technetium derivatives. J Clin Sci Mol Med, 1978; 54:265-272.

15. Sato M, Grasser W, Endo N, Akins R, Simmons H, Thompson DD, et al. Biphosphonate action. Alendronate localization in rat bone and effects on osteoclast ultrastructure. J Clin Invest, 1991; 88:2095-2105.

16. Larsson A, Rohlin M. In vivo distribution of C-labelled ethylene-1- hydroxy-1, 1-diphosphonate in normal and treated young rats. An autoradiographic and ultrastructural study. Toxicology and Applied Pharmacology, 1980; 52:391-399.

17. Wingen F, Schmahl D. Distribution of 3- amino-1-hydroxypropane-1, 1-diphosphonic acid in rats and effects on rat osteosarcoma. Arzneimittelforschung, 1985; 35:1565-1571.

18. Monkkonen J, Koponen HM, Ylitalo P. Comparison of the distribution of three bisphosphonates in mice. Pharmacol Toxicol, 1990; 66:294-298.

19. The Endocrine Society. Editorial Long-Term Safety of Biphosphonates. The Journal of Clinical Endocrinology & Metabolism, 2005; 90:1897-1899.

20. Melo DM, Obeid G. Osteonecrosis of the Maxilla in a Patient with a History of Biphosphonate Therapy. J Can Dent Assoc, 2005; 71:111-1113.

21. Woodward J, Coleman R, Holen I. Preclinical evidence for the effects of biphosphonates and cytotoxic drugs on tumour cell invasion. Anticancer Drugs, 2005; 16:11-19.

22. Hughes DE, Wright KR, Uy HL, Sasaki A, Yoneda T, Roodman GD, Mundy GR, Boyce BF. Bisphosphonates promote apoptosis in murine osteoclasts in vitro and in vivo. Journal of Bone and Mineral Research, 1995; 10:1478-1487.

23. Figara G, Beninati F, Rubino I, Vannucchi A, Longo G, Tonelli P, Pini Prato G. Osteonecrosis of the jaws in periodontal patients with a history of biphosphonates treatment. J Clin Periodont, 2005; 141:4793-4796.

24. King WR, Francis MD, Michael WR. Effect of disodium ethane-1-hydroxy-1,1-biphosphonate on bone formation. Clinical Orthopaedics and Related Research, 1971; 78:251-270.

25. Flora L, Hassing GS, Parfitt AM, Villanueva AR. Comparative skeletal effects of two biphosphonates in dogs. Metabolic Bone Disease & Related Research, 1980; 2:389-407.

26. Bukowski JF, Dascher CC, Das H. Alternative biphosphonate targets and mechanisms of action. Biochemical and Biophysical Research Communications, 2005; 328:746-750.

27. Pavlakis N, Schmidt R, Stockler M. Bisphosphonates for breast cancer. The Cochrane Database of Systematic Reviews, 2005; CD003474

28. Smetana S, Michlin A, Rosenman E, Biro A, Boaz M, Katzir Z. Pamidronate-induced nephrotoxic tubular necrosis:a case report. Clinical Nephrology, 2004; 61:63-67.

29. Dicuonzo G, Vincenzi B, Santini D, Avvisati G, Rocci L, Battistoni F, et al. Fever after zoledronic acid administration is due to increase in TNF-alpha and IL-6. Journal of Interferon and Cytokine Research, 2003; 23:649-654.

30. Teramoto S, Matsuse T, Ouchi Y. Increased cytokines and pamidronate-induced bone pain in adults with cystic fibrosis. Lancet, 1999; 353:750.

31. Merigo E, Manfredi M, Meleti M, Corradi D, Vescovi P. Jaw bone necrosis without previous dental extractions associated with the use of biphosphonates (pamidronate and zoledronate): a four-case report. J Oral Pathol Med, 2005; 34:613-617.

32. Bouquot JE, McMahon RE. Neuropathic pain in maxillofacial osteonecrosis. J Oral Maxillofac Surg, 2000; 58:1003-1020.


33. Assouline-Dayan Y,Chang C, Greenspan A, Shoenfeld Y, Gershwin ME. Pathogenesis and natural history of osteonecrosis. Seminars in Arthritis and Rheumatism, 2002; 32:94-124.

34. Gruppo R, Glueck CJ, McMahon RE, Bouquot J, Rabinovich BA, Becker A, et al. The pathophysiology of alveolar osteonecrosis of the jaw: anticardiolipin antibodies thrombophilia and hypofibrinolysis. J Lab Clin Med, 1996; 127:481-488.

35. Zigic TM, Marcous C, Hungerford DS, Dansereau JV, Stevens MB. Corticosteroid therapy associated with ischemic necrosis of bone in systemic lupus erythematosis. Am J Med, 1985; 79:596.

36. Marx ER, Sawatari Y, Fortin M, Broumand V. Biphosphonate-induced exposed bone (Osteonecrosis/Osteopetrosis) of the jaws: Risk factors, recognition, prevention and treatment. J Oral Maxillofac Surg, 2005; 63:1567-1575.

37. Melo DM, Obeid G. Osteonecrosis of the jaws in patients with a history of receiving biphosphonate therapy. Strategies for prevention and early recognition. J Am Dent Assoc, 2005; 136:1675-1681.

38. Russel RG, Rogers MJ, Frith JC, Luckman SP, Coxon FP, Benford HL, et al. The pharmacology of biphosphonates and new insights into their mechanisms of action. J Bone Miner Res, 1999; 14:53-65.

39. Ruggiero LS, Mehrotra B, Rosenberg JT, Engroff SL. Osteonecrosis of the Jaws Associated with the Use of Biphosphonates: A Review of 63 Cases. J Oral Maxillofac Surg, 2004; 62:527-534.

40. Schwartz HC. Osteonecrosis and biphosphonates: correlation versus causation. J Oral Maxillofac Surg, 2004; 62:763-764.

41. Carter GD, Goss AN, Doecke C. Bisphosphonates and avascular necrosis of the jaw: a possible association. Medical Journal of Australia, 2005; 182:413-415.

42. Marx RE. Pamidronate (Aredia) and zoledronate (Zometa) induced avascular necrosis of the jaws: a growing epidemic. J Oral Maxillofac Surg, 2003; 61:1115-1117.

43. Migliorati CA. Biphosphonates and oral cavity avascular bone necrosis. J Clin Oncol, 2003; 21:4253-4254.

44. Dimitrakopoulos I, Magopoulos C, Karakasis D. Biphosphonates-induced avascular osteonecrosis of the jaws: a clinical report of 11 cases. J Oral Maxillofac Surg, 2006; 35:588-593.

45. Lipton A. Towards New Horizons. The Future of Biphosphonate Therapy. The Oncologist, 2004; 9:38-47.

Correspondence and request for offprints to:

Petros Papadopoulos542 48, ThessalonikiGreeceE-mail: [email protected]

SUMMARYSeveral topical and systemic factors have been reported to influence

the eruption of teeth. Some of the local lesions include eruption cysts, erup-tion sequestra, fibrous developmental malformations and dentigerous cysts. The systemic factors include Down’s syndrome, cleidocranial dysostosis, hypothyroidism, hypopituitarism and achondroplastic dwarfism. All these lesions and factors generally influence the eruption of the primary, as well as the permanent dentition. The purpose of this review article is to present up-to-date aspects of these conditions.Keywords: Eruption cysts; Dentigerous Cysts; Down’s Syndrome; Cleidocranial Dysostosis; Hypothyroidism; Hypopituitarism; Dwarfism, achondroplastic

Vasiliki Boka, Anastasios K. Markopoulos, Athanassios K. Poulopoulos

Aristotle University, School of DentistryDepartment of Oral Medicine & Maxillofacial PathologyThessaloniki, Greece

REVIEW PAPER (RP)Balk J Stom, 2009; 13:11-14

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Tooth Eruption: Topical and Systemic Factors that Influence the Process

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Introduction

Numerous studies have been performed to understand the process of tooth eruption better. The most common general symptoms during tooth eruption include anxiety (15%), diarrhea (13%), a combination of the two (8%), fever1 and increased salivation2. Apart from general symptoms that end up to normal eruption of the teeth, several local and systemic factors have been reported to influence the eruption of teeth. The exact nature of the factors responsible for tooth eruption is not fully understood. It is believed that these factors influence the matrix formation and the calcification process.

The most important local conditions that influence tooth eruption are: eruption cysts, eruption sequestra, fibrous developmental malformations and dentigerous cysts. Systemic factors include Down’s syndrome, cleidocranial dysostosis, hypothyroidism, hypopituitarism and achondroplastic dwarfism.

The purpose of this review article is to present the current aspects of these conditions.

Eruption Cysts

Eruption cysts occur within the mucosa overlying a tooth that is about to erupt3. They develop as a result of separation of the dental follicle from around a crown of an

erupting tooth. They are considered soft tissue analogues of the dentigerous cysts. Lately, eruption cysts are described as a possible adverse effect of cyclosporine-A (CyA) administration during tooth eruption4.

There is a gender predilection; the male to female ratio is 2:15,6. They usually appear in the region of the molars7. Eruption cysts clinically appear as soft translucent swelling in the gingival mucosa. Their colour varies between deep blue and azure7.

Surface trauma may result in a considerable amount of blood in the cystic fluid. Such lesions are sometimes referred as eruption haematomas. Their basic clinical characteristics are swelling, fluctuation and deep blue colour6. Pain may appear only if the cyst is traumatized7. Histologically, they are characterized by non-keratinized, squamous epithelium lining in the cystic wall7. Differential diagnosis includes haematoma, amalgam tattoo, cysts and haemangioma8,9.

The treatment of the eruption cysts is surgical and includes the excision of tissues over the crowns of the responsible teeth. In most cases, even this treatment is not necessary, because the cysts rupture and never appear again3.

Eruption Sequestrum

The eruption sequestrum usually appears during the eruption of the first permanent molars. Intraorally, the

12 V. Boka et al. Balk J Stom, Vol 13, 2009

lesions presents as a small hard tissue fragment, white in colour, and with bone-like hardness on the occlusal surface of the mandibular second molar that was erupting10. Histopathologically, the fragments consist of necrotized cortical bone11. Studies involving X-ray micro-analyzer revealed that the percentages of calcium and phosphorous (by weight) were 78.41% and 21.59%, respectively, with a calcium to phosphorous ratio of 3.63, which was higher than that seen in normal osseous tissue11. Generally, the sequestra have little clinical significance as they can appear and disappear. However, they may retain plaque in close association with the newly erupting tooth12. The retained eruption sequestrum may lead to pericoronitis or pit and fissure caries13. In dental practice the presence of multiple developmental dental anomalies expressing simultaneous defects in different stages of tooth development should raise suspicion of possible manifestation of an underlying systemic abnormality, such as Ehlers-Danlos syndrome14.

Treatment is not always necessary. Surgical removal is usually chosen only if it is usually traumatized or annoys the patient2.

Fibrous Developmental Malformation

In most cases, fibrous developmental malformation manifests as enlargement of the gingiva, often correlated with the eruption of deciduous or permanent teeth15. Gingival fibromatosis may be familial or idiopathic. The familial variations may occur as isolated finding or in association with hereditary syndromes, such as Zimmermann-Laband syndrome, Rutherford syndrome or multiple hamartomas.

Tagaki et al16 described 6 categories of fibrous developmental malformation; (1) isolated familial gingival fibromatosis; (2) isolated idiopathic gingival fibromatosis; (3) gingival fibromatosis associated with hypertrichosis; (4) gingival fibromatosis associated with hypertrichosis and mental retardation, or epilepsy, or both; (5) gingival fibromatosis associated with mental retardation, or epilepsy, or both; (6) gingival fibromatosis associated with hereditary syndromes.

In most cases the enlargement begins before the age of 20. The gingiva is firm, normal in colour and covered by a smooth surface17-21. Histopathologically, fibrous developmental malformations consist of poorly cellular, richly collagenous fibrous connective tissue underneath a normal or acanthotic epithelium. Mild peri-vascular chronic inflammation and small foci of dystrophic calcification may be observed22.

Treatment is required only if the lesion annoys the patient. Surgical removal is the treatment of choice23.

Inflammatory Dentigerous Cysts

Inflammatory dentigerous cysts are the most common type of developmental odontogenic cysts and mostly they are found in the mixed dentition24. They are usually single and they are located in the posterior mandible25. They are associated with the roots of non-vital deciduous teeth and the crown of their unerupted permanent successors26. The cysts are not painful except in the case of secondary infection, or unless their size has created a pathological fracture24.

There are 2 leading theories about the formation of dentigerous cysts24. The first begins with fluid accumulation between the reduced enamel epithelium and the crown of the tooth. The other theory begins with a breakdown of the stellate reticulum, which forms a fluid between the inner and outer enamel epithelium.

Radiographically, the tooth may be displaced: it is not surprising to see teeth displaced to the condylar neck, the nasal floor or high in the maxillary sinus approaching the orbit24. Histologically, they are composed of a thin connective tissue wall lining the lumen. The epithelium is usually parakeratinized or orthokeratinized. Rete peg formation is usually absent and an inflammatory cell infiltration of the connective tissue is common. In about 50% of cases, dentigerous cysts can cause resorption of the adjacent unerupted teeth.

Treatment of choice is the extraction of the infected deciduous tooth and continuous drainage of the cyst27. Simultaneous with the eruption of the permanent tooth, ossification of the bony defect can take place28. The reparatory process is completed in 1-2 years26. Marsupialization is less ideal; it runs the risk of allowing an ameloblastoma in situ24,29. This treatment is indicated only in 2 situations: (1) if it will allow a tooth to spontaneously erupt or to be orthodontically guided into a functional position in the arch; or (2) if the surgeon identifies a realistic risk of damaging developing teeth or neurovascular bundles during the enucleation24.

Down’s Syndrome

Down’s syndrome (trisomy 21) is one of the congenital pathologic conditions in which delayed eruption of the teeth is frequently observed. Various studies in children with Down’s syndrome have shown that delayed tooth eruption is common, but sporadic30,31. The eruption usually follows an abnormal sequence and some of the deciduous teeth may be retained until the age of 15 years. The eruption abnormalities are associated with retardation in the growth of maxilla and mandible. A reduction of the anterior skull base and protrusion of lower incisors is often observed, which is related to a tendency to anterior cross-bite and, to a lesser extent, to diminished overbite32.

Balk J Stom, Vol 13, 2009 Factors that Influence Tooth Eruption 13

Cleidocranial Dysplasia

Cleidocranial dysplasia is a hereditary disorder characterized by abnormal clavicles, delayed fusion of the bones in the skull, extra teeth and short stature. Other bones, such as the ribs, pelvis and bones of the hands and feet may also be affected. Most patients with cleidocranial dysplasia do not have significant physical or mental disability33.

The development of the dentition is delayed and may reach the age of 15 years. Oral radiographs usually show many unerupted and supernumerary permanent teeth. Even after extraction of the deciduous or supernumerary tooth, eruption of the permanent dentition may be delayed without the proper orthodontic intervention34.

Hypothyroidism

Undetected and untreated congenital hypothyroidism is a rare condition that leads to mental deficiency and dwarfism. This pathologic entity is known as cretinism. The head of these patients is disproportionately large. They are obese and their extremities are abnormally short. The dentition of the child with cretinism is delayed in all stages, including the primary and the permanent dentition. Due to the small size of the jaws teeth are usually crowded. The tongue is large and often causes anterior open bite and malocclusion. Delayed eruption of the permanent dentition may also be observed in juvenile hypothyroidism (acquired hypothyroidism), which usually occurs between 6 and 12 years of age. Because juvenile hypothyroidisms appears after the period of rapid growth, its orofacial manifestations are more mild compared to congenital hypothyroidism35.

Hypopituitarism

Hypopituarism in children leads to nanism. Characteristic orofacial features are the maldevelopment of the face, the defective development of jaws and the delayed eruption of teeth. Cases of long delays of the absorption of primary teeth roots have been reported, which results in the delay of permanent teeth eruption36. This delay usually lasts 1-3 months for the teeth that erupt during the first decade, and 3 to 10 years for the teeth that erupt during the second decade of life. Another frequent finding is the absence of germs of the third mandibular molars37.

Frohlich’s syndrome, or lipogenetic dystrophy, is usually caused by neoplasms of the pituitary region and

often results in hypopituitarism. The dental findings of the syndrome include delayed eruption of the teeth.

Hutchinson-Gilford disease or progery is caused by anterior pituitary lobe malfunction. Delayed eruption of the teeth is also included in the clinical findings of this disease.

Achondroplastic Dwarfism

Achondroplastic dwarfism is the most common type of dwarfism and is clinically manifested with a characteristic appearance. There are short muscular extremities, brachycephalus, and bowed legs. The oral manifestations include retruded maxilla, disparity in the size of the jaws resulting in malocclusion, and delayed eruption of the teeth38.

References

1. Peretz B, Ram D, Hermida L, Otero MM. Systemic manifestations during eruption of primary teeth in infants. J Dent Child, 2003; 70:170-173.

2. Mc Donald RE, Avery DR. Dentistry for the child and adolescent. 7th ed. St Louis: Mosby, 2000; pp 162-163, 186-187.

3. Kramer IR, Pindborg JJ, Shear M. The World Health Organization histological typing of odontogenic tumours. Introducing the second edition. Eur J Cancer Oral Oncology, 1993; 29:169-171.

4. Kuczek A, Beikler T, Herbst H, Flemming TF. Eruption cyst formation associated with cyclosporin A: a case report. J Clin Periodontol, 2003; 30:462-466.

5. Boj JR, Poirier C, Espasa E, Hernandez M, Jacobson B. Eruption cyst treated with a laser powered hydrokinetic system. J Clin Pediatr Dent, 2006; 30:199-202.

6. Bodner L, Goldstein J, Sarnat H. Eruption cysts: a clinical report of 24 new cases. J Clin Pediatr Dent, 2004; 28:183-186.

7. Aguilo L, Cibrian R, Bagan IV, et al. Eruption cysts: retrospective clinical study of 36 cases. ASDC J Dent Child, 1998; 65:102-106.

8. Chiang ML, Huang WH. Odontogenic keratocyst clinically mimicking an eruption cyst: report of a case. J Oral Pathol Med, 2004; 33:373-375.

9. Nunn JH. Eruption problems: a cautionary tale. J Dent Child, 1993; 60:207–209.

10. Priddy RW, Price C. The so-called eruption sequestrum. Oral Surg Oral Med Oral Pathol, 1984; 58:321-326.

11. Maki K, Ansai T, Nishida I, et al. Eruption sequestrum: x-ray microanalysis and microscopic findings. J Clin Pediatr Dent, 2005; 29:245-247.

12. Ho KH. Eruption sequestrum. Ann Acad Med Singapore, 1986; 15:454-455.

13. Schuler JL, Camm JH,Houston GH. Bilateral eruption sequestra: report of case. ASDC J Dent Child, 1992; 59:70-72.

14 V. Boka et al. Balk J Stom, Vol 13, 2009

14. Yassin OM, Rihani FB. Multiple developmental dental anomalies and hypermobility type Ehlers-Danlos syndrome. J Clin Pediatr Dent, 2006; 30:337-341.

15. Kavvadia K, Pepelassi E, Alexandridis C, et al. Gingival fibromatosis and significant tooth eruption delay in an 11-year-old male: a 30-month follow-up. Int J Pediatr Dent, 2005; 15:294-302.

16. Takagi M, Yamamoto H, Mega H, et al. Heterogeneity in the gingival fibromatoses. Cancer, 1991; 68:2202-2209.

17. Bakaeen G, Scully C. Hereditary gingival fibromatosis in a family with Zimermann- Laband syndrome. J Oral Pathol Med, 1991; 20:457-459.

18. Coletta RD, Graner E. Hereditary gingival fibromatosis: a systematic review. J Periodontol, 2006; 77:753-764.

19. Lata J, Singh R. Idiopathic gingival fibromatosis. A case report. Indian J Dent Res, 2003; 14:234-237.

20. Jorgensson RJ, Cocker ME. Variations in inheritance and expression of gingival fibromatosis. J Periodontol, 1974; 45:472-476.

21. Denloye O, Bankole OO, Aderinokun GA. Teething myths among community health officers. Odontostomatol Trop, 2005; 28:19-22.

22. Gunhan O, Gardner DG, Bostanci H, et al. Familial gingival fibromatosis with unusual histologic findings. J Periodontol, 1995; 66:1008-1011.

23. Odessey EA, Cohn AB, Casper F, Schechter LS. Hereditary gingival fibromatosis: aggressive 2-stage surgical resection in lieu of traditional therapy. Ann Plast Surg, 2006; 57:557-560.

24. Delbem AC, Cunha RF, Afonso RL, Bianco KG, Idem AP. Dentigerous cysts in primary dentition: report of 2 cases. Pediatr Dent, 2006; 28:269-272.

25. Kozelj V, Sotosek B. Inflammatory dentigerous cysts of children treated by tooth extraction and decompression-report of four cases. Br Dent J, 1999; 187:11.

26. Slater LJ. Dentigerous cyst versus paradental cyst versus eruption pocket cyst. J Oral Maxillofac Surg, 2003; 61:149.

27. Naclerio H, Simoes WA, Zindel D, Chilvarquer I, Aparecida TA. Dentigerous cyst associated with an upper permanent central incisor: case report and literature review. J Clin Pediatr Dent, 2002; 26:187-192.

28. Ertas U, Yavuz MS. Interesting eruption of 4 teeth associated with a large dentigerous cyst in mandible by only marsupiulization. J Oral Maxillofac Surg, 2003; 61:728-730.

29. Kavadia-Tsatala S, Tsalikis L, Kaklamanos EG, Sidiropoulou S, Antoniades K. Orthodontic and periodontal considerations in managing teeth exhibiting significant delay in eruption. World J Orthod, 2004; 5:224-229.

30. Jara L, Ondarza A, Blanco R, Valenzuela C. The sequence of eruption of the permanent dentition in a Chilean sample with Down’s syndrome. Arch Oral Biol, 1993; 38:85-89.

31. Ondarza A, Jara L, Munoz P, Blanco R. Sequence of eruption of deciduous dentition in a Chilean sample with Down’s syndrome. Arch Oral Biol, 1997; 42:401-406.

32. Quintanilla JS, Biedma BM, Rodriguez MQ, et al. Cephalometrics in children with Down’s syndrome. Pediatr Radiol, 2002; 32:635-643.

33. Gorlin RJ, Cohen MM, Levin LS. Cleidocranial dysplasia. In: Syndromes of the Head and Neck. 3rd ed. New York: Oxford Press, 1990; pp 249-253.

34. Trimble LD, West RA, McNeil RW. Cleidocranial dysplasia: Comprehensive treatment of the dentofacial abnormalities. J Am Dent Assoc, 1982; 105:661-666.

35. Scully C, Cawson RA. Medical problems in Dentistry. 4th ed. Oxford: Wright, 1998; pp 277-280.

36. Kosowicz J, Rzymski K. Abnormalities of tooth development in pituitary dwarfism. Oral Surg Oral Med Oral Pathol, 1977; 44:853-863.

37. Sarnat H, Kaplan I, Pertzelan A, et al. Comparison of dental findings in patients with isolated growth hormone deficiency treated with human growth hormone (hGH) and in untreated patients with Laron-type dwarfism. Oral Surg Oral Med Oral Pathol, 1988; 66:581-586.

38. Collins WO, Choi SS. Otolaryngologic manifestations of achondroplasia. Arch Otolaryngol Head Neck Surg, 2007; 133:237-244.


Dr. A. MarkopoulosDept. of Oral Medicine and Maxillofacial PathologySchool of Dentistry, Aristotle University54006 Thessaloniki, GreeceE-mail: [email protected]

SUMMARYEarly childhood caries (ECC), as the most common oral disease occur-

ring in infants and pre-school children, is steel very frequent in most Balkan countries. The reason for this is existing old fashion attempt to control it by early diagnosing, preventing its further development by secondary preven-tion, treatment with expensive curative measures without significant success, what leads to conclusion that ECC is a hopeless dental problem. Identification and elimination of caries risk factors before dental treatment is essential for successful caries management. Caries control measures must be establish as a first step towards caries suppression, which will cause long-term chan ges in the surrounding oral environment, with the aim of altering it from being cariogenic to non-cariogenic. Failing to do so, all restorative works done in cariogenic oral environment will stay for a very short period. In clini-cal management of caries, the dentist’s role consists in seeking the cause, correcting bad habits or deficiency states they may be contributing factors, restoring the teeth, and finally, making use of all available preventive and control measures. Therefore, a successful management of the ECC prob-lem demands integrated approach of preventive and restorative measures, such as carefully completed dental and medical history, the use of currently accepted diagnostic aids, application of sound principles of restorative den-tistry, a comprehensive preventive programme, and regular recall appoint-ments for maintenance work and reemphasis of the preventive procedures. Keywords: Early Childhood Caries; Prevention; Rehabilitation

M. Carević, M. Vulović , M. Šindolić

University of Belgrade, Faculty of Dentistry Clinic of Paedodontics and Preventive Dentistry Belgrade, Serbia

REVIEW PAPER (RP)Balk J Stom, 2009; 13:15-20


Integrated Approach in Combating Early Childhood Caries

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Introduction

Early childhood caries (ECC) is a special form of rampant tooth decay that affects primary dentition in infants, toddlers and pre-school children. This type of caries has an early onset (evident in children ≤ 1-year-old) and is initially located on the smooth surfaces of primary teeth, followed by a very fast progression. First signs of ECC are in the form of white-spot lesions on anterior primary teeth, leading quickly to complete tooth destruction, pulp involvement, infections, thus impairing overall child’s health (Fig. 1)15,16.

In direct relation to age and primary teeth eruption chronology, different patterns of ECC were observed. 2 main categories of caries are recognized in children from birth to age 6: (1) ECC is caries on at least one surface

of any primary tooth; (2) Severe ECC is stratified by age and described for each year to age of 6. Criteria for definition of severe ECC are: (a) for children up to 3 years old - present lesion on any smooth surface; (b) for children from 3 to 6 years old - caries lesions and cavities on upper frontal teeth, extracted or filled teeth, dmfs = 4 for age 3, dmfs = 5 for age 4, dmfs = 6 for age 5, respectively. At the workshop that was organized by National Institute of Dental and Craniofacial Research (NIDCR) in 1999, following 4 different ECC patterns were suggested: (1) caries lesion on any surface of maxillary incisors (Fig. 2a); (2) caries lesion on occlusal surface of the first molars; (3) caries lesions in pits and fissures of the second molars, on maxillary lingual and mandibular vestibular surfaces, respectively (Fig. 2b); (4) caries lesions on smooth surfaces of other primary teeth 1,2.

16 M. Carević et al. Balk J Stom, Vol 13, 2009

Earlier attempts to identify causes of ECC were based on limited number of variables, predominantly on nutritional and biological factors. Such research approach resulted with prediction models high in sensitivity, but low in specificity. It became obvious that it is mandatory to take into account interaction of nutritional, biological, cultural, social and environmental factors for better understanding caries risk and caries development in infants and toddlers7,17-19.

ECC is also known as baby bottle tooth decay, nursing bottle caries, milk bottle syndrome, melanodontia, molted teeth and etc. Since ECC is considered as a multifactor infectious disease with behavioural, systemic and social component, the term early childhood caries was adopted lately to emphasize the complexity of etiological factors associated with this disease12,20,34.

Etiological factors contributing to the occurrence of ECC are found to bee parental lack of information regarding the disease, forwarding poor habits to the child, inappropriate feeding practices, poor oral hygiene, inadequate fluoride intake, maternal caries status, socioeconomic status and genetics7,4,18,21-24.

ECC can cause serious problems concerning oral and general health (Fig. 3), such as infections, abscesses, pain, fear, sleeplessness, chewing and eating difficulty, malnutrition, gastrointestinal disorders and other, which can lead to failure to thrive, delay in proper development, malocclusion, poor aesthetics and speech articulation, caries in the permanent dentition, thus affecting child’s quality of life12-14,34.

Despite the recent improvements in the oral health of children, ECC remains to be the most common oral disease in toddlers and pre-school children, presenting a serious challenge to child’s wellbeing. Estimated prevalence in developed countries ranges from 18-25% of children 2-6 year olds, while in some ethnic groups prevalence is as high as 40-45%. (California Department of Health Services, 1995). However, in developing countries and in disadvantaged groups within developed countries, the prevalence could be as high as 70%1,10. The reason for this is the existing approach to control the disease by early diagnosing (absence of widely accepted standards), preventing its progression by secondary prevention, treatment with expensive curative measures which may lead to the conclusion that ECC is a never ending dental problem12,25,26,34.

For many centuries dental decay has been the number one problem in dentistry because dentists have been treating just the consequences of the disease. The tendency has been ever since to treat these patients as one’s that have mechanical dental problems. They therefore had a false belief that restored teeth are equal to good dental health12,27.

Dental caries today is considered to be the result of a disturbance in the ecologic balance of the oral cavity. This balance is resembled by aggressive (demineralization) factors and defensive (re-mineralizing) factors. If and when factors that promote demineralization prevail, the balance will shift in favour of enamel demineralization and the formation of caries lesion12,15,29.

Therefore successful management of ECC must be accomplished by integrated (joint) approach and implementation of the following procedures:1. Conditioning (re-modification) of oral environment (primary prevention);2. Caries treatment (secondary prevention);3. Rehabilitation (tertiary prevention);4. Maintenance of achieved oral health.

Conditioning of Oral Environment (Primary Prevention)

Caries control measures must be establish as a first step towards caries reduction, which will cause long-term changes in the oral environment, with the aim

Figure 1. (a) First signs of ECC; (b) Complete teeth destruction by ECC

Figure 2. (a). Caries lesions on maxillary incisors; (b) Caries lesions on molar surfaces

Figure 3. ECC can cause serious problems

a b

a b

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Balk J Stom, Vol 13, 2009 Early Childhood Caries 17

of transforming it from cariogenic to non-cariogenic. Failing to achieve this, the restorative work done in cariogenic oral environment will have a short-term effect. Collectively, identification and elimination of all (risk) factors prior to dental treatment is essential for successful caries management.

Identification of factors that caused the diseaseTaking into consideration that etiological factors

of oral diseases are relatively well known today, identification of factors that can cause the disease must be made and actions has to be taken in order to neutralize risk that can cause problems in future.

Caries risk for dental caries can be diagnosed and effective measures offered to prevent or reduce the prevalence. At this point, we are able of identifying patient’s level of risk for cavities and utilize specific treatment options to prevent caries from occurring and progressing. To accomplish this task information that we need can be obtained by:

a. Case history;b. Clinical investigation;c. “Caries risk tests”.

A. Case History By interviewing the patient, we are trying to find out

factors that may influence the disease. Such factors usually belong to one or more of the following groups:

- General information about diseases (beside general information about the present oral disease, attention must be focused on existence of general diseases as well. Several diseases may directly or indirectly influence oral diseases, ether through affecting saliva properties, dietary patterns or by use of various medicines);

- Oral hygiene (good or bad);- Use of fluorides (yes or no);- Dietary habits (it is well known that in making up

the “risk profile” of the patient, diet and dietary habits are of great importance. Information about the diet of the patient can bi obtained by the “interview method”, the “three-day record” and by presence of bad feeding/eating habits);

- Drug use (frequent use of sweet medication against certain diseases in early childhood could contribute ECC formation);

- Socio-economic background (the common finding is that families from a lower socio-economic background may experience lack of understanding regarding oral hygiene, increased consumption of high cariogenic diet, vertical transmission of cariogenic bacteria to their children and difficulties in getting proper dental health services).

B. Clinical FindingsThe aim of clinical findings is to get a proper

information about severity of the caries problem. It can

also give us information about motivation and behavioural habits of the child and family to follow recommendations for oral health care.

Caries prevalence can be estimated by noticing: number of teeth missing, number of fillings, and number of cavities, incipient lesions or deep tissue lesions.

Aggravating factors can be checked by noticing: crowded teeth, deep fissures, overhangs, enamel or dentin disturbances (hypocalcification - local, systemic or hereditary disturbance), and acquired tooth defects (abrasion, erosions).

Assessing presence of factors ultimately involved in the caries process

- Oral hygiene - Saliva factors

C. Caries “Chair Side Tests” for Some Selected FactorsAvailable “chair side tests” for identification of caries

risk factors are: plaque accumulation rate test, salivary flow rate test, salivary buffer capacity test, Mutans streptococci level test, and Lactobacilli level test.

Plaque accumulation rate test (Fig. 4) is based on the amount of plaque which deposits within 24 hours after professional tooth cleaning. For estimation of plaque accumulation rate, the simplified “OHI debris index” according to Green and Vermillion can be used.

Figure 4. Plaque accumulation

Figure 5. Salivary buffer capacity test -“Dentobuff”

a b

Salivary flow rate test is a natural first step in obtaining a general information of saliva factors. It can be disturbed by: medication, radiation therapy, salivary stone or other local factors, anorexia nervosa, diabetes mellitus etc.

Salivary buffer capacity test is giving us a general idea about the quality or ability of saliva to control pH of the oral environment in physiological borders. It can be measured by “Dentobuff” kit (Fig. 5).

a b


Fissure sealing should be applied as a primary preventive measure to non-carious and the patients judged to be at some risk to caries formation12,28,32,33.

Caries Treatment (Secondary Prevention)

Following the clinical findings, on the basis of child’s medical history and the treatment needs, a thorough treatment plan must be designed. The most important objective is to get the disease under control as soon as possible.

A clinical protocol for treating ECC includes proper diagnosis and effective disease control. The main objectives for the placement of dental restorations (Fig. 8) are: reconstruction of the lost tooth surfaces, prevention of further complications, regaining basic functions (feeding, speech, phonetic articulation), maintaining space and, finally, aesthetic and communication rehabilitation.

Caries removal and temporization are designed to eliminate the presence of bacteria as quickly as possible. Once the caries lesion is completely removed, restorations

High count of Mutans streptococci in saliva indicates high risk for caries formation. This levels can be recorded by Mutans streptococci level test

High frequency of sucrose consumption and dietary carbohydrates intake causes higher salivary concentrations of Lactobacilli colonies which are most responsible for dental caries formation. the amount of salivary lactobacilli can be measured by Lactobacilli level test using “Dentocult LB” kit (Fig. 6).

Professional tooth-cleaning means removal of all supragingival and clinically visible hard and soft coatings by dentally educated professional personnel.

Topical application of high and low concentrated fluorides is effective for remineralization of early lesion (Fig. 7). The presence of fluorides in oral cavity strongly prejudices the remineralization/demineralization equation towards remineralization. Beside the crystals containing fluoride are more resistant to acid dissolution, it is a highly effective antimicrobial that is specific to acid-producing organisms. Fluoride toothpaste should be used daily at home and fluoride varnish or foam can be applied by the dentist periodically.

a b

Figure 6. Lactobacilli level test - “Dentocult LB”

Figure 7. Fluoride topical application

Figure 8. Caries treatment

Risk factors control (elimination of factors that caused the disease)

Risk factors control, or elimination of factors that caused the disease, can be accomplish by applying professionally instructed home-preventive measures and chair-side prevention programme in order to suppress caries promotion factors and modify oral environment from being high to low risk for ECC occurrence.

A. Professional basis of home-applied preventive measures

Home-applied preventive measures comprise: dietary guidance, oral hygiene counselling and fluoride application on regular basis.

The basic connections between caries and nutrition are well known. The most important basics of practical recommendation on dietary guidance are as follow: correction of bad feeding/eating habits; avoidance of sugar-containing food; the use of sucrose alternatives; and decreasing the frequency of snacks between meals.

First objective of proper oral hygiene counselling is to prevent plaque formation, or to remove it completely as early as possible, which can be seen as a basic caries home-preventive measure.

Use of fluoride-containing preparations in caries prevention is of great importance for improvement of oral health. It can be accomplished by: fluoride-containing dentifrices, fluoride tablets; and home fluorides mouth rinses.

B. Chair side prevention programmeBeside home-applied preventive measures to maintain

achieved oral health, “chair side preventive programme” is recommended as well to keep oral environment at low risk for caries disease for longer time period.

a b

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Balk J Stom, Vol 13, 2009 Early Childhood Caries 19

of lost tooth surfaces are recommended with the use of fluoride-release restorative materials (glass ionomer restorations). Endodontic therapy is performed only if the tooth is restorable. Any tooth that cannot be restored has to be extracted.

The basic idea of radical EEC treatment (tooth extractions) is to: (1) eliminate sources of infections; (2) prevent further infection progression (bacteraemia); and (3) improve child health and the quality of life12,29,34.

Rehabilitation (Tertiary Prevention)

Beside having basic functional problems in terms of chewing and eating, which can cause disturbances in growth and development, the consequences of early tooth loss have shown that social isolation can have a detrimental effect upon a young person general health as well. Obviously, social support plays an important role in enhancing general health-related behaviours, as well as

providing emotional support and enhancing child’s sense of self-worth (in itself important for health).

Similarly to eating problem, speech is also affected. Ability to speak “normally” is one of the primary ways in which one makes contact with others in the surroundings. If ability to speak is affected, clearly, this could have a detrimental effect upon basic social interaction. Such children may increasingly begin to dread occasions when they have to socialize and interact (communicate) with their friends and playmates. This could, in the worst-case scenario, result in withdrawal, social isolation and a negative spiral in which the individual loses confidence in himself and draw further away from the social world.

Therefore, the rationale solution for the rehabilitation of lost oral structures (Fig. 9) in this early life period must provide: proper food consumption, aesthetic and communication rehabilitation, and maintaining space. This can be accomplished with removable space retainers which can serve as small partial prosthetic appliance that can satisfied all the mentioned demands as well29,30,34.

a cbFigure 9. Oral rehabilitation

Maintenance of Achieved Oral Health

Maintenance of the achieved oral health is to be kept further on by regular recalls or check-up visits, performing caries control-preventing programmes, which will consider: (1) evaluation of the effect of casual treatment and rehabilitation; (2) caries risk factors control with comprehensive preventive programs; and (3) prediction and suppression regarding further development or continuation of the disease. Frequency of regular recalls or check-up visits should be organised on individual basis, regarding patients potential risk susceptibility and the already achieved level of oral health rehabilitation30,31.

Conclusion

Combating ECC consists of addressing the cause, correcting bad habits or deficiency that may act as

contributing factors and restoring the function by using all available preventive and control measures. Therefore successful management of early childhood caries demands integrated approach of preventive and restorative measures. These measures include carefully completed dental and medical history, use of currently accepted diagnostic aids, application of comprehensive preventive programs, use of sound principles of restorative dentistry, as well as regular recall appointments in order to maintain health and reemphasize preventive measures.

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35. Levin RP. Marketing and preventive dentistry. In: Professional prevention in dentistry. Advances in dentistry 1. Williams & Wilkins, 1994; 6:143-156.

36. Einwag J. Oral health maintenance by plaque control. In: Professional prevention in dentistry. Advances in dentistry 1. Williams & Wilkins, 1994; 3:71-108.

37. Ernst CP, Willershusen-Zonnchen B. Professional toothcleaning. In: Professional prevention in dentistry. Advances in dentistry 1. Williams & Wilkins, 1994; 5:129-139.

38. Beloica D, et al. Paediatric Dentistry. Belgrade: Elit-Medica, 2003; pp 131-167. (in Serb)


Prof. M. CarevićFaculty of DentistryClinic of Paedodontics and Preventive Dentistry11000 Belgrade, Serbia

SUMMARYThe retention and caries preventive efficacy of light-cured resin-based

fluoride fissure sealant (RBS) in comparison with glass ionomer cement (GIC) were studied during chemotherapy. The survival rates of GIC and RBS were: 44.8% and 51.7% at 3 months, 26.2% and 43.9% at 12 months, respectively. The percentage of fully retained sealants at month 3 was 25.9% in GIC group and 12% in RBS group. At 12 months, the difference between the percentages was insignificant in both groups. The percentage of carious lesions seen in GIC sealant and RBS group was 6.9% at month 3. At month 12, 7.3% carious molar was found in RBS group, whereas the same estima-tion was 19% in GIC group. Regarding caries development on molars at 12 months, in which sealants were fully disappeared at month 3, the percentage was 29.3% for RBS and 33.3% for GIC groups. Caries preventive efficacy and survival rate of GIC were not found superior compared to RBS at the end of 12 months.Keywords: Chemotherapy; Pit-Fissure Sealant; Caries Prevention; Children

Çiğdem Elbek Çubukçu

Uludağ University, Faculty of MedicinePediatric Dental Care UnitBursa, Turkey

ORIGINAL PAPER (OP)Balk J Stom, 2009; 13:21-25


Retention of Glass Ionomer Cement and Resin-Based Fissure Sealant and Their Effect on Caries Outcome During Chemotherapy: A Pilot Study

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Introduction

Various reports have indicated the relationship between dental caries and chemotherapy1-4. These studies suggested that children with malignant diseases had more carious teeth compared to healthy subjects. Depending on the reduced buffer and antibacterial action of saliva encountered during chemotherapy, cariogenic flora increases, and this results in an increased susceptibility to dental caries. This fact indicates the need for preventive strategies to promote dental health and to avoid the development of caries prior to chemotherapy.

A number of caries preventive measures have been developed for children with malignant diseases, as well as the healthy ones2,3,5. These include cleaning tooth surfaces with a toothbrush and a fluoridated toothpaste6,7, application of a fluoride varnish8, application of a chlorhexidine varnish, sealing pits and fissures with a

composite resin and/or a glass ionomer9,10, and different combinations of these preventive measures. Only effective clinical regimen available for preventing occlusal caries is the use of pit-and-fissure sealants11,12.

Pit-and-fissure sealing has been described as a procedure of introducing a material into the occlusal pits and fissures of caries-susceptible teeth, therefore forming a micro-mechanically bonded protective layer that blocks nutrients of caries-producing bacteria13. To the best of our knowledge, neither retention nor caries preventive efficacy of sealing materials has been investigated in children who were on chemotherapy. In the present study, the retention and caries preventive efficacy of glass ionomer cement (GIC) in comparison with light-cured fluoride resin-based sealant (RBS) were studied intra-individually in a period of 1 year in children who were on chemotherapy for solid tumours.

22 Ç.E. Çubukçu Balk J Stom, Vol 13, 2009

Materials and Methods

Sample SelectionEligible subjects among the children diagnosed with

solid tumours between 2002 and 2005 in the Department of Pediatric Oncology, Faculty of Medicine of Uludağ University were included in this prospective clinical study. Criteria for eligibility were as follows: The patient should suffer from solid tumour, be hospitalized for chemotherapy, and had no carious teeth; patients should have no stain and/or soft debris, and supragingival calculus covering not more than one third of their exposed tooth surface14, and should follow the same oral care guideline during the therapy. In order to follow oral care guideline, teeth and tongue were cleaned 4 times a day (after meals and before bed time) with a soft-bristled brush to remove plaque and debris. Once brushing was completed, 10 ml of 8.4% sterile sodium bicarbonate (Drogsan®, Turkey) was administered as a rinse to remove loose debris and to irrigate healthy tissue.

All the first permanent molars should fully be erupted and sound, with absence of mobility due to periodontal disease, and with no evidence of hypoplasia or history of previous sealant application.

Pre-Operative AssessmentThe study was approved by the Ethics Review

Committee of the faculty. Informed written consents were obtained from each family using separate forms written in simple clear native language. A systematic and precise dental examination was performed and the teeth were examined for caries with a No.4 plain mirror and a No.6 right-angle probe.

Assignment of the Teeth to the Study GroupsThe material was randomized with respect to teeth,

mandibular and maxillary, and left and right side. The study consisted of 33 children with a total of 132 molars. 66 maxillary and mandibular first permanent molars were sealed with a RBS (Alpha-Seal®, Dental Technologies, Inc.) and a GIC (Fuji IX®, GC Europe).

Sealant Procedure The sealant procedure was performed on every

child by a resident dentist in Pediatric Dental Care Unit. Following the initial dental examination, the sealant materials were applied on molars of each child in 1 session before chemotherapy has been initiated. The occlusal surfaces of the teeth where RBS material was applied were cleaned with a brush mounted on a low speed engine, washed and dried, and isolated with cotton wool rolls and high volume suction. The teeth were etched for 30 seconds using 37% orthophosphoric acid, washed for 10 seconds, and dried for a further 10 seconds. The occlusal surface was checked for the characteristic chalky white matt

appearance, indicative of appropriate etching. The RBS material was applied by using the tip of a small excavator and cured by applying visible light for 30 seconds using a dental-curing unit (LA 500, Model Blue-light, Apoza Enterprise Co, Taiwan).

The occlusal surfaces of molars where GIC material was applied, was cleaned with a brush mounted on a low speed engine, washed and dried, and isolated with cotton wool rolls and high volume suction. The occlusal surfaces of each tooth were conditioned with polyacrylic acid for 10-15 seconds, and dried for a further 10 seconds. The GIC was applied according to the ART manual15. Subjects were instructed not to eat for at least 1 hour.

Post-Operative AssessmentAfter completion of treatment, 2 calibrated dentists,

who were not operators, carried out the evaluation at 3 months, during intensive chemotherapy, and at 12 months when the therapy was completed using the criteria described by Frencken et al (Table 1)15. The follow-up examination was performed using a No.4 plain mirror and a No.6 right-angle probe. It was decided that if caries was detected clinically in any of the teeth included in the study, the patient would be appointed for restorative care and the specific tooth/teeth would be excluded from the study. The inter-examiner reliability was assessed by examination of an independent sample of sealants of children who attended for reviews (5 molars during each of the 3 and 12 month follow-up periods), by the 2 examiners. Each examiner was unaware of the other examiner’s findings. This ensured a constant check on the reliability of the examiners.

Table 1. Evaluation criteria of the GIC and RBS

Scores Evaluation criteria0 Present, good seal

1 Partly present, visible pits and/or fissures are free of active caries; no sealant needed

2 Partly present, visible pits and/or fissures show signs of active caries; treatment needed

3 Not present, pits and/or fissures show no signs of active caries; no treatment needed

4 Not present, pits and/or fissures show signs of active caries; treatment needed

5 Unable to diagnose

Survival: Scores 0 and 1Failure: Scores 3 and 4Retention: Scores 0, 1, and 2No retention: Scores 3 and 4

Statistical AnalysisThe data were entered into a database, checked for

errors and analyzed using SPSS software (Release 11.0 version). All the data in this study were categorical and

Balk J Stom, Vol 13, 2009 Control of Caries During Chemotherapy 23

Table 3. The number and percentage of sealed teeth lost to follow-up after 3 and 12 month

Sealant material No. placed No. evaluated % lost to follow-upAt 3-months At 12-months At 3-months At 12-months

GIC (Fuji IX®) 66 58 42 12% 36.3%RBS (Alpha-Seal®) 66 58 41 12% 37.9%

Table 4. The cumulative survival percentage of sealants according to the evaluation periods

Time span (months) No. failures No. survival No. transfers(teeth without caries) Survival rate (%/SD)

GIC (Fuji IX®)0-3 32 26 54 44.8/1.23-12 31 11 34 26.2/3.3RBS (Alpha-Seal®)0-3 28 30 54 51.7/1.33-12 23 18 38 43.9/1.6

SD: standard deviationSurvival: Scores 0 and 1Failure: Scores 3 and 4

therefore non-parametric statistics was used. Analysis of the data was carried out using Chi-square test, which is used to assess quantitatively whether or not the observed frequencies differ significantly from those expected on the basis of the null hypothesis. For purposes of analysis of sealant procedure, we considered the tooth and not the patient to be the unit sample. Retention was considered present for the combined scores 0, 1, and 2. Scores 3 and 4 represented no retention. Survival of the sealants placed was identified with the combined scores of 0 and 1. Caries scores 0, 1, and 3 were combined in the analyses as sound. Caries was considered present for the combined scores 2 and 4. A probability value less than 0.05 were considered significant16.

Results

In this study, 33 children who were on chemotherapy for solid tumours (mean age 9.2±1.8 years - 7-14 yr; male/female ratio: 18/15) were included (Tab. 2).

Table 2. Description of the sample

Patient characteristics n

Males 18Females 15Age (years)MeanRange

9.2 yr7-14 yr

Type of cancerMedulloblastomaOsteosarcomaLymphoma

15414

The Number of Molars Evaluated at 3 and 12 Months Follow-Ups

At the beginning of the study, a total of 132 sealants were placed on occlusal surfaces of molar teeth. After 3 months, 116 molars were available in 29 children. 4 children did not attend their follow-up. At evaluation on month 12, there were 21 children available, with a total of 83 molars. Table 3 presents the number and percentage of teeth lost at follow-ups at 3 and 12 months.

Retention Rates at 3 and 12 Months Follow-Ups

Almost 1 out of the 2 RBSs (51.7%) and GIC sealants (44.8%) had found disappeared at evaluation on month 3 (p>0.05). However, the evaluation made at month 12 indicated a survival rate of 43.9% for RBS material, whereas the same estimation was determined to be 26.2 in GIC group, and the difference was significant (Tab. 4). The number of fully retained (score 0) GIC sealants at month 3

was 15 (25.9%), whereas 7 RBS (12%) were fully retained (p<0.05). At evaluation on month 12, fully retention was detected on 3 RBSs out of 41 (7.3%). However, the result was found significantly different (p<0.05) in the 7 GIC sealants out of 42 teeth (16.6%).

Caries Rates at 3 and 12 Months Follow-UpsThe percentages of caries development in GIC

sealant and RBS groups were: 6.9% (n=4 for each group)

24 Ç.E. Çubukçu Balk J Stom, Vol 13, 2009

at 3 months and 19% (n=8) and 7.3% (n=3) at 12 months, respectively. The results obtained on month 12 in GIC group were significantly different (p<0.01) from those obtained on month 3. Additionally, the results obtained on month 12 in GIC and RBS groups were also significantly different (p<0.01) from each other. The percentages of children with carious molars in GIC sealant and RBS groups were: 13.8% (n=4) at 3 months and 28.6% (n=6) at 12 months, respectively. Out of 4 subjects, 1 patient was excluded from the study at month 3 since the patient had developed caries on 4 molar teeth.

Evaluation for Caries Development on Molars on Month 12, in which Sealants were Fully Disappeared (Score 3) at Month 3

The percentages of carious molars in GIC sealant and RBS groups were 7% (n=3) and 2.4% (n=1), respectively. In the RBS group, no caries development was detected in 29.3% of molars (n=12), whereas in the GIC sealant group, it was as high as 33.3%. The difference between the percentages was insignificant (p>0.05).

Discussion

The results of this study provided data on retention and caries preventive efficacy of GIC and RBS applied to children with solid tumours during chemotherapy. In the literature, other investigations on this subject were held only in healthy children from different socioeconomic status17.

The present investigation has preliminary results. Therefore, the power calculation was not performed. However, it was still possible to randomize the sealants over the first molars by the jaw of the mouth. Another important aspect that needs discussion is that the cumulated lost to follow-up observed in the present study was high (37.1%). This can be explained by the fact that children and their parents became too debilitated to stick to regular dental follow-ups during intensive chemotherapy.

Fissure sealant application is one of the preventive measures recommended before the onset of chemotherapy to ameliorate its impact on dental tissues. 2 materials are commonly used as a sealant material: composite resin and glass ionomer. It is generally accepted that composite resin as a sealant retains longer than glass ionomer18-20.

Many researchers demonstrated low retention rates for glass ionomer when it is used as a fissure sealant in periods of 6 months and 7 years20,21. A total retention rate of polyacid-modified resin composite was found 20% after 1-year follow-up18. In our study, RBS indicated a lower complete retention rate (7.3%) from those obtained in the trial conducted by Aranda et al18. Some authors19,21 observed a 10% total retention rate after 3- and 7-year follow-ups of a conventional glass ionomer used as

fissure sealant, thus demonstrated worse results than in this study after 1 years of clinical evaluation (16.6%). The difference between survival rates of these 2 materials was statistically insignificant at the month 3. However, our findings obtained at month 12 clearly indicated that the survival rate of the resin based sealant was significantly higher than that of the glass ionomer material.

To the best of our knowledge, clinical trials related to effectiveness of glass ionomer materials have usually discouraged their use as fissure sealants22,23. But, all of them were held on healthy subjects17. However, the present study investigated the efficacy of this material on patients receiving chemotherapy.

Although, recently published clinical trials have consistently found poorer retention of glass-ionomers than resin-based materials18-21,24,25, there appears no difference in their caries preventive effect over a long period19-21,25,26. Williams et al26 found no difference in the effect on caries 2 or 4 years after the sealant application. However, Forss and Halme21 found an increased risk of caries in glass-ionomer-sealed teeth compared with resin-sealed-teeth after a 7-year follow-up. This later finding is consistent with clinical results of GIC we have reported previously. However, evaluation of caries development on molars where sealants fully disappeared (Score 3) at month 3 were in accordance with the results conducted by Williams et al26.

Chemotherapy regimen of the subjects varied according to the diagnosis, which comprised BFM-95 (Berlin-Frankfurt-Munsten-95), ABVD (Adriamycine-Bleomycine-Vinblastine-DTIC), carboplastine, vincristine, CCNU and/or VP-16 agents. However, the subjects with medulloblastoma (n=15) were provided post radiotherapy chemotherapy. Before chemotherapy was initiated, the children had cranial radiotherapy 180 cGy per day within 5 days (total 5400 cGy irradiation). Then these subjects with this disease (45% of the study population) had carboblastine, vincristine, CCNU and/or VP-16 agents.

Intensive chemotherapy combined with and without therapeutic radiation to the head can result in both short- and long-term debilitating oral side-effects, such as mucositis, loss of salivary function, and taste loss. These side-effects, particularly oral mucositis and loss of salivary function, may cause lowered pH in oral environment and resultant demineralization of enamel, dentinal hypersensitivity, and dental caries27. Therefore, it is logic to assume that the complete retention rates of sealants in children undergoing cancer therapy would be lower compared to healthy children, even they are in high-risk group for dental caries.

All subjects had the same oral care regimen during this highly oral-toxic therapy. It is known that the intensive oral care may not completely eliminate the deteriorative effect of chemotherapy on dental tissues28. Additionally, the subjects and parents may not stick to regular dental care during the therapy. This could be the possible reason of the low survival rates of these 2 materials during chemotherapy (at 3 months).

Balk J Stom, Vol 13, 2009 Control of Caries During Chemotherapy 25

Despite the higher rate of complete retention of GIC sealants at the end of 3 months; their caries preventive effect and survival rate was found unsatisfactory compared to RBS at the end of 12 months. Therefore, application of RBS was recommended as a caries preventive measure in children with malignancy before chemotherapy was initiated. It is obvious that further long-term comparative clinical studies, in which additional measures are established to maintain oral health, such as regular applications of fluoride and artificial saliva, are needed to discuss the longevity of GIC sealant and RBS in the presence of chemotherapy.

Acknowledgements: We express our gratitude to Vedat Gültekin, Doctor of Oral Surgery in the Centre of Oral Health Care of Ministry of Health, and Alper Sönmez, Doctor of Orthodontics in Bursa, for their invaluable help with the evaluation period of the study.

References

1. Duggal MS, Curzon MEJ, Bailey CC, et al. Dental parameters in the long term survivors of childhood cancer compared with siblings. Oral Oncol, 1997; 33:348-353.

2. Joyston-Bechal S. Prevention of dental diseases following radiotherapy and chemotherapy. Int Dent J, 1992; 42:47-53.

3. Sonis S, Kunz A. Impact of improved dental services on the frequency of oral complications of cancer therapy for patients with non head and neck malignancies. Oral Surg Oral Med Oral Pathol, 1988; 65:19-22.

4. Pajari U, Ollila P, Lanning M. Incidence of dental caries in children with acute lymphoblastic leukaemia is related to the therapy used. ASDC J Dent Child, 1995; 62:349-352.

5. Fayle SA, Duggal MS, Williams SA. Oral problems and the dentists’ role in the management of paediatric oncology patients. Dental Update, 1992; 5:152-159.

6. Carvalho JC, Thylstrup A, Ekstrand KR. Results after 3 years of non-operative occlusal caries treatment of erupting first permanent molars. Community Dent Oral Epidemiol, 1992; 20:187-192.

7. Arrow P. Oral hygiene in the control of occlusal caries. Community Dent Oral Epidemiol, 1998; 26:323-330.

8. Zimmer S, Robke FJ, Roulet J-F. Caries prevention with fluoride varnish in a socially deprived community. Community Dent Oral Epidemiol, 1999; 27:103-108.

9. Arrow P, Riordan PJ. Retention and caries-preventive effects of a GIC and a resin-based fissure sealant. Community Dent Oral Epidemiol, 1995; 23:282-285.

10. Morphis TL, Toumba KJ. Retention of two fluoride pit-and-fissure sealants in comparison to a conventional sealant. Int J Paed Dent, 1998; 8:203-208.

11. Weintraub JA. The effectiveness of pit and fissure sealants. J Public Health Dent, 1989; 49:317-330.

12. Simonsen RJ. Retention and effectiveness of dental sealant after 15 years. J Am Dent Assoc, 1991; 122:34-42.

13. Simonsen RJ. Chapter 2: Pit and fissure sealants. In: Clinical Applications of the Acid Etch Technique. 1st ed. Chicago, Ill: Quintessence Publishing Co, 1978; pp 19-42.

14. Oral hygiene index. WHO Oral Health Country/Area Profile Programme, Department of Noncommunicable Diseases Surveillance/Oral Health. Available in: whocollab.od.mah.se/expl/ohigv60.html

15. Frencken JE, Makoni F, Sithole WD. Atraumatic restorative treatment and glass-ionomer sealants in a school oral health programme in Zimbabwe: evaluation after 1 year. Caries Res, 1996; 30:428-433.

16. Armitage P, Berry G. Inferences from proportions. In: Statistical methods in Medical Research. Oxford, UK: Blackwell Scientific Co, 1994; pp 118-132.

17. Ahovuo-Saloranta A, Hiiri A, Nordblad A, Worthington H, Makela M. Pit and fissure sealants for preventing dental decay in the permanent teeth of children and adolescents. Cochrane Database Syst Rev 3: CD001830. Comment in: Evid Based Dent, 5:93-94, 2004.

18. Aranda M, Garcia-Godoy F. Clinical evaluation of the retention and wear of a light-cured pit and fissure glass ionomer sealant. J Clin Pediatr Dent, 1995; 19:273-287.

19. Karlzen-Reuterving G, van Dijken JW. A three-year follow-up of glass ionomer cement and resin fissure sealants. ASDC J Dent Child, 1995; 62: 108-110.

20. Simonsen RJ. Glass ionomer as fissure sealant: A critical review. J Public Health Dent, 1996; 56:146-149.

21. Forss H, Halme E. Retention of a glass ionomer cement and a resin-based fissure sealant and effect on caries outcome after 7 years. Community Dent Oral Epidemiol, 1998; 26:21-25.

22. Komatsu H, Shimokobe H, Kawakami S, Yoshimura M. Caries preventive effect of glass ionomer sealant reapplication: Study presents 3-year results. J Am Dent Assoc, 1994; 125:43-49.

23. Waggoner WF, Siegal M. Pit and fissure sealant application: updating the technique. J Am Dent Assoc, 1996; 127:351-361.

24. Poulsen S, Beiruti N, Sadat N. A comparison of retention and the effect on caries of fissure sealing with a glass-ionomer and a resin-based sealant. Community Dent Oral Epidemiol, 2001; 29:298-301.

25. Mejare I, Mjör IA. Glass ionomer and resin-based fissure sealants: a clinical study. Scand J Dent Res, 1990; 98:345-350.

26. Williams B, Laxton L, Holt RD, Winter GB. Fissure sealants: a 4-year clinical trial comparing experimental glass polyalkenoate cement with a bis glycidil methacrylate resin used as fissure sealants. Br Dent J, 1996; 180:104-108.

27. Jansma J, Vissink A, Spijkervet FLK, Roodenburg JLN, Panders AK, Vermey A, et al. Protocol for the prevention and treatment of oral sequelae resulting from head and neck radiation therapy. Cancer, 1992; 70:2171-2179.

28. Borowski E, Benhamon E, Pico JL, Laplanche A, Margainaud JP, Hayat M. Prevention of oral mucositis in patients treated with high-dose chemotherapy and bone marrow transplantation. A randomized controlled trial comparing two protocols of dental care. Oral Oncol Eur J Cancer, 1994; 30:93-97.


Çiğdem Elbek ÇubukçuPediatric Dental CareUludağ University, Faculty of MedicineBursa, TurkeyE-mail: [email protected]

SUMMARYThe purpose of the present study was to compare the shear bond strength

to human dentin of 2 root canal sealers: Sultan U/P (zinc-oxide euge nol) and 2seal (epoxy resin). The dentin specimens were divided randomly into 2 groups (A, B) of 12 specimens each, and etched with 3 ml of EDTA 17% before rinsing with NaOCl 2.5% and distilled water. The 2 sealers were mixed according to the manufacturer instructions and placed on dentin surfaces. Bond strength was tested using a universal test machine at a cross-head speed of 0.5 mm/min.

Data were analyzed with Student t-test. The results indicated that 2seal presented statistically significant higher values of bond strength than Sultan U/P.Keywords: Shear Bond Strength; Root Canal Sealers

P. Beltes, M. Pashali, N. Economides, C. Gogos

Aristotle University of ThessalonikiFaculty of DentistryThessaloniki, Greece



Shear Bond Strength of 2 Root Canal Sealers to Human Dentin

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Introduction

The main goal of endodontic treatment is the 3-dimensional obturation of the root canal system with biocompatible materials, such as gutta-percha in combination with a sealer. One of the basic properties of a root canal sealer is to have good sealing ability and to adhere firmly to dentinal walls. The inadequate bond strength of a sealer can lead to an increased possibility of subsequent microleakage and failure of endodontic treatment.

Zinc oxide-eugenol (ZOE) sealers have been used widely in clinical praxis and they are based on Grossman’s formula. However, problems regarding their setting time7, microleakage2 and adhesion to dentin6 have been reported. Epoxy resin-based root canal sealers are characterized by the reactive epoxy ring and are polymerized by the breaking of this ring. These sealers have good adhesion to dentin1,3,4,9,12 and this property is improved by the removal of smear layer12. 2-seal is a relatively new epoxy resin-based sealer, and in the literature there is no information about the adhesion of this material to dentin.

The purpose of the present study was to compare the shear bond strength of Sultan U/P (zinc oxide-eugenol sealer, Sultan Chemists, USA) and 2seal (epoxy resin-based sealer) to human root dentin.

Materials and Methods

The dentin substrate was obtained from 12 single-rooted human teeth. The teeth were stored in the distilled water at -20°C. Before use, they were debrided with ultrasonic scalers and washed several times in water. A low-speed diamond disk saw (Isomet, Buehler, USA) was used to cut off the apical and cervical parts of the roots. The remaining sections were split longitudinally in a bucco-lingual direction using the diamond disk. The portions of the root surface where the canal had been located were ground flat against #600 grit SiC paper. Teflon tape with a circular hole 3 mm in diameter was then centred on the dentin surface to standardize the exposed area. The dentin samples were mounted on a single plane shear test assembly, as described by Watanabe et al10.

The dentin specimens were divided randomly into 2 groups (A, B) of 12 specimens each and etched with 3 ml of EDTA 17% (Pulpdent) before rinsing with NaOCl 2.5% and distilled water. Finally, the dentin surfaces were dried with paper points.

The 2 sealers (2seal - group A; Sultan - group B) were mixed according to the manufacturer instructions and placed on dentin surfaces. The entire assemblies (plates, dentin specimens, and bonded materials) were transferred to an incubator (37°C, 100% relative humidity) for 1 month.

Bond strength was tested using a test machine (Accuforce III; Ametec) by subjecting samples to a shear load at a cross-head speed of 0.5 mm/min. The force required to break the bond between the cements and dentin was recorded in kg using a personal computer connected to the testing machine. Shear bond strength was calculated in mega-Pascals (MPa) using the formula BSMPa=MVKg/BA * 9.80665 (where BSMPa= bond strength in MPa, MVKg = measured value in kg, BA= bonding area = π*r2 = 3.14 * 1.52 = 7.065 mm2 and 9.80665 is the equivalent in MPa of kg/mm2).

Data were analyzed with Student t-test. The selected level of significance was 0.01.

Results

The results are presented in figure 1. The mean shear bond strength in group A (2seal) was 5.43 MPa ± 1.53 and in group B (Sultan) was 1.97 MPa ± 0.75.

Statistical analysis showed that there a was a statistically significant difference between the 2 groups (p<0.01).

Figure 1. Means (MPa) and SDs of the experimental groups

Discussion

Many different methods have been used for measuring the adhesion of endodontic sealers. These methods include tensile strength test, shear testing and push-out test. However, none of them seems to be generally accepted.

The shear test is a common method for the bond strength evaluation. The main problem with this test is the difficulty in the placement of the shear-loading device in close alignment with the bond interface. The load is offset at some distance from the bonded interface, resulting in unpredictable torque loading of the specimen. The single plane shear test assembly, as used in the present

study, fixes the shear loading device in-line with the bond interface zone and applies the stress through this zone in a specific plane, thereby minimizing the offsetting problem11.

In this study the dentin substrate was pre-treated with NaOCl and EDTA. This combination removes the smear layer from the dentin surface and permits the penetration of sealers into the dentinal tubules, allowing the creation of mechanical interlocking which may increase the bond strength values8.

The best results in the present study were observed in the 2seal group. There was a statistically significant difference in bond strength between 2seal and Sultan.

The epoxy resin-based sealers in many studies have shown that they have both good sealing ability and high bond strength to dentin. Lee et al6 compared the adhesion of 4 root canal sealers both to dentin and gutta-percha. The sealers evaluated were a ZOE root canal sealer (Kerr), an epoxy resin-based root canal sealer (AH-26), a calcium hydroxide sealer (Sealapex) and a glass-ionomer sealer (Ketac-Endo). AH-26 sealer gave better results than the other materials, with statistically significant differences. In another study, the Topseal, an epoxy resin sealer, showed higher adhesion than Endion and CRCS, although the best results were obtained with Fibrefill (a methacrylate resin-based sealer)4.

The results obtained with epoxy resin-based sealers may be associated with their ability to react with any exposed amino groups in collagen to form covalent bonds between the resin and collagen when the epoxide ring opens6, although other mechanisms may also contribute to the observed bond strength.

The results of the present study showed that, the adhesion between Sultan and dentin was very weak. This finding is in agreement with the results of Gettleman et al3 who found that AH-26 bonded to dentin better than Sultan. One potential problem with the ZOE sealers is their long setting time7, which may contribute to their low adhesion to dentin.

It should be stated that the adhesive properties of sealers can not be correlated directly with microleakage; however, the weak bonding of ZOE sealers to dentin may explain their lower sealing ability than epoxy resin sealers2,5.

References

1. De Gee AJ, Wu MK, Wesselink PR. Sealing properties of Ketac-Endo glass ionomer cement and AH26 root canal sealers. Int Endod J, 1994; 27:239-244.

2. Economides N, Liolios E, Kolokuris I. Beltes P. Long-term evaluation of the influence of smear layer removal on the sealing ability of different sealers. J Endod, 1999; 25:123-125.

5.43 ± 1.97

1.53 ± 0.75

0

1

2

3

4

5

6

7

8

MPa

2seal

Sultan

Balk J Stom, Vol 13, 2009 Root Canal Sealers and Human Dentin 27

28 P. Beltes et al. Balk J Stom, Vol 13, 2009

3. Gettleman BH, Messer HH, El Deeb ME. Adhesion of sealer cements to dentin with and without the smear layer. J Endod, 1991; 17:15-20.

4. Gogos C, Economides N, Stavrianos C, Kolokouris I, Kokorikos I. Adhesion of a new methacrylate resin-based sealer to human dentin. J Endod, 2004; 30:238-240.

5. Khayat A, Jahanbin A. The influence of smear layer on coronal leakage of Roth 801 and AH26 root canal sealers. Aust Endod J, 2005; 31:66-68.

6. Lee KW, Williams MC, Camps JJ, Pashley DH. Adhesion of endodontic sealers to dentin and gutta-percha. J Endod, 2002; 28:684-688.

7. Mazinis E, Eliades G, Lambrianides T. An FTIR study of the setting reaction of various endodontic sealers. J Endod, 2007; 33:616-620.

8. Saleh IM, Ruyter IE, Haapasalo M, Orstavik D. The effects of dentine pretreatment on the adhesion of root-canal sealers. Int Endod J, 2002; 35:859-866.

9. Tagger M, Tagger E, Tjan AH, Bakland LK. Measurement of adhesion of endodontic sealers to dentin. J Endod, 2002; 28:351-354.

10. Watanabe LG, Marshall GW Jr, Marshall SJ. Dentin shear strength: effects of tubule orientation and intratooth location. Dent Mater, 1996; 12:109-115.

11. Watanabe LG, Marshall G Jr, Marshall SJ. Variables influence on shear bond strength testing to dentin. In: Tagami J, Prati C (eds). Advanced adhesive dentistry. Granada International Symposium, 3-4 December 1999, Como: Kuraray Co, 2000; pp 75-90.

12. Wennberg A, Orstavik D. Adhesion of root canal sealers to bovine dentine and gutta-percha. Int Endod J, 1990; 23:13-19.


Dr. Christos GogosAristotle University Faculty of DentistryThessaloniki, GreeceE-mail: [email protected]

SUMMARYThe aim of this study was to examine restored human teeth in order to

evaluate tissue changes in primary dentin or in primary-secondary dentin continuum. 16 non-carious and restored human molars were used. All teeth were processed for scanning electron microscopic (SEM) analysis. Analysis was focalised at 3 parts of the dentin matrix; at the dentin-restoration inter-face, at the middle part of the remaining dentinal thickness and at the dentin-pulp interface.

The results showed that in most cases dentinal tubules were wide open, from the dentin-restoration interface to the dentin-pulp interface. No sign of dentinal sclerosis or tubular obturation was found. Consequently, dentinal tubules could provide a pathway for bacteria to penetrate the dentin pulp complex. Nevertheless, dentinal tubules under composite resin restorations seemed to have been sealed by the composite material, at the dentin-resto-ration interface. Parameters like the age of the patient, the reason of extrac-tion or longevity of restoration did not, indirectly, affect by any way dentin continuum. In general, it can be concluded that unlike previously reported studies, dentinal sclerosis was absent in most of the teeth studied.Keywords: Dentin Pulp Complex; Pulp Inflammation; Tubule Obturation; Restorative Material

K. Kodonas

Aristotle University, School of DentistryDepartment of EndodontologyThessaloniki, Greece



Intra-Tubular Reactions in Restored Human Teeth:A SEM Study

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Introduction

The bulk of the structure of the tooth, both crown and root, is made up of a mineralized tissue known as dentin1. The most prominent features of dentin are the dentinal tubules1,2. In the periphery, there are approximately 10.000 to 25.000 tubules per square millimeter with a diameter of 0.5μm. On the contrary, near the pulp there are about 45.000-90.000 tubules per square millimeter, each having a diameter of 2.5 to 3μm2,3. Thus, from a clinical point of view, it should be recognized that dentin beneath a deep cavity preparation is much more permeable than dentin underlying a shallow cavity3.

During time, dentinal tubules progressively narrow by the deposition of peritubular dentin in their walls1,4. Additionally, dentinal tubules could be blocked by the precipitation of hydroxyapatite and whitlockite crystals within their structure. These biologic procedures represent dentinal sclerosis3. Partial or complete obturation of

dentinal tubules may occur as a result of aging, dental caries, or can develop in response to any kind of stimuli, including the affect of some properties of the restorative materials used3,5-7.

Biologic reactions in dentin pulp complex must be at the centre of attention in restorative dentistry7-9. With all the steps involved in restorative procedure, it is apparent that the biologic effects on dental tissues are multifactorial and the effect from 1 factor alone is impossible to separate from the combined effect of all factors8.

Many investigators have studied the effect of dental materials on mineralized dental tissues. Some data are available on the effect of amalgam, resin composite, zinc oxide eugenol cement, and calcium hydroxide on dentin8. Besides chemical toxicity, some of the properties of the materials used that are capable of producing injury include acidity, absorption of water, production of heat during setting, or poor marginal adaptation10-12. The aim of this study was to examine non-carious and restored human

30 K. Kodonas Balk J Stom, Vol 13, 2009

teeth in order to evaluate tissue changes in primary dentin or in primary-secondary dentin continuum.

Materials and Method

16 volunteers of both sexes, ranging in age from 12 to 72 years, enrolled the study. All had been scheduled to undergo tooth extraction for various therapeutic reasons, including orthodontic therapy, prosthetic rehabilitation or periodontal treatment. In all cases the extracted teeth were molars. Each tooth carried an amalgam or resin composite restoration, had no sign of clinically, or by x-ray, diagnosed secondary caries, and no sign of pulp necrosis, as pulp vitality tests indicated.

Teeth were previously denuded of any soft tissue and stored in 10% formalin. The apical third of the root was removed in order the specimen to consolidate fast. After teeth were vertically sectioned in 2 by a mechanical fracture, they were cleaned in water, immersed in 0.5% sodium hypochlorite solution and gradually dehydrated in alcohol.

Table 1. Teeth processed for SEM evaluation

Groups Number of teeth Restorative materialA 7 5 amalgam, 2 compositeB 6 5 amalgam, 1 compositeC 3 1 amalgam, 2 composite

Table 2. Specimen details

Teeth Reason ofextraction Pain symptoms* Age

A1 periodontitis no 66A2 prosthetic no 52A3 periodontitis no 58A4 prosthetic no 72A5 prosthetic no 52A6 prosthetic no 63A7 periodontitis no 53B1 periodontitis no 38B2 unknown no 34B3 prosthetic no 37B4 periodontitis no 40B5 prosthetic no 35B6 prosthetic no 33C1 orthodontic no 12C2 orthodontic no 15C3 orthodontic no 13

*Vitality tests took place when needed

Teeth were divided into 3 groups according to the patient’s age. In group A patients were at least 40 years old, in group B between 20 and 40 years old, and in group C they were at most 20 years old (Tab. 1). For each the extracted tooth, details concerning the reason of extraction, the presence of symptoms, or longevity of restoration were recorded (Tab. 2).

All teeth were processed for scanning electron microscopic analysis in a JEOL JSM-840 A SEM. When needed, Energy Dispersive (EDS) analysis was performed for qualitative examination of the chemical composition of the material at the tooth-restoration interfaces. In all cases SEM analysis was focused at 3 parts of the dentin matrix; at the dentin-restoration interface, at the middle part of the remaining dentinal thickness and at the dentin-pulp interface (Fig. 1).

Figure 1. Parts that analysis was focalized at (specimen A1). (a) dentin-restoration interface, (b) middle part of the remaining dentinal thickness,

(c) dentin-pulp interface.

Results

The results of the SEM analysis showed that dentinal tubules were wide open in most of the cases. No sign of dentinal sclerosis or tubular obturation was found (Tab. 3). Occlusion of dentinal tubules was absent, not only at the dentin-restoration interface, but also at the middle part of dentin and at the dentin-pulp interface. In some cases (specimen B3, A4, B4), it was quite obvious that their structural continuity formed a wide pathway towards the pulp chamber (Fig. 2).

The protective cavity base or liner used under amalgam restoration could not be easily identified using EDS analysis. Nevertheless, no sign of dentinal sclerosis was found under the cavity base application sites.

Balk J Stom, Vol 13, 2009 Intra-Tubular Reactions in Restored Teeth 31

Discussion

No material that has been developed to date is ideal for all situations, nor is any absolutely perfect for any one situation13. It has long been recognized that dentinal tubules are the main pathways from any prepared surface to the pulp8. Consequently, occlusion of dentinal tubules reduces dentin permeability and eliminates pulpal reactions to restorative procedures and materials1,3,8. As stated before, tissue changes in dentin continuum may occur as an accelerated formation of peri-tubular dentin or by the precipitation of dissolved mineral salts within the tubules3,8. Additionally, mechanical obturation of dentinal tubules may be achieved by the application of adhesive filling materials8.

Table 3. Results of electron microscopic analysis

Teeth Restorative material Open tubules EDS analysis

A1 amalgam + Ca , P , ZnA2 amalgam + Ca , PA3 amalgam + Ca(0H)2A4 amalgam + ZnA5 resin composite - Ca , PA6 amalgam + Ca , P , ZnA7 resin composite - Ca , PB1 amalgam + Ca , P , ZnB2 amalgam + Ca , P , ZnB3 amalgam + Ca , P , ZnB4 amalgam + Zn , Sr, SnB5 amalgam + Ca , P , ZnB6 resin composite - Ca , PC1 amalgam + Ca , P , ZnC2 resin composite - Ca , PC3 resin composite - Ca , P

In 5 cases (specimens A5, A7, B6, C2, C3), where the restorative material was composite resin, it was obvious that tubules at the dentin restoration interface were infiltrated by the resin monomer. Thus, tubules seemed to have been sealed, but only at that specific part of dentin. The rest dentinal matrix and the dentin-pulp interface showed tubules being open, with no sign of obturation or infiltration by any kind of material (Figs. 3 and 4).

Figure 3. Dentin-restoration interface (specimen A5)

Figure 4. Detail of figure 3

Figure 2. Occlusion of dentinal tubules was absent not only at the dentin-restoration interface (a), but also at the middle part of dentin (b) and at the dentin-pulp interface (c) (specimen B2)


These biological changes in dentin seem to be multifactorial as they depend on many factors, including the type of the material used. Amalgam, still widely used in restorative dentistry, is not considered injurious to the pulp, but requires protection in deep cavities14,15. In spite of its limitations, it is very popular because of its strength, longevity, low cost and relatively ease of handling16. One of the most significant disadvantages of amalgam that leads to marginal leakage is lack of adhesion to tooth structure. Amalgam may also discolour dentin because of penetration of mercury8. Nevertheless, that is unlikely to initiate any biologic reaction in dentin and is of no importance compared with the amount of mercury released in the oral cavity8.

Resin based materials are included among direct adhesive restorative materials. To achieve optimal bonding to dentin, the adhesive must penetrate the de-mineralized dentin, enter the dentinal tubules and their branches and then be polymerized8. Beside the variety of the different bonding systems that are commercially available, they all have a unique bonding protocol. In detail, phosphoric acid etching removes the smear layer and de-mineralizes dentin. After conditioning of dentin with acid solution,

a collagen fibril network is exposed8. Resin monomers are then infiltrated into the collagen network as the primer and resin or a combined primer-resin is applied8. However, some concerns remain about pulpal reactions, hypersensitivity and longevity of restoration of this material17,18. Specifically, it has been well documented that using composite resin as a filling material, without a protective base or liner, in deep cavities could impair irreversible pulp damage, due to the diffusion of un-polymerized and toxic components of the material to the pulp through the remaining dentin17,18.

Apart from toxic or allergenic agents in restorative materials, bacteria and their products are also capable of eliciting an inflammatory reaction19,20. The invasion of dentinal tubules by oral bacteria has been clearly demonstrated by many in vivo and in vitro studies21,22. Thus, bacteria present within dentinal tubules may be responsible for pulp infection. In this study, dentinal tubules could provide a pathway for bacteria to penetrate the dentin pulp complex23. In detail, the tubule width, as estimated by SEM, was more than 0.5μm, which is the average diameter of many bacteria species23 (Figs. 5 and 6).

Figure 5. Detail of 3 dentinal tubules with no sign of obturation (specimen B4)

Figure 6. Application site of Ca(OH)2 , with no sign of tubular occlusion (specimen A3)

Unlike previously published data, in this report it is well shown that obturation of dentinal tubules did not occur apart from 5 cases, when resin composite was used as a filling material5. In these cases obturation took place only at the dentin-restoration interface (Figs. 3 and 4). These data are completely justified considering the nature of resin based composite adhesion to dentin. Doubtless, the results found in 5 teeth restored with resin composite indicate a surface seal but not institute anything more.

In this report, parameters like the age of the patient, the reason of the extraction or longevity of restoration did not, indirectly, affect by any way dentin continuum. The

most important factor seemed to be the type of the filling material used in each case.

Information about the base cements and liners used in the tested teeth is limited. Generally, it has been documented that zinc oxide-eugenol cements inhibit bacterial growth and promote slight, but statistically significant, increase in hardness on cavity walls8,10. Calcium hydroxide is a substance that promotes limited sclerosis when applied to dentin24. Sclerosis is caused by the precipitation of a crystalline material produced by calcium ions within dentinal tubules24-26. Additionally, it has important but time limited antibacterial effect,

Balk J Stom, Vol 13, 2009 Intra-Tubular Reactions in Restored Teeth 33

attributed to its high PH25-27. On the other hand, glass-ionomer cements have advantages including chemical bonding to mineralized tissues and release of fluorides to the dentin-material interface28.

In this study, EDS analysis showed that most of the intermediate materials used were eugenol based. At all cases, no sign of tubular obturation was found under the cavity base application sites. Additionally, no precipitation of crystalline material occurred when calcium hydroxide was used (Fig. 6). However, it should be well understood that there are other factors determining biological changes at the dentin-base interface, such as the application procedure followed in each case.

Unexceptionably, the procedure followed by each dentist affects the interplay between injury, defence and repair, events of dentin pulp complex15,29. In all cases where amalgam was used, parameters like possible lack of condensation or the low degree of perfection of easily purchasable materials used, contribute to our findings. Nevertheless, it should be well recognised that in order to achieve a surface seal under a restoration, not only materials used should be standardized by international associations, but new materials that provide optimal bonding with dentin should be preferable.

Acknowledgments: The author wishes to express sincere appreciation to Professor Dimitrios Tziafas for his instruction and guidance in this study.

References

1. Olgart L, Bergenholtz G. The dentin pulp complex: responses to adverse influences. In: Bergenholtz G, Horsted P, Reit C (ed). Textbook of Edodontology. Oxford: Blackwell Publishing, 2003; pp 21-42.

2. Mjor I, Sveen O, Heyeraas K. Pulp dentin biology in restorative dentistry. Part 1: Normal structure and physiology. Quintessence Int, 2001; 32:427-446.

3. Trowbridge H, Kim S, Suda H. Structure and functions of the dentin pulp complex. In: Cohen S, Burns S (ed). Pathways of the Pulp. 8th ed. Philadelphia: CV Mosby, 2002; pp 411-455.

4. Morse D. Age-related changes of the dental pulp complex and their relationship to systemic aging. Oral Surg Oral Med Oral Pathol, 1991; 72:721-745.

5. Klinge R. The ultra structure of copper amalgam-covered dentin from human deciduous teeth. Acta Odontol Scand, 1993; 51:223-228.

6. Orchardson R, Gillam D. Managing dentin hypersensitivity. J Am Dent Assoc, 2006; 137:990-998.

7. Hahn C, Liewehr F. Relationships between caries bacteria, host responses, and clinical signs and symptoms of pulpitis. J Endod, 2007; 33:213-219.

8. Mjor I, Ferrari M. Pulp dentin biology in restorative dentistry. Part 6. Reactions to restorative materials, tooth restoration interfaces and adhesive techniques. Quintessence Int, 2002; 33:35-62.

9. Mjor I. Pulp dentin biology in restorative dentistry. Part 2: Initial reactions to preparation of teeth for restorative procedures. Quintessence Int, 2001; 32:537-553.

10. Smith A, Murray P, Cox C. Bacterial microleakage and pulp inflammation associated with various restorative materials. Dent Mater, 2002; 18:470-478.

11. Ngo N, Mount G, Peters M. A study of a glass ionomer cement and its interface with enamel and dentin using a low temperature, high-resolution scanning electron microscopic technique. Quintessence Int, 1997; 28:63-69.

12. Demarco P, Tarquino S, Jaeger M, Matson K. Pulp response and cytotoxicity evaluation of 2 dentin bonding agents. Quintessence Int, 2001; 32:211-218.

13. Hilton T. Cavity sealers, liners, and bases: current philosophies and indications for use. Oper Dent, 1996; 21:134-146.

14. Wisithphrom K, Murray PE, About I, Windsor LJ. Interactions between cavity preparation and restoration events and their effects on pulp vitality. Int J Periodontics Restorative Dent, 2006; 26:596-605.

15. Tyler D, Thurmeier J. Amalgam Bonding. Visualization and clinical implications of adhesive displacement during amalgam condensation. Oper Dent, 2001; 26:81-86.

16. Marchiori S, Baratiery L, Andrada M, Monteiro S, Ritter A. The use of liners under amalgam restorations: An in vitro study on marginal leakage. Quintessence Int, 1998; 29:637-641.

17. Seki Y, Shimada Y, Foxton RM, Tagami J. Pulpal response to a newly developed MMA based resin cement for bonding tooth-colored indirect restorations. Am J Dent, 2006; 19:297-302.

18. Huang FM, Chang YC. Cytotoxicity of resin-based restorative materials on human pulp cell cultures. Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 2002; 94:361-365.

19. Pashley DH, Pashley EL, Carvalho RM, Tay FR. The effects of dentin permeability on restorative dentistry. Dent Clin North Am, 2002; 46:211-245.

20. Cox CF, Hafez AA. Biocomposition and reaction of pulp tissues to restorative treatments. Dent Clin North Am, 2001; 45:31-48.

21. Love R, McMillan MD, Park Y, Jenkinson HF. Coinvasion of dentinal tubules by Porphyromonas gingivalis and Streptococcus gordonii depends upon binding specificity of streptococcal antigen I/II adhesion. Infect Immun, 2000; 68:1359-1365.

22. Love R. The effect of tissue molecules on bacterial invasion of dentine. Oral Microbiol Immunol, 2002; 17:32-37.

23. Love R, Jenkinson H. Invasion of dentinal tubules by oral bacteria. Crit Rev Oral Biol, 2002; 13:171-183.

24. Tronstad L. Reaction of the exposed pulp to Dycal treatment. Oral Surg Oral Med Oral Pathol, 1974; 38:945-953.


25. Olsson H, Petersson K, Rohlin M. Formation of a hard tissue barrier after pulp cappings in humans. A systematic review. Int Endod J, 2006; 39:429-442.

26. Ranly D, Garcia F. Current and potential pulp therapies for primary and young permanent teeth. J Dent, 2000; 28:153-161.

27. Smith A. Pulpal responses to caries and dental repair. Caries Res, 2002; 36:223-232.

28. Smith D. Development of glass-ionomer cement systems. Biomaterials, 1998; 19:467-478.

29. Singer L. Evidence-based dental plans: dentistry’s future is now. J Am Coll Dent, 1999; 66:21-26.


K.KodonasKaukasou 2654632, Sykies ThessalonikiGreeceE-mail: [email protected]

SUMMARYBackground. Silicone-based soft lining materials have been found to

be more susceptible to Candidal adhesion. Denture hygiene is essential to maintain the serviceability of the denture, and denture cleaners have been suggested for denture disinfection.

Purpose. The purposes of this study were to investigate the Candida albicans adhesion, and determine the effectiveness of peroxide-type denture cleaners in the disinfection of silicone-based soft lining materials.

Material and Methods. 2 different silicone-based soft lining mate-rials have been used in this study (Molloplast-B and Luci-Sof). For each soft lining materials, 7 specimens have been prepared (10mm×10mm×3mm in diameter). Sterile specimens have been contaminated with Candida albicans and immersed in 4 different denture cleaners (Efferdent, Polident, Steradent, Correga tabs). The reduction in viable, adherent cells have been calculated by comparison with appropriate control specimens that have been treated in same way as test specimens, but without a disinfection regime.

Results. Both soft liners showed Candidal adherence, but Luci-Sof soft liner exhibited higher Candidal adherence than Molloplast-B soft liner. Alkaline peroxide-type denture cleaners have been found effective in the dis-infection of silicone-based soft liners contaminated with C. albicans.

Conclusion. Alkaline peroxide-type denture cleansers can be used in order to maintain effective denture hygiene.

Clinical Implications. Heat cured silicone based soft liners materials could be safely disinfected with alkaline peroxide type denture cleansers.Keywords: Denture Cleansers; Soft Lining Materials; Candida Albicans

Hale Gedik1, Yasemin Kulak Özkan2

1Haydarpaşa Hospital, Istanbul, Turkey2University of MarmaraDepartment of Prosthetic DentistryIstanbul, Turkey

ORIGINAL PAPER (OP)Bakj J Stom, 2009; 13:35-40


Cleaning Efficiency of Alkaline Peroxide Type Denture Cleansers on Silicone-Based Soft Lining Materials Colonized With Candida Albicans

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Introduction

Resilient denture lining materials are widely used in prosthetic dentistry because they can assist the clinician in restoring health to the inflamed and distorted denture supporting tissues1-5. However, these materials have some physical and microbial disadvantages. One of the most serious problems has been colonisation and infection of the material surface by Candida albicans and related Candida species, resulting in the denture induced stomatitis. Also, effective denture plague control is indispensable for clinical use of these materials, because bacterial and yeast

plaque is a major factor of denture stomatitis6-17. Denture plaque is important factor in the pathogenesis of denture stomatitis18-20. Therefore, denture cleansing should include removal of Candida organisms that have been reported to be closely related to the disease 6,21.

Chemical cleansing with immersion denture cleansers is suggested as the first choice for plaque control with these soft-lining materials, since brushing is likely to damage the liners, and ultrasonic treatment per se is not effective22-24. Also, geriatric or handicapped denture wearers can use chemical cleansers more advantageously24-26.

36 H. Gedik, Y.K. Özkan Balk J Stom, Vol 13, 2009

A variety of experimental approaches have been tested in attempt to examine the efficacy of denture cleansers. Some authors have investigated the minimal inhibitory or minimal bactericidal concentration of these agents27, while others have examined the fungicidal effects28,30, Candida lytic effects28-30, or the agents’ ability to remove attached Candida cells from acrylic resins 25-27.

Many types of cleansers have been commercialised; sparse data are available on the efficacy of denture cleansing agents. These agents may be classified as alkaline peroxides, neutral peroxide with enzymes, crude drugs, acid detergents, and mouthrinses for dentures31.

The purposes of this study were to examine: (1) the ability of Candida albicans to adhere to 2 permanent soft liners; and (2) the effectiveness of alkaline peroxide-type denture cleansers in the disinfection of long-term soft lining materials contaminated with Candida albicans.

Material and Methods

Preparation of Specimens2 heat-cured soft lining materials (Molloplast-B,

Regneri GmbH and Co; and Luci-Sof, Dentsply,) were used in this study (Tab. 1). Square of specimens for each soft liners were prepared (10mm×10mm×3mm) and polymerized according to recommendation of the manufacturer. They were prepared in a stainless-steel mould with highly polished surfaces to produce reproducible results. All specimens were saturated with sterile water for 24 hours at room temperature32-34. Specimens for each soft liner were randomly divided into 5 subgroups; 4 of test and 1 of control (n: 7).

Table 1. Type and manufacturer of soft denture materials

Material Type Manufacturer Molloplast-B (Group I)

Heat-cured silicone rubber Regneri GmbH and Co.

Luci-Sof (Group II)

Heat-cured silicone rubber Dentsply, IntL, Pa.

Preparation of Candida AlbicansA reference C. albicans (ATCC 2091, Istanbul

University, School of Medicine, Kükens) was used to investigate the efficacy of disinfection. Candida strains were incubated in Sabouraud’s broth supplemented with sucrose 500 mmol/L overnight at 37°C. This medium was used because previous studies have shown increased Candidal adherence to acrylic resin after culture in Sabouraud’s broth supplemented with sucrose34. Candidal growth was harvested after 24 hours by centrifugation (3000 g 15 minutes, 10ºC). The Candidal cells were

washed in phosphate-buffered saline solution (PBS), 0.15 mol/L, pH 7.234,35. This procedure was repeated 2 times.

Adherence AssayThe principle of the experiment was to contaminate

sterile specimens of Molloplast-B and Luci-Sof soft lining materials with Candida albicans and to determine any reduction in count of viable adherent cells after test disinfection regimes. The reduction in viable, adherent cells were calculated by comparison with appropriate control specimens that were treated in the same way as test specimens, but without a disinfection regime36. At the commencement of the experiment, specimens were autoclaved at a temperature of 121ºC for 15 minutes. Sterile specimens were deposited in 20 ml yeast suspensions inserting the sterile universal bottles. They were incubated for 1 hour at room temperature to provide the adherence of Candida albicans34,35,37,38. All specimens were washed with PBS for 1 minute.

Table 2. Type and manufacturers of denture cleansers

Material Type Manufacturer

Efferdent (A) Alkaline-peroxide Warner-Lambert, NJ

Polident double action (B) Alkaline-peroxide Block Drug, NJ

Steradent triple action (C) Alkaline-peroxide Reckitt & Colman

Ltd, NJ

Correga (D) Alkaline-peroxide Stafford-Miller Ltd, UK

ProcedureControl groups were stored in 40 ml sterile distilled

water for 2 hours before fixation period. Disinfection regimes were carried out for each test group34. 4 denture cleaners (Efferdent - A, Polident duble action - B, Steradent triple action - C , and Correga - D) were used for the disinfection regime. Denture cleaner solutions were prepared according to manufacturers’ instructions. The test specimens were immersed in 40 ml of disinfection solutions in sterile universal bottles at 37ºC for 2 hours39-41 .

All specimens were washed twice with PBS (Phosphate Buffer Solutions) with gentle rocking to remove non-adherent cells after discarding disinfection solutions and sterile water. Excess of PBS solution was drained from specimens. After they were dried, adherent cells were fixed in methanol, stained with crystal violet and examined by light microscopy. Adherent cells in 30 fields of view (0.25 mm2 per field) were enumerated by light microscopy and the results were expressed as yeast cells/mm2 of material remaining after each cleanser in comparison with the control group34,39. Scheffe F-test was used to analyze the data.

Balk J Stom, Vol 13, 2009 Cleaning Efficiency of Alkaline Peroxide Cleaners 37

Results

Both soft liners showed Candidal adherence. At disinfection period, inhibition was observed for Candida albicans for both tested soft lining materials. Table 3 shows the mean and standard deviation values of Candida albicans adherence to the silicone-based soft lining materials before and after the disinfection. Before

disinfection, adhesion of Candida albicans to the Luci-Sof soft liner was found statistically higher than to the Molloplast-B in control groups (p<0.0001). There were statistical differences between the soft liners and denture cleansers (Tab. 4). After disinfection, Cleaner B showed the highest cleaning efficiency for the 2 tested lining materials. However, Cleaner D and A was found the least effective for Group 1 and 2, respectively (Tab. 5).

Table 3. Mean and SD of the tested materials

Denture cleanser Control A B C D Totals

Group 1 7130 (35)

730 (26)

721(7)

732(19)

733(26) 35

49

Group 2 7486 (123)

7286 (169)

7141 (76)

7183 (152)

7196 (97)

35258

Totals 14 308

1481

14114

14108

14158

70154

Table 4. Two-way ANOVA results

Source df Sum of square Mean square F-test P valueMollo-Luci (A) 1 764836 764836 9 0.0001Denture cleansers (B) 4 457966 114492 13 0.0001AB 4 129717 32429 4 0.0079Error 60 510067 8501

Table 5. Scheffe-F tests results; comparison denture cleanser and soft lining materials

Denture cleansers Molloplast-B denture liners

Lucisoft denture liners.

Co. vs B S SCo. vs D S SCo. vs C S SCo. vs A S SB vs D NS NSB vs C NS NSB vs A NS SD vs C NS NSD vs A NS NSC vs A NS S

Scheffe-F test: Significant at 95 %, NS: Non-significant

Discussion

Bacterial and yeast plaque on dentures is thought to be an important factor in the pathogenesis of denture stomatitis18,20. Since these fungi have been reported

to colonize easily and penetrate denture materials34,42, particularly tissue conditioners, and mechanical cleaning per se is insufficient to remove harboured Candida and harmful to soft liners43,44, chemical cleansing is suggested to be indispensable to denture plaque control43,45. Therefore, many denture cleansers have been marketed for removal or reduction of denture plaque.

For the past years, resilient denture-lining materials have been widely used in prosthodontic treatment. However, severe deterioration of these materials have been reported to be caused by some denture cleansers36,43,45 in a relatively short period, depending upon the combination of the soft liners and cleansers. The deteriorated surface of soft liners should facilitate further plaque accumulation. Therefore, denture cleansers used for plaque control with tissue-conditioned dentures should consider both microbial and physical requirements41.

Plaque control for soft-lining materials has not been stressed by either clinicians or researchers, and there are scant data available on either the material or microbiologic aspects of denture cleansers. This may be a result of the lack of recognition of the importance of plaque control for soft liners, since the prevention of Candida invasion and denture plaque formation may be achieved not only by plaque but also by replacement of the lining materials every few days. However, plaque control is particularly


essential in the clinical use of soft liners and aetiology of denture stomatitis18,20. Accordingly, the purposes of this study were to examine the ability of Candida albicans to adhere to 2 permanent soft liners, and the effectiveness of alkaline peroxide-type denture cleansers in the disinfection of long-term soft lining materials contaminated with Candida albicans.

The adherence of a microorganism to a surface is classically considered to be a 2-stage process. The initial interactions between the 2 surfaces are non-specific and reversible, although the secondary phase is caused by specific intermolecular interactions. Many approaches have been used to explain the initial adherence of microorganisms to surfaces, including the thermodynamic approach to adhesion, which describes the adhesion of microorganisms to surfaces in terms of free energies of the surfaces and the microorganisms. In addition, the hydrophobicity of the microorganisms has been theorized as a reason for high adherence and also for electrostatic interactions between surfaces. The second phase of the adhesion process involves specific adhesin-receptor interactions. The microorganism carries adhesins that bind stereo-chemically to complementary receptors on the surface. This stage is necessary for the tight binding of the microorganisms to the surface, which permits colonization. In addition to tightly binding the microorganisms to the surface, the irreversible interactions are also responsible for the site-specific colonization of the oral microorganisms, which provides a selective advantage for microorganisms that possess relevant adhesins. Adhesins have been postulated to be associated with the microorganisms surface appendages that, by virtue of their small radius, are unable to overcome the energetic barrier of the primary force37.

Other factors associated with the adherence of yeast to surfaces include surface roughness, presence of salivary proteins, presence of other adherent microorganisms, strain variability, concentration, viability of yeast cells, and culture conditions37 .

In this study, a simple in vitro model was used to compare the adherence of C. albicans with 2 soft lining materials. We aimed to provide a reproducible variables that could be examined in future studies. In light of this, the material surfaces were reproduced in a stainless-steel mould; the variability of surface roughness was therefore not examined. The concentration, viability, and culture conditions of the assay were kept constant. Adhesion was initially carried out on surfaces with no saliva coating to produce a reproducible assay before the introduction of variables. Only one dye - crystal violet - used within the study is commonly used in microbiology. Because crystal violet stains all cells present, with no ghost cells evident34.

Even though this study did not evaluate the fungicidal effects of denture cleansers, there are many studies that examine the fungicidal effects of denture cleansers. Nikawa et al28,29 reported that fungicidal effects of some

denture cleansers tested was less effective with a soaking period of 30 minutes, as compared with 2-hour incubation periods, in accordance with the conclusions of other investigators43,46. Thus, a 2-hour incubation period was used to asses the efficacy of the cleansers28,29.

In this study, surface roughness and concentration, viability, and culture conditions of the assay were kept constant except surface free energy and chemical properties of the materials tested. Conflicting reports have been published regarding the role of the materials’ surface free energy on the degree of microorganism adhesion. It has been reported that the higher the surface free energy of the substrata, the higher the amount of adhesion of microorganisms47,48. This unclear situation highlights the importance of the surface properties of the lining materials and surface tensions of the suspending denture cleansing medium, both not measured. Therefore, there is need for further investigations.

The results of the experiment clearly indicated that all peroxide-type denture cleansers were effective in the 2-hour test period. In this study, peroxide-type denture cleansers were used for disinfection regimes, because these cleansers are commonly used by denture wearers and more often found in the markets.

Conclusion

The ability of Candida albicans to adhere to 2 permanent soft liners and the effectiveness of alkaline peroxide-type denture cleansers in the disinfection of long-term soft lining materials contaminated with Candida albicans were examined. The following conclusions may be made:

Both Luci-Sof and Molloplast-B soft liners showed Candidal adherence;

Luci-Sof soft liner exhibited higher Candidal adherence than Molloplast-B soft liner;

2-hour immersion period was found effective to reduce Candidal colonization clinically;

Alkaline peroxide-type denture cleansers can be used in order to maintain effective denture hygiene;

There is a need for further investigations to explain if there is any relation between Candidal adherence and surface free energy of the materials and microorganisms.

Acknowledgements: The study is based on a thesis submitted to the Dental faculty, University of Marmara, in partial fulfilment of the requirements for the MS degree. This investigation was supported in part by Research Grant from the TUBITAK.

Balk J Stom, Vol 13, 2009 Cleaning Efficiency of Alkaline Peroxide Cleaners 39

References

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2. Mack PJ. Denture soft lining materials: clinical indications. Aus Dent J, 1989; 34:54-58.

3. Maginnis MJ, Gaubert GT. Soft liners. In: Morrow R, Rudd K, Rhoads J (eds). Dental Laboratory procedures: Complete dentures. St Louis: Mosby, 1986; pp 441-459.

4. Van Noort R. Dental materials: 1992 literature review. J Dent, 1994; 22:5-28.

5. Brown D. Resilient soft liners and tissue conditioners. Br Dent J, 1988; 164:357-359.

6. Budtz-Jorgensen E, Bertram U. Denture Stomatitis. I. The etiology in relation to trauma and infection. Acta Odont Scand, 1970; 28:71-92.

7. Bascom PW. Resilient denture base materials. J Prosthet Dent, 1966; 16:646-649.

8. Graham BS, Jones DW. In vivo fungal presence and growth on two resilient denture liners. J Prosthet Dent, 1991; 65:528-532.

9. Wrigth PS, Young KA, Riggs PD, Parker S, Kalachandra S. Evaluating the effect of soft lining materials on the growth of yeast. J Prosthet Dent, 1998; 79:404-409.

10. Masella RP, Dlaln CT, Laney WR. The prevention of the growth of Candida on Silastic 390 soft liner for dentures. J Prosthet Dent, 1975; 33:250-257.

11. Waters MGJ, Williams DW, Jagger RG. Adherence of Candida albicans to experimental denture soft lining materials. J Prosthet Dent, 1997; 77:306-312.

12. Radford DR, Sweet SP, Challacombe SJ, Walter JD. Adherence of Candida albicans to denture-base materials with different surface finishes. J Dent, 1998; 26:577-583.

13. Wrigth PS, Clark P, Hardie M. The prevalence and significance of yeasts in persons wearing complete dentures with soft-lining materials. J Dent Res, 1985; 64:122-125.

14. Nikawa H, Hamada T, Makihira S, Kumagai H Murata H. Interactions between thermal cycled resilient denture lining materials, salivary and serum pellicles and Candida albicans in vitro: Part II. Effect on fungal colonization. J Oral Rehabil, 2000; 27:124-130.

15. Fenlon MR, Sherriff M, Walter JD. Factors associated with the presence of denture related stomatitis in complete denture wearers: a preliminary investigation. Eur J Prosthodont Rest Dent, 1998; 6:145-147.

16. Rodrigez LO, Minah GE, DriscollCF. Candida albicans colonization of surface-sealed interim soft liners. J Prosthodont, 2000; 9:184-188.

17. Nikawa H, Iwanaga H, Kameda M, Hamada T. In vitro evaluation of Candida albicans adherence to soft-lining materials. J Prosthet Dent, 1992; 68:804-808.

18. Budtz-Jorgensen E. The significance of Candida albicans in denture stomatitis. Scan J Dent Res, 1974; 82:151-190.

19. Arendorf TM, Walker DM. Denture stomatitis; a review. J Oral Rehabil, 1987; 14:217-227.

20. Budtz-Jorgensen E, Stenderup A, Grabowski M. An epidemiologic study of yeasts in elderly denture wearers. Community Dent Oral Epidemiol, 1975; 3:115-119.

21. Davenport JC. The oral distribution of Candida in denture stomatitis. Br Dent J, 1970; 129:151-156.

22. Lambert JP, Kolstad R. Effect of a benzoic acid-detergent germicide on denture-borne Candida albicans. J Prosthet Dent, 1986; 55:699-700.

23. Palenic CJ, Miller CH. In vitro testing of three denture-cleaning system. J Prosthet Dent, 1984; 51:751-754.

24. Dills S, Olshan AM, Goldner S, Brogdon AC. Comparison of the antimicrobial capability of an abrasive paste and chemical-soak denture cleaners. J Prosthet Dent, 1988; 60:467-470.

25. Keng SB, Lim M. Denture plaque distribution and the effectiveness of a perborate-containing denture cleanser. Quintesence Int, 1996; 27:341-345.

26. Ödman PA. The effectiveness of an enzyme-containing denture cleanser. Quintessence Int, 1992; 23:187-190.

27. Nakamoto K, Tamamoto M, Hamada T. A review of in vitro and in vivo methods to evaluate the efficacy of denture cleansers. Int J Prosthodont, 1999; 12:153-159.

28. Nikawa H, Yamamoto T, Hamada T, Rahardjo MB, Murata H. Commercial denture cleansers-cleansing efficacy against Candida albicans biofilm and compatibility with soft denture-lining materials. Int J Prosthodont, 1995; 8:434-444.

29. Nikawa H, Yamamoto T, Hamada T, Sadamori S, Agrawal S. Cleansing efficacy of commercial denture cleansers: Ability to reduce Candida albicans biofilm activity. Int J Prosthodont, 1995; 8:527-534.

30. Nakamoto K, Tamamoto M, Hamada T. Evaluation of denture cleansers with and without Candida albicans. J Prosthet Dent, 1991; 66:792-795.

31. Chan ECS, Iugovaz I, Siboo R, Bilyk M Barolet R, Amsel R, Wooley C, Klitorinos A. Comparison of two popular methods for removal and killing of bacteria from dentures. Journal, 1991; 57:937-939.

32. Dixon DL, Breeding LC, Faler TA. Microwave disinfection of denture base materials colonized with Candida albicans. J Prosthet Dent, 1999; 81:207-214.

33. Waters MG, Jagger RG, Winter RW. Water absorption of (RTV) silicone denture soft lining material. J Dent, 1996; 24:105-108.

34. Waters MG, Jagger RG, Winter RW. Adherence of Candida albicans to experimental denture soft lining materials. J Prosthet Dent, 1997; 77:306-312.

35. Samaranayake LP, McCourtie J, Macfarlane TW. An in-vitro study of the adherence of Candida albicans to acrylic surfaces. Arch Oral Biol, 1980; 25:603-609.

36. Baysan A, Whiley R, Wrigth PS. Use of microwave energy to disinfect a long-term soft lining material contaminated with Candida albicans or Staphylococcus aureus. J Prosthet Dent, 1998; 79:454-458.

37. Samaranayake LP, McCourtie J, Macfarlane TW. Factors affecting the in-vitro adherence of Candida albicans to acrylic surfaces. Arch Oral Biol, 1980; 25:611-615.

38. Verran J, Motteram KL. The effect of adherent oral streptococci on the subsequent adherence of Candida albicans to acrylic in vitro. J Dent, 1987;15:73-76.

39. Nakamoto K, Tamamoto M, Hamada T. Evaluation of denture cleansers with and without enzymes against Candida albicans. J Prosthet Dent, 1991; 66:792-795.

40. Nikawa H, Yamamoto T, Hamada T, Sadamori S, Agrawal S. Cleansing efficacy of commercial denture cleansers: Ability to reduce Candida albicans biofilm activity. Int Prosthodont, 1995; 8:527-534.


41. Nikawa H, Yamamoto T, Hamada T, Rahardjo MB, Murata H. Commercial denture cleansers-Cleansing efficacy against Candida albicans biofilm and compatibility with soft denture lining materials. Int Prosthodont, 1995; 8:434-444.

42. Allison RT, Douglas WH. Micro-colonization of the denture-fitting surface by Candida albicans. J Dent, 1973; 1:198.

43. Harrison A, Basker RM, Smith IS. The compatibility of temporary soft materials with immersion denture cleansers. Int J Prosthodont, 1989; 2:254-258.

44. Connor JNE, Schoenfeld CM, Taylor RL. An evaluation of an enzyme denture cleanser. J Prosthet Dent, 1977; 37:147-157.

45. Davenport JC, Wilson HJ, Basker RM. The compatibility of tissue conditioners with denture cleansers and chlorhexidine. J Dent, 1978; 6:239-246.

46. Palenik CJ, Miller CH. In vitro testing of three denture-cleaning systems. J Prosthet Dent, 1984; 51:751-754.

47. Van Dijk J, Herkstrorer F, Busscher H, Weerkamp A, Jansen H, Arends J. Surface-free energy and bacterial adhesion. An in vivo study in beagle dogs. J Clin Periodontol, 1987; 14:300-304.

48. Dexter SC, Sullivan JD, Williams J, Watson SW. Influence of substrata wettability on the attachment of marine bacteria to various surfaces. Appl Microbiol, 1975; 30:298-308.


Prof. Yasemin OzkanUniversity of Marmara, Faculty of DentistryGüzelbahçe Büyükçiftlik Sok. No.634365 Nişantaşı, IstanbulTurkeyE-mails: [email protected], [email protected]

SUMMARYObjective: The purpose of this in vitro study was to evaluate the effect

of shade and thickness of porcelain veneers on depth of cure of 2 light-cured resin-based luting cements with 2 different shades.

Material and Methods: Veneer samples (Empress 2 -Ivoclar) were pre-pared in 1mm and 1.8 mm thickness and 10mm diameter (shade 1M2, 2M2). The test materials (RelyX and Variolink II Base; A1 and A3 shade) of this study were cured through the porcelain samples. Measurements of depth of cure were performed according to ISO 4049. Statistical analysis was per-formed with Tukey HSD test.

Results: The highest depth of cure results were obtained with Vario-link II Base (A1) covered with Empress 2 (1M2 shade - 1mm thickness) as 3.051mm. 0.937mm was the lowest data which was obtained with RelyX (A3) covered with Empress 2 (2M2 shade - 1.8mm thickness) (p<0.05).

Conclusions: Darker shade of the resin-based luting material is a sig-nificant factor on decreasing depth of cure, especially for RelyX. Thickness of porcelain veneers had a greater influence on the depth of cure than the shade of porcelain. Keywords: Porcelain Thickness; Resin Cement; Cure, depth

Temel Koksal1, Arzu Civelek2, Ender Kazazoglu1, Mubin Soyman2

Faculty of Dentistry, Yeditepe UniversityIstanbul, Turkey1Department of Prosthodontics2Department of Operative Dentistry



Effect of Shade and Thickness of Porcelain Veneers on Depth of Cure of Light-Cured Resin-Based Luting Cement

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Introduction

Porcelain veneers are an increasing demand of the patients to achieve aesthetic indirect anterior restorations and improve the smile design. These restorations enable to change the colour, form and/or position of anterior teeth, which are important elements of anterior aesthetics.

The porcelain veneer technique includes the bonding procedure of a porcelain laminate to teeth using an adhesive system and a luting material. These adhesive systems comprise dual cured1, self-cured2 and light-cured resin based cements3. Light activated luting resins are used for anterior porcelain veneers, while thick posterior ceramic restorations require the use of dual activated, self-cured resin cements or resin modified glass ionomer cements2. Light-cured resin luting materials may be preferred to dual-cured and self-cured resin luting

materials because of their simplicity to manipulate and more timesaving properties. Besides, dual-cured and self-cured luting materials have some disadvantages because of the catalysts they incorporate. These are the potential for discoloration of the luting resin and for interference with some self-etching adhesives, which causes lower bond strength4,5. Therefore, using solely light-curing composite resin would have certain clinical advantages.

The success of the porcelains can be affected by the exposed dental hard tissue (enamel or dentin), bond strength of the luting material and the occlusal relationship. Luting materials’ performance depends on the physical and mechanical properties of the material, which includes especially bond strength, viscosity, elastic modulus and depth of cure. Adequate polymerization is a crucial factor in obtaining optimal physical properties and a satisfying clinical performance of composite resin luting materials. Inadequate polymerization causes inferior

42 T. Koksal et al. Balk J Stom, Vol 13, 2009

physical properties and changes in strength, stiffness, water sorption and colour stability1,6.

The depth of polymerization is very important in direct composite application and in cementation of veneers7. The curing capacity (depth of cure) of light-cured luting cements depends on the translucency8 and the thickness9 of the porcelain material. Light source also plays an important role on the depth of cure. Type of light1,6,10, light intensity1,11,12, mode1,13 and exposure period10 are the effecting factors. Additionally, formulation, photo-sensitizer and shade of the resin-based cement can be influencing factors on the polymerization of the luting material through the porcelain veneer.

Different methods can be used to evaluate the efficiency of light-cured materials. Measuring micro-hardness or depth of cure tests are the most common methods for this purpose1. Micro-hardness tests are used as an indirect measurement of degree of cure rate8,9, whereas micrometer evaluation is a direct determination method of depth of cure, which is used in the present study.

The purpose of this in vitro study was to evaluate the effect of shade and thickness of porcelain veneers on depth of cure of 2 light-cured resin-based luting cements with 2 different shades.

Material and Method

In this study, veneer samples (IPS-Empress 2, Ivoclar Vivadent, Liechtenstein) were prepared in 1mm and 1.8mm thicknesses, 1M2 and 2M2 shades and 10mm diameter. The Rely X Veneer (3M ESPE, Canada) and Variolink II Base (Ivoclar Vivadent, Liechtenstein) composite resin-based cements were used for determination of depth of cure in 2 different shades (A1 and A3). Rely X Veneer is used for only light-curing purposes, whereas Variolink II can be used as light-cured or dual-cured luting material. In this study Variolink II base (light-cured) was used to compare with Rely X Veneer. Measurements of depth of cure were performed according to ISO 4049:2000.

The experimental procedure was as follows: A stainless steel mould was used for the preparation of a cylindrical luting composite resin (8mm long x 4mm in diameter). A black bottom was chosen for preparing the samples. The mould was placed onto a strip of transparent film on a glass microscope slide on the black bottom. The mould was filled with the test material (Rely X Veneer and Variolink II Base; A1 or A2 shade), prepared according to the manufacturer’s instructions and care was taken to avoid air bubbles. The mould was overfilled slightly and a second strip of the transparent film was placed on the top, followed by the second microscope slide. The mould and strips of film were pressed between the glass slides to displace excess material. Polymerization (Kavo Polylux II, 750-mW/cm2) was performed for 40 seconds after placing

Empress 2 porcelain sample (Vitapan 1M2 or 2M2 shade) on the mould.

The specimens were removed from the mould and the inadequately cured soft luting material was removed from the bottom of the mould with a plastic spatula. The height of the cylinder of the cured material was measured with a digital micrometer (Mitutoyo, UK Ltd) to an accuracy of ±0.1mm (Mount & others, 2002; Fan & others, 2002; Cobb & others, 2000). The obtained values were divided by 2 and recorded as the depth of cure, according to ISO 4049:2000.

The data were analyzed by ANOVA (SPSS 15.0 package programme) and for multiple comparisons Tukey HSD was used.

Results

Mean depth of cure values and standard deviations are given in table 1, figure 1 and figure 2. The highest curing depth results were obtained with Variolink II Base (shade A1) under the porcelain laminate with the shade of 1M2 and thickness of 1mm. The mean value for this group was 3.05 ± 0.04 mm. 0.93 ± 0.01 mm was the lowest data which was obtained with Rely X (shade A3) under the porcelain laminate with the shade of 2M2 and 1.8 mm thickness. Rely X (shade A3) gave the lowest values under all porcelain laminate specimen groups when compared with the other luting cements. Under the porcelain specimens with the shade of 2M2 and thickness of 1.8mm, the depth of cure values of all resin cement groups were lowest.

Table 1. Mean and standard deviation of the depth of cure values

Shade and thickness of porcelain specimens

Shade of theluting cement

Mean (mm) (±) S.D.

1M2, 1mm

Rely X, A1 2.72 0.10

Rely X, A3 1.01 0.04

Variolink, A1 3.05 0.04Variolink, A3 2.43 0.04

1M2, 1,8mm

Rely X, A1 2.42 0.03Rely X, A3 0.94 0.02


2M2, 1mm

Rely X, A1 2.79 0.09Rely X, A3 1.02 0.03


2M2, 1,8mm

Rely X, A1 2.37 0.03Rely X, A3 0.93 0.01


Balk J Stom, Vol 13, 2009 Depth of Cure of Light-Cured Resin-Based Luting Cement 43

Table 2. Comparison of the mean depth of cure values under same porcelain specimens

Luting material 1M2, 1mm

1M2, 1.8mm

2M2, 1mm

2M2, 1.8mm

Rely X A1 a e h k

Rely X A3 b f i l

Variolink A1 c g h m

Variolink A3 d e j k

Same letters in the same column indicate non-significant differences(p>0.05, Tukey HSD test)

Figure 1: Mean depth of cure values of each luting cement under different porcelain specimens

Figure 2: Mean depth of cure values of different luting cements under same porcelain specimen group

Table 3. Comparison of the mean depth of cure values under different porcelain specimens

Porcelain specimens Rely X A1

Rely X A3

Variolink A1

Variolink A3

1M2, 1mm a d f i

1M2, 1.8mm b e g i k

2M2, 1mm a d g k l

2M2, 1.8mm b c e h l

Same letters in the same column indicate non-significant differences (p>0.05, Tukey HSD test)

Table 4. Tests of between-subject effects

Source Type IIISum of Squares df Mean Square F Sig.

Type of porcelain ,890 3 ,297 77,063 .000

Resin cement 39,023 3 13,008 3379,036 .000

Type of porcelain & Resin cement ,648 9 ,072 18,713 .000

Comparisons of the mean depth of cure values under the same and different porcelain specimens are given in tables 2 and 3. Under the porcelain specimen group with the shade of 1M2 and thickness of 1mm, the depth of cure values of all resin cement groups were significantly different from each other (p<0.05).

According to the analysis of variance (ANOVA), the effects of both luting cements and porcelain specimens either separately or together on depth of cure were found to be significant - p<0.001 (Tab. 4).

Discussion

The thickness, opacity and shade of composite resin materials were reported to reduce the available light energy to polymerize light cured resin systems14,15. Therefore in this study the effect of shade and thickness of porcelain veneers on depth of cure of 2 light-cured resin-based luting cements with 2 different shades was evaluated. To evaluate the effect of the curing capacity of the luting cement, depth of cure test method was used. As stated by Fan et al16 the ISO scraping test used to

44 T. Koksal et al. Balk J Stom, Vol 13, 2009

determine depth of cure requires minimal instrumentation and can be performed easily. For this reason this method is also advisable for practitioners to establish the appropriate curing times for the various resin based composites used in the dental office and periodically verify the adequacy of the curing light and composite performance.

It is reported that light curing systems must emit radiation between 400 and 500nm9, while the radiation intensity must be at least 280 mW/cm2 to polymerize a 1mm thickness of composite resin17. For composite resins, generally, a light intensity of more than 400 mW/cm2 is recommended1. Therefore in the present study, a halogen light cure device (Kavo Polylux II) of 750-mW/ cm2

was used.The depth of satisfactory polymerization is very

unpredictable in areas where the composite thickness is greater than 2mm18. This concept is important in direct composite application. But a very thin layer of luting resin is sufficient to cement porcelain veneers. Therefore the thickness and opacity of porcelain becomes more important in effecting the polymerization of luting resin cement. O’Keefe et al19 and Strang et al20 determined that thickness of a porcelain veneer affects the intensity of the light source to a greater extent than shade and opacity. The results of this study supported these findings.

Chan and Boyer21 reported similar findings and established a formula to predict the required exposure time of composite resins under porcelain of varying shades and thicknesses. In the present study, similar to the study performed by Jung et al1, 40 seconds of exposure time was assumed to be enough for a satisfactory polymerization because of the light intensity of the light-curing device used.

The results obtained in this study showed that the composition (different brands) and shade of the luting material affected the depth of cure. Besides these affecting factors, porcelain thickness and porcelain shade is also an influencing variable on depth of cure.

The obtained results showed that darker shade of the resin-based luting material is a significant factor on decreasing depth of cure. Especially, Rely X (Shade A3) decreased the depth of cure dramatically (nearly 2.5 times). According to our results, when a dark shade of resin cement is needed, Variolink is a better alternative compared to Rely X. When shade of the resin cement is a lighter one (A1), the depth of cure values showed differences between Variolink and Rely X. But it seems not to be of clinical importance.

The second finding was that the thickness of porcelain veneers influenced the depth of cure, except Variolink A3. But also these differences could not be interpreted as clinically important.

The shade of porcelain affected the depth of cure of Variolink luting material significantly, but this difference is clinically non-significant.

The present study showed that data obtained from Variolink A1, A3 and RelyX A1 resemble each other and that they can be used safely in clinical application.

Conclusions

Within the limitations of this in vitro study, the following conclusions can be drawn:1. The shade of a luting resin material is an important

influencing factor on depth of cure. When the shade gets darker, the depth of cure significantly decreases;

2. The porcelain thickness affects the depth of cure significantly (except Variolink A3). However, the porcelain shade exerts no effect on the depth of cure;

3. When the resin cement Variolink gets darker (A3), the porcelain thickness (1mm and 1.8mm) has no influence on the depth of cure; however, the shade does have an effect.

References

1. Jung H, Friedl KH, Hiller KA, Haller A, Schmalz B. Curing efficiency of different polymerization methods through ceramic restorations. Clin Oral Invest, 2001; 5:156-161.

2. van Dijken JW. Resin-modified glass ionomer cement and self-cured resin composite luted ceramic inlays. A 5-year clinical evaluation. Dent Mater, 2003; 19:670-674.

3. Horn HR. Porcelain Laminate Veneers bonded to etched enamel. Dent Clin North Am, 1983; 27:671-684.

4. Cheong C, King NM, Pashley DH, Ferrari M, Toledano M, Tay FR. Incompatibility of self-etch adhesives with chemical/dual-cured composites: two-step vs. one-step systems. Oper Dent, 2003; 28:747-755.

5. Tay FR, Pashley DH, Yiu CK, Sanares AM, Wei SH. Factors contributing to the incompatibility between simplified-step adhesives and chemically-cured or dual-cured composites. Part I. Single-step self-etching adhesive. J Adhes Dent, 2003; 5:27-40.

6. Usumez A, Ozturk AN, Usumez S, Ozturk B. The efficiency of different light sources to polymerize resin cement beneath porcelain laminate veneers. J Oral Rehabil, 2004; 31:160–165.

7. Rasetto FH, Driscoll CF, von Frauenhofer JA. Effect of light source and time on the polymerization of resin cement through ceramic veneers. J Prosthodont, 2001; 10:133-139.

8. Koch A, Kroeger M, Hartung M, Manetsberger I, Hiller KA, Schmalz G, Friedl KH. Influence of ceramic translucency on curing efficacy of different light-curing units. J Adhes Dent, 2007; 9:449-462.

9. Jung H, Friedl KH, Hiller KA, Furch H, Bernhart S, Schmalz G. Polymerization efficiency of different photocuring units through ceramic discs. Oper Dent, 2006; 31(1):68-77.

10. Barghi N, McAlister EH. LED and halogen lights: effect of ceramic thickness and shade on curing luting resin. Compen Contin Educ Dent, 2003; 24:497-500.

Balk J Stom, Vol 13, 2009 Depth of Cure of Light-Cured Resin-Based Luting Cement 45

11. Gagliani M, Fadini L, Ritzmann JM. Depth of cure efficacy of high-power curing devices vs. traditional halogen lams. J Adhes Dent, 2002; 4:41- 47.

12. Mills RV, Jandt KD, Ashworth SH. Dental composite depth of cure with halogen and blue light emitting diode technology. Br Dent J, 1999; 186:388-390.

13. Hammesfahr PD, O’Connor MT, Xiuling W. Light-curing technology: past, present, and future. Compen Contin Educ Dent, 2002; 23(Suppl 1):18-24.

14. Moseley H, Strang R, Stephen KW. An assessment of visible-light polymerizing sources. J Oral Rehabil, 1986; 13:215-224.

15. Kanca J 3rd. The effect of thickness and shade on the polymerization of light-activated posterior composite resins. Quintessence Int, 1986; 17:809-811.

16. Fan PL, Schumacher RM, Azzolin K, Geary R, Eichmiller FC. Curing-light intensity and depth of cure of resin-based composites tested according to international standards. J Am Dent Assoc, 2002; 133:429-434.

17. Rueggeberg FA, Jordan DM. Effect of light tip distance on polymerization on resin composite. Int J Prosthodont, 1993; 6:364-370.

18. Rueggeberg FA, Caughman WF, Curtis JW. Effect of light intensity and exposure duration on cure of resin composite. Oper Dent, 1994; 19:26-32.

19. O’Keefe KL, Pease PL, Herrin HK. Variables affecting the spectral transmittance of light through porcelain veneer samples. J Prosthet Dent, 1991; 66:434-438.

20. Strang R, McCrosson J, Muirhead GM, Richardson SA. The setting of visible light-cured resins beneath etched porcelain veneers. Br Dent J, 1987; 163:149-151.

21. Chan KC, Boyer DB. Curing light-activated composite cement through porcelain. J Dent Res, 1989; 68:476-480.


Temel KoksalYeditepe UniversitesiDis Hekimligi FakultesiBagdat Caddesi No: 238Goztepe 34728, IstanbulTurkeyE-mail: [email protected]

SUMMARYObjectives: The purpose of this study was to investigate and compare

age, gender, menopause, duration of symptoms, laboratory results, location of burning symptoms, type of denture and the psychological aspects accor-ding to the type of burning mouth syndrome (BMS) in a sample of Turkish population.

Methods: 63 patients complaining of burning, pain and xerostomia over the last 6 months or longer were examined clinically and radiographi-cally; laboratory evaluation was performed as well. Non-stimulated whole salivary flow rate was determined. Psychological disturbances were eva-luated by the Speilberger State-Trait Anxiety Inventory for anxiety and Zung Self-Rating Depression Scale for depression.

Results: Of the total of 63 cases, 50 (79.4%) were females and 13 (20.6%) were males. 34 of these subjects were Type 1 and 29 were Type 2 BMS. There was no statistically significant difference for age, gender, meno-pause, location of burning symptoms and type of denture between Type 1 and Type 2 groups (p>0.05). Non-stimulated whole salivary flow rate and all data were within normal ranges for both groups. For anxiety and depres-sion, there were no statistically significant differences between Type 1 and Type 2 BMS patients (p>0.05), but anxiety scores (SAI and TAI) of both groups were found to be significantly higher than normal ranges. How ever, Zung Depression Scores for both groups were within normal ranges. All patients had cancer-phobia, and the mean VAS scores were 3.32±0.91 and 3.55±0.95 for Type 1 and Type 2 BMS patients, respectively.

Conclusion: The psychological element has been an important aspect of the pathological picture for BMS, and anxiety is the most important factor in both types of BMS.Keywords: Anxiety; Depression; Psychological Disturbance; Visual Analogue Scale

F.N. Pekiner, B. Gümrü, S. Özbayrak

Marmara University, Faculty of Dentistry Department of Oral Diagnosis and Radiology Istanbul, Turkey



Burning Mouth Syndrome in a Sample of Turkish Population

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Introduction

The term Burning Mouth Syndrome (BMS) is in widespread use, although in the past, terms such as glossodynia, glossalgia, stomatodynia, stomatopyrosis and oral dysaesthesia have been used to describe patients complaining of intra-oral burning symptoms. When the burning symptoms persist for over 6 months, and objective clinical findings of local and systemic disorders have not been demonstrated, in contrast to the clinically normal appearance of the oral mucosa, patients with burning symptoms pronounce excessive complaints,

often accompanied by other phenomena, such as dryness, paraesthesia and changes in the sensations of taste (predominantly bitter or metallic) and smell. This condition is known as BMS7-10,18,19,25-27,36,40,42. The aetiology and pathogenesis are unknown2,3,5,6,16,21,23,26-28,32,34,38-41, but recently, the psychological element has been an important aspect of the pathological picture4,12,15,17,18,32,37,42. The prevalence of BMS is unknown25, but international estimates of the prevalence vary from 0.7% to 15%27,35,40, and a higher prevalence is found among middle-aged women8,18,20,36, mean age ranging between 55-60 years8,18,36. The site of burning is variable, but most often affects the

tongue, followed by the palate, upper alveolus, lips and the lower denture bearing area. More than 1 site is usually affected and there is nearly always a bilateral involvement. Other sites in the oral mucosa and the throat may be involved8,9,20,30,33,35,37,38.

The pattern of daily symptoms seems fairly stable for the individual patient. The symptoms of BMS tend to fall into three broad categories: Type 1, Type 2 and Type 3. There are similarities between these subtypes. In Type 1 BMS, patients suffer no symptoms on waking, but the burning begins and increases in severity as the day goes on; in Type 2 BMS, patients suffer from burning on waking and it persists throughout the day; in Type 3 BMS, patients have symptom-free days and also complain of involvement at unusual sites, such as the floor of the mouth or the throat21.

The purpose of this study was to investigate and compare the age, gender, menopause, duration of symptoms, laboratory results, location of burning symptoms at the oral mucosa, type of dentures and the psychological aspects in relation to the type of BMS in a sample of Turkish population

Material and Methods

A total of 63 patients with burning or pain symptoms were examined in the Department of Oral Diagnosis and Radiology, Faculty of Dentistry, Marmara University in Istanbul, Turkey. The diagnosis of BMS was based on established diagnostic criteria7,12,20,21,24,27,31: (1) Patients were initially interviewed for complaints of dysgesia, xerostomia, burning, and/or painful sensations in the oral cavity; (2) All patients underwent a thorough clinical examination of the head and neck region to the oral cavity and dental status. If dentures were worn then their design and condition were assessed; (3) All patients underwent radiographic examination including panoramic radiographs and additional radiographs as necessary to exclude organic findings; (4) Laboratory evaluation included fasting blood glucose, haemoglobin, haematocrit, levels of vitamin B12, serum iron, total iron binding capacity, folic acid; (5) Non-stimulated whole salivary flow rate (UWSFR) was determined in all patients; 6. Patients suffering from systemic or local conditions, such as diabetes mellitus, lichen planus, neuralgia, chronic pain conditions in other regions and geographic tongue were excluded from the study; (7) Patients were interviewed if the complaints could be relieved by eating or drinking; (8) History of regularity of BMS over the last 6 months or longer; (9) Type of the BMS was recorded - in Type 1 BMS, patients suffer no symptoms on waking, but the burning begins and increases in severity as the day goes on; in Type 2 BMS, patients suffer from burning on waking and it

persists throughout the day; in Type 3 BMS, patients have symptoms-free days.

The patients were requested to sign a written informed consent statement. The study was carried out according to the recommendations of the Helsinki declaration.

At their first examination, the patients were given a chart containing a 10 cm horizontal visual analogue scale (VAS) to record the degree of their discomfort due to the pain. The left end of the scale indicated “no discomfort” and the right end “unendurable discomfort”7,20. Patients were asked about possible “symptoms of the climacteric” and “cancer-phobia”20.

Saliva collections were always performed between 9 and 11 am. Subjects were instructed not to eat, consume fluids, brush teeth and smoke for 1 hour prior to the investigation. Non-stimulated whole saliva was collected from all of the patients. The patients were asked to bend their heads forward and after an initial swallow, to allow saliva to flow into the mouth. Subjects expectorated the saliva into a test tube once per min for 5 min, and the flow rate was recorded in ml/min. UWSFR of <0.1 ml/min was considered very low, 0.1-0.2 ml/min low, and >0.2 ml/min normal24.

In this study, we investigated 63 patients using the Speilberger State-Trait Anxiety Inventory for anxiety (SAI-TAI)18 and Zung Self-Rating Depression Scale for depression (ZDS)44. The border line of the SAI-TAI for adults is 33.97 and 42.65, respectively. The answers given to each question in ZDS were graded from 1 to 4. According to this, the following grading system was used to determine the severity of depression: less than 50 - within normal range, no psychopathology; 50-59 - mild depression; 60-69 - moderate depression; 70 and above - severe depression.

Statistical analysis of the study was performed by using GraphPad Prisma V.3 programme. Descriptive statistical methods (mean, standard deviation) were used for the evaluation of the data. Independent t-test was used for the comparison of 2 groups and the quantitative data was compared by chi-squared test. The value of p<0.05 was considered significant.

Results

Of the total of 63 cases of BMS identified, 50 (79.4%) were females and 13 (20.6%) were males. No statistically significant difference was found in relation to age between female and male patients (Tab. 1). Type 1 BMS was detected in 34 and Type 2 BMS in 29 of these subjects; no Type 3 BMS patients were detected in this study (Tab. 2).

The comparison of Type 1 and Type 2 BMS patients was performed using independent t-test. The mean ages

Balk J Stom, Vol 13, 2009 Burning Mouth Syndrome 47

48 F.N. Pekiner et al. Balk J Stom, Vol 13, 2009

of Type 1 and Type 2 BMS patients were 49.41±13.45 and 52.45±9.69, the mean duration of symptoms reported by these patients were 2.54±3.21 and 3.24±2.38 years, and the mean UWSFR of 2 groups were 0.45±0.06 and 0.33±0.04 ml/min, respectively. There were no statistically significant differences in age, duration of symptoms and UWSFR between Type 1 and Type 2 BMS patients (Tab. 2). In addition, UWSFR were within normal ranges for both groups.

Table1. Comparison of male and female patients with BMS according to age

Patients Male (n:13)mean±SD

Female (n:50)mean±SD t p

Age 52.08 ± 7.53 50.48 ± 12.81 0.42 >0.05

Table 2. Comparison of type 1 BMS and type 2 BMS patients according to age, duration of symptoms and non-stimulated

salivary flow rate (UWSFR)

Type 1 (n:34)mean±SD

Type 2 (n:29)mean±SD t p

Age 49.41 ± 13.45 52.45 ± 9.69 -1.01 >0.05Duration of stimulation (yr)

2.54 ± 3.21 3.24 ± 2.83 -0.91 >0.05

UWSFR (ml/min) 0.45 ± 0.06 0.33 ± 0.04 -0.21 >0.05

A chi-square test was applied to determine whether there was a difference in relation to gender, menopause, location of burning symptoms and types of denture between Type 1 and Type 2 BMS patients. No statistically significant relationships were observed in relation to all these parameters (Tab. 3).

Table 3 Evaluation of type 1 BMS and type 2 BMS patients according to gender, menapouse, type of denture and sites

Type 1 (n: 34)

Type 2 (n: 29)

GenderMale 8 (23.5%) 5 (17.2%) χ²:0.37

p>0.05Female 26 (76.5%) 24 (82.8%)

MenopausePost-menopause 9 (26.5%) 6 (20.7%)

χ²:2.33p>0.05Menopause 9 (26.5%) 13 (44.8%)

Non-menopause 8 (23.6%) 5 (17.3%)

Type of denture

No denture 5 (14.7%) 1 (3.4%)

χ²:6.80p>0.05

Full removable denture 6 (17.6%) 5 (17.2%)Partial removable denture 4 (11.8%) 7 (24.1%)Fixed denture 13 (38.2%) 6 (20.7%)Partial removable + fixed denture 6 (17.6%) 10 (34.5%)

SitesBuccal mucosa + lips 12 (46.2%) 4 (19%)

χ²:3.80p>0.05Buccal mucosa + tongue 9 (34.6%) 11(52.4%)

Buccal mucosa + palate + lips 5 (19.2%) 6 (28.6%)

Table 4. The laboratory tests of all BMS patients

Type 1 (n: 34)Mean ± SD

Type 2 (n: 29)Mean ± SD t p

Fasting blood glucose 91.65 ± 13.34 91.08 ± 15.63 0.16 >0.05Hb 13.72 ± 1.90 13.38 ± 1.68 0.76 >0.05Hct 40.24 ± 3.65 39.31 ± 4.53 0.91 >0.05Fe+2 99.29 ± 32.75 87.28 ± 35.75 1.39 >0.05Fe+2 binding 356.76 ± 71.62 335.59 ± 87.14 1.06 >0.05Vit. B12 332.76 ± 149.51 397.55 ± 181.69 -1.55 >0.05Folic acid 8.47 ± 3.30 8.72 ± 4.47 -0.26 >0.05

Normal values: Fasting blood sugar:70-120mg % Hb:14-17gr % male, 12-14gr% female Hct: 40-54ml % male, 37-47ml % female Fe+2: 40-150 UG/DL Fe+2 binding: 200-460 UG/DL Vit B12: 150-825 PG/ML Folic acid: 3-17 ng/ml


Table 4 presents the laboratory results of Type 1 and Type 2 BMS patients. There were no statistically significant differences in relation to the laboratory results between the investigated groups (p>0.05), and all laboratory results were within normal ranges.

Table 5 summarizes psychological component for Type 1 and Type 2 BMS patients. For anxiety and depression, there were no statistically significant differences between the groups (p>0.05), but anxiety scores (SAI and TAI) for both groups were found to be significantly higher than the normal ranges. However, mean Zung Depression scores for 2 groups were determined as 45.85±8.45 and 43.52±8.68, respectively, e.g. within normal ranges. In addition, all patients in this study had cancer-phobia, and the mean VAS scores were 3.32±0.91 and 3.55±0.95 for Type 1 and Type 2 BMS patients, respectively. There were no significant differences in relation to VAS scores (p>0.05).

Table 5. Comparison of type 1 BMS and type 2 BMS patients according to Visual Analogue Scale (VAS), The State and Trait Anxiety Inventory (SAI-TAI) and Zung-self Rating Depression

Scale (ZDS)

Type 1 (n:34)mean ± SD

Type 2 (n:29)Mean ± SD t p

VAS 3.32±0.91 3.55±0.95 -0.97 >0.05SAI 41.12±8.43 39.34±10.73 0.73 >0.05TAI 48.44±10.14 43.76±11.09 1.75 >0.05ZDS 45.85±8.45 43.52±8.68 1.08 >0.05

Discussion

In the present study, Type 1 and Type 2 BMS patients participating the study were mostly women (76.5% and 82.8%, respectively), and the mean ages of patients were 49.41±13.45 and 52.45±9.69, respectively, which is similar to the data published in the previous studies8,18,20,25,27,35,36.

The pain is mainly located in the anterior two thirds of the tongue (71-78%), followed by the dorsum and the right and left sides of the tongue, the anterior part of the hard palate and lips. Other sites in the oral mucosa and the throat may also be involved. More than one site is usually affected and there is nearly always bilateral involvement13,21,33,35,37,38. In the present study, we noted that more than one site was usually affected. The burning sensation was mostly in the buccal mucosa and lips for Type 1 and in the buccal mucosa and tongue for Type 2 BMS patients.

In previous studies, BMS was considered as a diagnosis in which a dental or medical cause has been excluded. The clinically normal appearance of the oral mucosa, which contrasts with the patient’s pronounced

complaints, and the time constitute important factors in differential diagnosis10,19,26,30,40.

This study showed that there seemed to be no correlations between denture usage, hormonal effects, nutritional disturbances, vitamin deficiency, anaemia, salivary flow rate and the type of the BMS. All data was within normal ranges. Clinically and radiographically, the soft and hard tissues were observed to be within normal limits. Therefore according to our study it can be mentioned that dental or medical reasons did not cause BMS.

The presence of a psychological component in the symptoms of the BMS patients has been suggested, such as elevation in anxiety, depression, somatic reactions to stress, neuroticism, and psychiatric disorders1,4,7,11,12,15,17,18

,29,37,42. Psychometric studies have discovered more severe psychiatric symptoms in BMS patients than in normal populations and other chronic patients, but less severe symptoms than in other psychiatric populations10,25,29,30,37. Zilli et al43 reported depression in 75% of cases and anxiety in 41% of cases. Similarly, Rojo et al29 reported that depression was the prevalent psychiatric diagnosis among patients with BMS (31%), anxiety was much less common and affected only 8 patients (10.8%). Contrary, anxiety was found to be a more important psychological factor in BMS than depression by Lamey and Lamb22 and Pekiner et al27.

In the present study, psychological component of BMS patients was measured by the Speilberger State-Trait Anxiety Inventory for anxiety and Zung Self-Rating Depression Scale for depression. No psychopathologic phenomenon was detected in Type 1 and Type 2 BMS patients and Zung Depression scores were within normal ranges; however, Speilberger State Anxiety Inventory and Speilberger Trait Anxiety Inventory score were significantly higher, which is in accordance to other studies29,43.

This condition may lead to cancer-phobia, and it is important that the dentist working with BMS patients cooperates with the patients’ physician, psychologist or a multidisciplinary pain clinic14,26.

In conclusion; many organic causes have been proposed as possible aetiological factors for burning symptoms, including local irritation by environmental factors, but the psychological element has been an important aspect of the pathological picture for BMS, and anxiety is the most important factor in all types of the condition. Detailed and correct history of the patients with psychosomatically originated BMS is an obligation for the definite diagnosis and skills of the clinician is required for that process. In addition, reference of such patients to experienced clinics or dentists is important in achieving the life quality standards and the proper treatments of all types of BMS patients.

50 F.N. Pekiner et al. Balk J Stom, Vol 13, 2009

References

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3. Botha PJ, van der Bijl, van Eyk AD. A literature review and pilot study to characterize the treatment of burning mouth syndrome. SADJ, 2001; 56:353-358.

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5. Carlson CR, Miller CS, Reid KI. Psychosocial profiles of patients with burning mouth syndrome. J Orofac Pain, 2000; 14:59-64.

6. Danhauer SC, Miller CS, Rhodus NL, Carlson CR. Impact of criteria-based diagnosis of burning mouth syndrome on treatment outcome. J Orofac Pain, 2002; 16:305-311.

7. Eli I, Kleinhauz M, Baht R, Littner M. Antecedents of burning mouth syndrome (glossodynia) - Recent life events vs. psychopathologic aspects. J Dent Res, 1994; 73:567-572.

8. Gorsky M, Silverman S, Chinn H. Clinical characteristics and management outcome in the burning mouth syndrome. An open study of 130 patients. Oral Surg Oral Med Oral Pathol, 1991; 72:192-195.

9. Grushka M, Ching V, Epstein J. Burning mouth syndrome. Adv Otorhinolaryngol, 2006; 63:278-287.

10. Gruskha M, Epstein JB, Gorsky M. Burning Mouth Syndrome. Am Farm Physician, 2002; 65:615-620.

11. Gruskha M, Sessle BJ, Hawley TP. Psychophysical assessment of tactile, pain and thermal sensory functions in burning mouth syndrome. Pain, 1987; 28:169-184.

12. Gruskha M, Sessle BJ, Miller R. Pain and personality profiles in burning mouth syndrome. Pain, 1987; 28:155-167.

13. Gruskha M. Clinical features of burning mouth syndrome. Oral Surg Oral Med Oral Pathol, 1987; 63:30-36.

14. Hakeberg M, Hallberg LR-M, Berggren U. Burning mouth syndrome: experience from the perspective of female patients. Eur J Oral Sci, 2003; 111:305-311.

15. Hampf G, Vikkula J, Ylipaavalniemi P, Aalberg V. Psychiatric disorders in orofacial dysaesthesia. Int J Maxillofac Surg, 1987; 16:402-407.

16. Hugoson A, Thorstensson B. Vitamin B status and response to replacement therapy in patients with burning mouth syndrome. Acta Odontol Scand, 1991; 49:367-375.

17. Jerlang B. Burning mouth syndrome (BMS) and the concept of alexithymia - A preliminary study. J Oral Pathol Med, 1997; 26:249-253.

18. Lamb AB, Lamey PJ, Reeve PE. Burning mouth syndrome: psychological aspects. Br Dent J, 1988; 165:256-260.

19. Lamey PJ, Hammond A, Allam BF, McIntosh WB. Vitamin status of patients with burning mouth syndrome and the response to replacement therapy. Br Dent J, 1986; 160:81-84.

20. Lamey PJ, Lamb AB. Lip component of burning mouth syndrome. Oral Surg Oral Med Oral Pathol, 1994; 78:590-593.

21. Lamey PJ, Lamb AB. Prospective study of aetiological factors in burning mouth syndrome. Br Med J, 1988; 296:1243-1246.

22. Lamey PJ, Lamb AB. The usefulness of the HAD scale in assessing anxiety and depression in patients with burning mouth syndrome. Oral Surg Oral Med Oral Pathol, 1989; 67:390-392.

23. Lamey PJ, Murray BM, Eddie SA, Freeman RE. The secretion of parotid saliva as stimulated by 10% citric acid is not related to precipitating factors in burning mouth syndrome. J Oral Pathol Med, 2001; 30:121-124.

24. Narhi TO, Meurman JH, Ainamo A, Nevalainen JM, Schmidt-Kaunisaho KG, et al. Association between salivary flow rate and the use of systemic medication among 76-, 81-, and 86-year-old inhabitants in Helsinki; Finland. J Dent Res, 1992; 71:1875-1880.

25. Palacios-Sanchez MF, Jordana-Comin X, Gracia-Sivoli CE. Burning mouth syndrome: A retrospective study of 140 cases in a sample of Catalan population. Med Oral Patol Oral Cir Bucal, 2005; 10:388-393.

26. Pedersen AML, Smidt D, Nauntofte B, Christiani CJ, Jerlang BB. Burning mouth syndrome: Etiopathogenic mechanisms, symptomatology, diagnosis and therapeutic approaches. Oral Biosci Med, 2004; 1:3-19.

27. Pekiner FN, Özbayrak S, Çanakçı E. Burning mouth syndrome in patients wearing prosthesis: Evaluation of type I and type II. The Pain Clinic, 2005; 17:269-273.

28. Pinto A, Stoopler ET, DeRossi SS, Sollecito TP, Popovic R. Burning mouth syndrome: guide for the general practitioner. Gen Dent, 2003; 51:458-461.

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34. Svensson P, Kaaber S. General health factors and denture function in patients with burning mouth syndrome and matched control subjects. J Oral Rehabil, 1995; 22:887-895.

35. Tammiala-Salonen T, Hiidenkari T, Parvinen T. Burning mouth syndrome in Finnish adult population. Community Dent Oral Epidemiol, 1993; 21:67-71.

36. Tourne LPM. Burning mouth syndrome. Critical review and proposed clinical management. Oral Surg Oral Med Oral Pathol, 1992; 74:158-167.


37. van der Ploeg HM, van der Waal N, Eijkman MAJ, van der Waal I. Psychological aspects of patients with burning mouth syndrome. Oral Surg Oral Med Oral Pathol, 1987; 63:664-668.

38. van der Waal I. The burning mouth syndrome. Copenhagen: Munksgaard, 1990; pp 5-90.

39. Vucicevic-Boras V, Topic B, Cekic-Arambasin A, Zadro R, Stavljenic-Rukavina A. Lack of association between burning mouth syndrome and hematinic deficiencies. Eur J Med Res, 2001; 6:409-412.

40. Zakrzewska JM, Glenny AM, Forssell H. Interventions for the treatment of burning mouth syndrome. Cochrane Database Syst Reu, 2005; (1):CD002779.

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Dr. Filiz PekinerMarmara Üniversitesi, Dişhekimliği FakültesiOral Diagnoz ve Radyoloji Anabilim DalıBüyükçiftlik Sok. No: 6 34365 NişantaşıIstanbul, TurkeyE-mail: [email protected]

SUMMARY

Dental implants are commonly used in dentistry. A fixed prosthesis is a generally the preferred method of replacing the missing teeth which are lost for various reasons. In this case, we aimed to evaluate the success of a different dental implant application supported with a full mouth-fixed bridge in a patient after 13 years of implantation. It seems that a combined implant application could be useful .

Keywords: Dental Implant; Full Mouth Bridge

Gönen Özcan1, Hakan Develioglu2, Bülent Kurtis1, Dilek Nalbant3

1Gazi University, Faculty of Dentistry Department of Periodontology, Ankara, Turkey2Cumhuriyet University, Faculty of Dentistry Department of Periodontology, Sivas, Turkey3Gazi University, Faculty of Dentistry Department of Prosthodontics, Ankara, Turkey

CASE REPORT (CR)Balk J Stom, 2009; 13:52-55


A Useful Approach to a Combined Implant Application:Report of a Case after a 13-Year Assessment

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Introduction

The long-term predictability of osseointegrated implants for tooth replacement have been reported by several longitudinal studies, resulting in a wide use of dental implants1,2. Factors that allegedly influence the survival rates of dental implants include the quantity and quality of bone in the selected site3, the lack of keratinized tissue around the implant4, the patients’ periodontal status5, the type of micro-flora in the sulci/pockets of the remaining natural teeth and implants6, the patients’ plaque control7, professional maintenance8, smoking9, parafunctional habits10, and the characteristics of dental implants11. A wide variety of implant designs are available to satisfy the varying needs of patients12. The fixed prostheses are generally preferred as a way of replacing missing teeth.

A 65-year-old woman patient applied for her dental cure and rehabilitation with a prosthodontic. The present case report aims: (1) to present a way of treatment of the patient with different dental implants and a full mouth-fixed prosthesis; and (2) to evaluate their long-term results.

Report of a Case

Clinical ExaminationPlaque and bleeding on probing was seen slightly.

Moreover, the tooth 33 needed a filling and in the teeth

26 and 27 caries was detected as well. In the mandible, except the present teeth 44, 43, 42, 32 and 33, there were the edentulous ridges bilaterally (Fig. 1).

Figure 1. Intraoral view of the first examination at baseline

Before planning an implant placement, teeth were filled and a periodontal therapy was retrieved for elimination the pockets. Additionally, plaque was reduced via audio-visual educations advised for the patient. And in general, no systemic disease except a mild hypertension and menopause was reported. Using any of the medicaments for this reason was also not emphasized.

Figure 5. Intraoral view of the full mouth bridge on the implants after 13 years

Radiographic ExaminationThe panoramic X-ray taken at first visit (March

1993) showed that the maxillary teeth 18, 16, and 28, and mandibular teeth 31, 34, 35, 36, 37, 38, 41, 45, 46, 47, 48 were missing. A fixed prosthesis was seen on the upper jaw right site between tooth 15 and 17. In addition, in some areas there was an alveolar bone loss area that was visible on the radiograph (Fig. 2).

for the patient. Oral hygiene instructions were repeated (Fig. 4).

After 13 years, in 2006, the patient was evaluated again, radiographically and clinically. A successful bone implant interrelationship was noted (Figs. 5 and 6).

Figure 2. Panoramic view of the jaws at baseline

Surgical ExaminationIn addition to the clinical examination and

radiographs, a model was obtained for better analyzing of the implant placement ridges. As first, a linear incision was performed on the gingiva for exposing the alveolar ridge. Flaps were removed carefully so that the alveolar ridges were visible. Then, holes were created with a special bur under saline irrigation on the right site of the alveolar ridge of the mandible, and holes were created with a special bur on the left site of the alveolar ridge for the blade and other root-form implants. The blade implant (Nobel Biocare AB, Goteborg,Sweden) was placed firmly and a drill was used with saline irrigation at ultralow speed to complete the root-form implant (ITI, Straumann, Switzerland) placements (Fig. 3). Care was taken not to do perforations in the mandibular alveolar ridge. The flaps were readapted and sutured with a 3-0 black silk. The patient was instructed to take postoperative Siprosan® (Drogsan, Ankara, Turkey) 4 times daily for 1 week. After 1 week, sutures were removed and recorded, and the healing appeared to be within normal limits, with no complications seen.

Post-op ExaminationAfter a 6-month healing period, we examined

the related sites and have noted that all implants had successfully integrated, both clinically and radiographically. Full mouth-fixed prosthetic restoration covered the remained mandibular teeth and placed implants fabricated

Figure 3. Intraoral view of the placed implant after the operation

Figure 4. Intraoral view of the full mouth bridge on the implants after treatment

Balk J Stom, Vol 13, 2009 Combined Implant Application 53

54 G. Özcan et al. Balk J Stom, Vol 13, 2009

Figure 6. Panoramic view of the case after completing all treatments after 13 years

Discussion

Dental implant treatment did not become a reliable way until 1952, when P I Branemark’s researches of bone marrow in the rabbit fibula evolved the idea of osseointegration. Osseointegration is known as a “direct structural and functional connection between ordered, living bone and the surface of a load-carrying implant”. It contains the incorporation of non-biological material within the human skeleton without initiating a rejection phenomenon and allows for permanent penetration of the soft tissues without a chronic inflammatory reaction. Osseointegration is a dynamic phenomenon that is possible due to the characteristics of the implants composition13. In our case, a good osseointegration was also observed.

In the literature there has not been found any case with implant combination14. Our case can have a significant role from this point of view. Postoperative panoramic films showed a successful implant bone correlation. Additionally, there was no evidence of implant failure in this case, and implant failure is very important in implantology14,15.

Partially edentulous patients with single or multiple missing teeth represent another viable treatment population, and introduce an additional challenge to achieve a long-lasting, successful rehabilitation16

. In the present case, the bridge was found physiologically and aesthetically acceptable17,18. For further evaluation, the patient has been invited to the recall programme.

In conclusion, we are of the opinion that in particular cases an application using different dental implants rehabilitated with a full prosthodontics could be useful and satisfactory for the patients.

References

1. Apse P, Ellen RP, Overall CM, Zarb GA. Microbiota and crevicular fluid collagenase activity in the osseointegrated dental implant sulcus: a comparison of sites in edentulous and partially edentulous patients. J Periodontal Res, 1989; 24(2):96-105.

2. Buser D, Schenk RK, Steinemann S, Fiorellini JP, Fox CH, Stich H. Influence of surface characteristics on bone integration of titanium implants. A histomorphometric study in miniature pigs. J Biomed Mater Res, 1991; 25(7):889-902.

3. Block MS, Gardiner D, Kent JN, Misiek DJ, Finger IM, Guerra L. Hydroxyapatite-coated cylindrical implants in the posterior mandible: 10-year observations. Int J Oral Maxillofac Implants, 1996; 20:36-40.

4. Artzi Z, Tal H, Moses O, Kozlovsky T. Mucosal considerations for osseointegrated implants. J Prosthet Dent, 1993; 70:427-432.

5. Bauman GR, Mills M, Rapley JW, Hallmon WW. Plaque-induced inflammation around implants. Int J Oral Maxillofac Implants, 1992; 7:330-337.

6. Kohavi D, Greenberg R, Raviv E, Sela MN. Subgingival and supragingival microflora around healthy osseointegrated implants in partially edentulous patients. Int J Oral Maxillofac Implants, 1994; 9:673-678.

7. Meffert RM, Langer B, Fritz ME. Dental Implants: A review. J Periodontol, 1992; 63:859-870.

8. Matarasso, Quaremba G, Coraggio F, Vaia E, Cafiero C, Lang NP. Maintenance of implants: An in vitro study of titanium implant surface modifications subsequent to the application of different prophylaxis procedures. Clin Oral Implant Res, 1996; 7:64-72.

9. De-Bruyn H, Collaert B. The effects of smoking on early implant failure. Clin Oral Implant Res, 1994; 5:260-264.

10. Becker W, Becker B. Replacement of maxillary and mandibular molars with single endoosseous implant restorations: A retrospective study. J Prosthet Dent, 1995; 74:51-55.

11. Gher ME, Quintero G, Assad D, Monaco E, Richardson AC. Bone grafting and guided bone regeneration for immediate dental implants in humans. J Periodontol, 1994; 65:881-891.

12. Josefovici N. Use of an extraction site for implant placement: case report. J Oral Implantol, 2001; 27:204-206.

13. Branemark PI, Zarb GA, Albrektsson T. Tissue integrated prostheses: osseointegration in clinical dentistry. Chicago: Quintessence, 1985.

14. Shen TC. The use of a combination of different dental implants in a patient. J Oral Implantol, 1987; 13(3): 454-460.

15. Susarla SM, CHuang SK, Dodson TB. Delayed versus immediate loading of implants: survival analysis and risk factors for dental implant failure. J Oral Maxillofac Surg, 2008; 66(2):251-255.

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16. Montes CC, Pereira FA, Thome G, Alves ED, Acedo RV,

de Souza JR, Melo AC, Trevilatto PC. Failing factors

associated with osseointegrated dental implant loss. Implant

Dent, 2007; 16(4):404-412.

17. Lekholm U, van Steenberghe D, Hermann I, et al.

Osseointegrated implants in the treatment of partially

edentulous jaws: A prospective 5-year multicenter study. Int

Oral Maxillofac Implants, 1994; 9:627.

18. Pylant T, Triplett RG, Key MC, Brunsvold MA. A retrospective evaluation of endosseous titanium implants in the partially edentulous patient. Int J Oral Maxillofac Implants, 1992; 7(2):195-202.


Dr. Hakan DeveliogluCumhuriyet University, Faculty of DentistryDepartment of PeriodontologySivas, 58140, TurkeyEmail: [email protected]

SUMMARYOdontomas are the most common odontogenic tumours. They are

usual ly asymptomatic and often are discovered during routine radiography. Here, we report a case of an odontoma located at the anterior maxilla that initially caused inflammatory reactions around the overlying teeth; later on, it was associated with a generalized inflammation of the area. Endodontic re-treatment of the 4 front maxillary incisors and 2 surgical procedures were performed aiming the patient to recover.Keywords: Odontoma; Maxilla; Endodontic Re-treatment; Apicectomy

Kleoniki Lyroudia, G. Stephanopoulos

Aristotle University, Dental SchoolDepartment of EndodontologyThessaloniki, Greece



Intraosseous Odontoma in the Maxilla and ItsImpact on Underlying Teeth. A Case Report

TUPNBUP

MP

HJDBM!!TPDJFUZ

Introduction

Odontoma, one of the most common odontogenic tumours, is a tumour-like malformation (hamartoma) in which enamel, dentin or cementum are present. 2 types are recognised using criteria of their histological appearance: compound and complex odontomas7. Complex odontomas are less common than the compound lesions in the ratio 1:22,4. They differ in that in the complex odontoma calcified tissues are presented as an irregular mass, while the compound type is composed of tooth-like structures that can be seen radiographically as opacities. The most homogenous tissue can be dentin, while enamel and pre-enamel related structures can be totally abnormal in their shape, size and site8. Using clinical criteria, 3 types are described: central (intraosseous) odontoma, peripheral and erupted odontoma. Central odontomas occur predominantly in the anterior maxilla and less frequently in the mandibular molar region. More specifically, in a rather extended study, it was shown that 55.7% of all odontoma cases were located in the maxilla while 44.3% in the mandible. The anterior portion of the maxilla was the most common location of odontomas3,4. In another study, the proportions regarding odontomas’ localization were for the maxilla (70%) and for the anterior region of the jaw (83%), particularly for the anterior maxilla (62%)1. Odontomas are in general inherited or they are shown after a genetic interference during tooth development. As main causes for the development of an odontoma are mentioned trauma, infection, or growth pressure5.

Case Report

A 40-year-old male reported to a general dentist in March 2004, complaining of pain to all front maxillary teeth (central and lateral incisors). The patient’s medical history was not contributory. Clinically, there were no facial asymmetries or localised swellings and the intraoral examination did not reveal any abnormalities. However, the radiological examination using panoramic and intradental periapical radiographs revealed a well defined radiopaque mass situated in bone and underlying the upper central and lateral incisors, but with a greater density than bone and equal to or greater than that of the teeth (Figs. 1 and 2). The pre-operative diagnosis was central compound odontoma and the diffused pain reported by the patient was attributed to its presence. Surgical intervention and extraction of the odontoma was the treatment of choice. The teeth 21 and 22 were already insufficiently treated endodontically, and an apicectomy of 21 and 22 was performed with amalgam used for retrograde filling (Fig. 3).

Figure1. Panoramic radiograph. The odontoma is seen overlying teeth 21 and 22

Figure 2. Intradental periapical radiograph of the case, before any surgical treatment

Figure 4. Intradental periapical radiograph following the endodontic re-treatment of the teeth 21 and 22

Figure 3. Intradental periapical radiograph 9 months after the first surgical procedure

Figure 5. Intradental periapical radiograph after endodontic re-treatment of 4 upper incisors

6 months later, the patient returned complaining for the same diffused pain to the front teeth and a general lip swelling. His dentist decided to treat endodontically the tooth 11 (Fig. 3).

3 months later, he was referred to the Department of Endodontology, Dental School, since the clinical symptoms have not subsided. The teeth 11, 12, 21 and 22 responded with great sensitivity to percussion and palpation tests. The patient complained of a light swelling of the area and especially of the upper lip. Teeth 11, 12, 21 and 22 were decided to be re-treated endodontically on the basis that all of them were under-filled, simultaneously showing signs of localized periapical inflammation

Balk J Stom, Vol 13, 2009 Intraosseous Odontoma 57

58 K. Lyroudia, G. Stephanopoulos Balk J Stom, Vol 13, 2009

(Figs. 4 and 5). Although re-treatment of all the above mentioned teeth was sufficiently completed, the patient still complained for diffuse pain in the area and therefore a second surgical clearance of the area was performed at the oral surgery department in order to eradicate any remnants of the “calcified structure” as it was thought that this was possible reason for continuous pain (Fig. 5). A biopsy of the upper lip was taken as well, as the patient complained for a light diffused swelling. Antibiotics were prescribed and given to the patient for a period of 2 weeks.

6 months later the symptoms totally subsided (Fig. 6) and permanent restorations were placed 1 year thereafter (Fig. 7).

Discussion

Odontomas are entities that can cause different complications in the related teeth. Delayed eruption of the neighbouring teeth, or occurrence of impacted permanent teeth, especially in relation with maxillary central incisor (27%), are mentioned1. Pain, expansion of the cortical bone and tooth displacement are referred as well. In the present case, the impacted odontoma was the cause of periapical inflammation of the underlying teeth. One of the problems that had to be solved was the endodontic re-treatment of the teeth with clinical signs of infection, as we believed that microflora in the root canals of the involved underlying teeth, was one of the probable reasons for the patients’ problems, in combination with microleakage. On the other hand, it is well known that in several cases amalgam used as a filling material in periapical surgery can produce hypersensitivity of the neighbouring soft tissues, or even the treated teeth fail to heal as a result of corrosion of the apical amalgam6.

Cases like that, may confuse diagnosis, since the signs are not totally clear and radiographically these cases could be held as various other lesions9. Therefore before any treatment plan is decided, there is a need to differentially diagnose cementoblastoma, osteoid osteoma, fibro-osseous lesions from odontomas. A cementoblastoma presents a well defined radiopaque mass attached to a tooth and root and surrounded by a radiolucent area10. Osteoid osteomas are characterized by a small ovoid or round radiolucent area surrounded by a rim of sclerotic bone; the central radiolucency exhibits some calcification as it matures. Cemento-ossifying fibroma is presented as a well-defined radiolucency with increasing degree of calcification as it matures; it is not surrounded by a radiolucent rim and it is diffused with normal bone10. One of the major drawbacks regarding diagnosis in this case was the lack of histological data for confirmation of the preoperative diagnosis.

In the present case, no eruption was mentioned or seen, although we assume that the case started during an eruption process that was followed by inflammation, which was extended and gave signs of periapical inflammation to the underlying teeth. Furthermore it can’t be assessed as well, to what extend the undertreatment of the involved teeth was the cause for the patient’s chief complaints or it was actually the remnants of the odontoma that caused the inflammation signs and discomfort of the patient, as both followed on the same time.

References

1. Chang JY, Wang JT, Wang YP, Liu BY, Sun A, Chiang CP. Odontoma: a clinicopathologic study of 81 cases. J Formos Med Assoc, 2003; 102:876-882.

Figure 6. Intradental periapical radiograph after the second apicectomy that followed for the upper incisors and removal of the odontoma’s

remnants

Figure 7. Periapical tissues radiographically show signs of healing 6 months later

Balk J Stom, Vol 13, 2009 Intraosseous Odontoma 59

2. Cohen DM, Bhattacharyya I. Ameloblastic fibroma, ameloblastic fibroodontoma and odontoma. Oral Maxillofac Surg Clin North Am, 2004; 16(3):375-384.

3. Crincoli V, Scivetti M, Di Bisceglie MB, Lucchese A, Favia G. Odontoma: a retrospective study and confocal laser scanning microscope analysis of 52 cases. Minerva Stomatol, 2007; 56(11-12):611-620.

4. Cuesta A, Albiol G, Aytes B, Escoda G. Review of 61 cases of odontoma. Presentation of an erupted complex odontoma. Med Oral, 2003; 8(5):366-373.

5. Hitchin AD. The aetiology of the calcified composite odontomas. Br Dent J, 1971; 130:475-482.

6. Hohenfeldt PR, Aurelio JA, Gerstein H. Electrochemical corrosion in the failure of apical amalgam. Report of two cases. Oral Surg Oral Med Oral Pathol, 1985; 60(6):658-660.

7. Kitano M, Tsuda-Yamada S, Semba I, Mimura T, Nozoe E, Setoyama M. Pigmented ameloblastic fibro-odontoma with melanophages. Oral Surg Oral Med Oral Pathol, 1994; 77(3):271-275.

8. Veis A, Tziafas D, Lambrianidis T. Delayed eruption of a central maxillary incisor: Clinical and microscopic evaluation. J Endod, 2000; 26(8):477-479.

9. Worth HM (ed). Odontomas and cysts of the jaws. In: Principles and practice of oral radiographic interpretation. Chicago: Year Book Medical, 1963; pp 420-424.

10. Wood NK, Goaz PW, Lehnert J. Mixed radiolucent-radiopaque lesions associated with teeth. In: Wood NK, Goaz PW (eds). Differential diagnosis of oral and maxillofacial lesions. Singapore: Harcourt Brace and Company Asia Pte Ltd, 1998; pp 289-314.


Kleoniki Lyroudia23, Papafi Str.54638 [email protected]

SUMMARYRhino-orbito-cerebral mucormycosis is a rare, opportunistic and often

fatal fungal infection usually occurring in immuno-compromised or diabetic patients. The treatment involves administration of Amphotericin B and surgi-cal debridement. Due to its lethal nature, early recognition of the infection is essential.

This paper reports a case of rhino-orbito-cerebral mucormycosis, which developed in a 60-year-old female patient with latent diabetes mellitus after a tooth extraction. The patient, unfortunately, succumbed due to the delayed diagnosis. This case study is combined with a review of the literature.

Keywords: Mucormycosis; Diabetes Mellitus

Doxa Mangoudi, Eleni Bourlidou, Gregory Venetis, Vasilis Antoniadis

Department of Oral and Maxillofacial SurgeryUniversity Clinic“G. Papanikolaou” General Hospital Thessaloniki, Greece



Rhino-Orbito-Cerebral Mucormycosis: A Case Report and Review of the Literature

TUPNBUP

MP

HJDBM!!TPDJFUZ

Introduction

Rhino-orbital-cerebral mucormycosis (ROCM) is an acute, opportunistic, often fatal fungal infection occurring mainly in diabetics, particularly those with ketoacidosis. Other predisposing factors include leukemia, lymphoma, disseminated neoplasms, extensive burn injuries and prolonged corticosteroid or immuno-suppressive therapy.

The disease provokes diffuse tissue necrosis. The fungi invade the walls of blood vessels, causing thrombosis and ischemia. Progression of the disease is rapid and intracranial dissemination may become fatal. The disease presents symptoms of sinusitis, nasal ulceration and palatal necrosis, while orbital invasion may lead to opthalmoplegia, proptosis, vision loss, and chemosis. Further progression of the disease may result in cerebral involvement with poor prognosis.

The principles of management comprise a high index of suspicion, early diagnosis and combined treatment with Amphotericin B and aggressive surgical debridement. Hyperbaric oxygen therapy has also been reported5,37,50.

The following report presents a case of ROCM, which developed in a patient with latent diabetes who unfortunately succumbed. A review of the literature is also presented.

Case Report

A 60-year-old female patient was admitted to “G. Papanikolaou” General hospital 2 days after a tooth extraction, with headache, malaise, left mid-facial pain, erythema, swelling and an abscess in the buccal vestibule resistant to surgical drainage. The patient was well-oriented and her vital signs were stable. Her past medical history was not significant, but laboratory examination immediately after the admission revealed uncontrolled diabetes. White blood cells were 18000 per mm3, the blood glucose level 380 mg/dl, while the urine analysis showed 3+ for glucose and ketones.

Within 14 hours the patient’s clinical picture deteriorated significantly. Physical examination showed left periorbital cellulitis, chemosis, a dilated left pupil non-reactive to light, proptosis with limited movement, and decreased vision acuity of the left eye (Fig. 1). Examination of the nasal cavity showed nothing significant, but the following day a necrotic lesion on the left side of the hard palate was revealed during oral examination. The patient rapidly developed necrotic lesions in the nose, upper lip and left infraorbital area, while chemosis and erythema progressively extended to the right side (Fig. 2). CT scan disclosed occupation of the left maxillary sinus,

The patient became progressively disoriented, pre-senting neck rigidity. Lumbar puncture was performed revealing cerebral involvement with a large count of

a perforated hard palate, and oedema of the left orbit, however, without any significant intracranial findings.

polymorphonuclear cells in the cerebrospinal fluid. The patient was finally intubated and admitted to the intensive care unit, where empiric treatment was given with intravenous metronidazole (500mg, 3 times daily), vancomycin (1gr, twice daily) and ceftriaxone (1gr, twice daily).

Figure 1. Presentation of the patient 14 hours after the admission and the drainage of the abscess

Figure 3. Photomicrographs showing non-septate right-angled branching hyphae of mucormycosis in the ground of necrotic tissue

(HE, 40x10)

Figure 4. Final picture of the patient in the intensive care unit. Note the extensive necrotic lesions in the left orbit, cheek, nose and the lips and

the chemosis and erythema covering almost all the face

Figure 2. Progressing chemosis and erythema of the left eye, expanding to the right eye. Necrotic lesions in the nose, upper lip and

infraorbital area

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62 D. Mangoud et al. Balk J Stom, Vol 13, 2009

A biopsy of the vestibule was performed. The histopathological findings revealed non-septate fungal hyphae consistent with mucormycosis (Fig. 3); the triple antibiotic scheme was stopped and Amphotericin B (0.25 mg/kg daily) was administered. However, the patient did not respond to the treatment. During the following 2 days the left eye became more proptotic and the facial necrosis rapidly spread, extending to the right side (Fig. 4). The neurological picture gradually deteriorated and the patient manifested renal failure and sepsis before unfortunately succumbing.

Discussion

ROCM is an acute opportunistic fatal fungal infection caused by the species Rhizopus, Rhizomucor and Absidia17,42,47. These saprophytic fungi can be found in soil, bread mould, rotten fruit and vegetables3,36,38,39,49,50, and seem to infect humans with compromised systemic health. The disease most commonly originates in the oral and nasal mucosa where in healthy individuals the spores normally parasitize, but are prevented from development by the mechanism of phagocytosis. In immuno-compromised patients this mechanism fails, resulting in the development of the infection.

The fungi show a remarkable affinity for arteries and grow along the internal elastic lamina causing thrombosis, ischemia and infraction6,19,20,22. The infection spreads from the oral and nasal cavity to the paranasal sinuses and enters the orbit via the ethmoid and maxillary sinuses, or through the nasolacrimal duct2. Further progression may lead to intra-cerebral extension from the orbit via the orbital apex, orbital vessels or via cribriform plate2. Diabetes, especially uncontrolled, predisposes to this infection8,19,28,38,50. The iron and glucose rich acidic environment in diabetics creates suitable conditions for fungal proliferation14,50. Other factors predisposing to mucormycosis include haematological malignancies, extensive burn injuries, chemotherapy, transplantation, prolonged corticosteroid or immuno-suppressive therapy and, rarely, AIDS10,25,34,40,41,47. Also, patients under deferoxamine therapy should be highly suspect for mucormycosis as deferoxamine provides iron to Mucorales, facilitating their growth11-13,16,33,45.

ROCM presents with a characteristic clinical picture, consisting of fever, malaise, sinusitis, chemosis, black nasal eschar, peri-orbital cellulites, and palatal necrosis. Paranasal sinuses were involved in all patients7 while sinus involvement was found in 69% and 79% according to other authors19,50. As the infection progresses to the orbit, the patient manifests ophthalmoplegia, proptosis, chemosis, vision loss due to ischemic necrosis of the intraorbital cranial nerves, orbital cellulites or ocular invasion of the mucorales4,9,43,48,50. Intracranial extension presents with

altered sensorium, hemiparesis and meningeal signs40. Patients with keto-acidosis whose clinical picture does not improve after appropriate treatment, may suggest mucormycosis28. Cavernous sinus thrombosis results from spread of infection from the orbit and presents with early vision loss. Internal carotid artery thrombosis is a rare complication leading to cerebral ischemia and infarction.

Diagnosis can be made by direct microscopy, histopathological examination or by culturing on Sabroud’s agar. Cultures are often negative, but this should not affect treatment and prognosis47,50. The fungi can be easily detected as aseptate hyphae with right-angled branching on Haematoxylin and Eosin stained sections; with periodic acid-Schiff reaction; or by Grocott-Gomonii methenamine silver nitrate stained section1,8,29,40,44,37. The predominant histological findings are ischemia and haemorrhaging necrosis, moderate suppurative inflammation and vascular thrombosis8,29,44. Plain orbit or sinus radiography are non-specific, while CT or MRI are useful imaging modalities for evaluating the extension of the disease.

Initial cerebritis is presented with bifrontal lucencies without mass. Abscess formation and bone destruction can be easily detected1,8,24. In areas of anatomic complexity, where CT or MRI are not helpful, angiography or surgical exploration should be performed1,15,23. Cerebrospinal fluid findings are usually non specific and blood cultures are rarely positive35.

The treatment of ROCM includes correction of any underlying disorder, administration of Amphotericin B, and prompt surgical intervention1. In diabetics, management of the keto-acidosis and dehydration improve overall survival rate, while the management of the immuno-suppressed patients is more difficult to achieve. Hyperbaric oxygen therapy has been reported as an adjunctive modality5,48, as it not only exerts a fungistatic effect but also boosts neovascularization30,31,37.

Amphotericin B is a fungostatic agent that is usually ineffective in eradicating the primary lesion, but it can control early micro-metastases41. Doses of 0.7-1 mg/kg/day are usually recommended26. In the past, Amphotericin B was administered after a test dose and, depending on the patient’s response, the dosage could be gradually increased. In cases of rapid progression, a sharp increase is recommended if the degree of adverse reaction is tolerated48. Medication side-effects are fever, headaches, nausea, vomiting, hypokalemia, thrombophlebitis, azotemia and renal dysfunction. The last years Liposomal Amphotericin B replaced conventional Amphotericin B, as it is less nephrotoxic and may enhance delivery properties to infected areas21,40. The lethal dose (LD50) is 10-15 higher than that of conventional Amphotericin B27. The recommended dose can be raised to 5mg/kg/day.

Extensive surgical debridement enhances survival rate and is necessary except in cases with terminal neoplasms1. Orbital exenteration is required in patients with ocular involvement or signs of retinal artery thrombosis8.

Balk J Stom, Vol 13, 2009 Rhino-Orbito-Cerebral Mucormycosis 63

Prognosis depends on the nature of the underlying disease, early diagnosis and prompt management1. Diabetics seem to have a better survival rate1,8. Indicators of poor prognosis are hemiparesis or hemiplegia, bilateral infection, renal disease leukaemia, deferoxamine therapy, palatal and facial necrosis8,48,50. Considering the fact that even when appropriate treatment is instituted, only about half of the ROCM cases survive, it can be easily concluded that early diagnosis and immediate, aggressive treatment are of great importance.

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6. Berger CJ, Disque FC, Topazian RG. Rhinocerebral mucormycosis: Diagnosis and treatment. Report of two cases. Oral Surg Oral Med Oral Path, 1975; 40:27-33.

7. Bhansali A, Bhadad S, Sharma A, Suresh V, Gupta A, Singh P, Chekarbanti A, Dash RJ. Postgrad Med J, 2004; 80:670-674.

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13. Boelaert JR, Van Roost GF, Vergauwe PL, et al. The role of desferrioxamine in dialysis-associated mucormycosis: Report of three cases and review of the literature. Clin Nephrol, 1988; 29:261-266.

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Doxa MangoudiP.O. Box 34570-10, Elta AsvestochoriThessalonikiGreeceE-mail: [email protected]

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