By S.Gnana Sekar

Post Graduate Student Dept. of Periodontics ,

GDC,VIJAYAWADA.

CONTENTS :

WHAT IS A BONE ? COMPOSITION OF BONE .

IS THERE ANY DIFFERENCE BETWEEN ALVEOLAR BONE AND NORMAL BONE ?

DEVELOPMENT OF ALVEOLAR PROCESS

STRUCTURE OF ALVEOLAR PROCESS

NERVE SUPPLY OF ALVEOLAR BONE

BLOOD SUPPLLY OF ALVEOLAR BONE

LYMPHATIC DRAINAGE OF ALVEOLAR BONEALVEOLAR BONE; RADIOGRAPHIC INTERORETATION

AGE CHANGES IN ALVEOLAR PROCESS

HISTOLOGY OF ALVEOLAR BONE

REMODELLING OF BONE

FACTORS REGULATING BONE FORMATION

FACTORS REGULATING BONE RESORPTION

REGULATION OF BONE BY SYSTEMIC HORMONES

BONE COUPLING

ALVEOLAR BONE IN DISEASE

(a)Bone destruction caused by extension of gingival inflammation

(b) Pharmacologic Agents & Bone Resorption

(c)Bone destruction caused by trauma of occlusion

BONE REGERATIVE PROCEDURES

REFERENCES

WHAT IS A BONE ?????

Inorganic material – 65%        Hydroxyapatite

Organic material – 35%

         Collagen (Type – I) 88% - 89% Noncollagen 11% - 12% -         Glycoproteins 6.5% - 10% -         Proteoglycans 0.8% -         Sialoproteins - 0.35%

-  Lipids - 0.4%

Only a subset of BMPs, most notably BMP 2,4,6,7,9 has osteoinductive activity.

COMPOSITION :

Osteocalcin - also known as bone gamma-carboxyglutamic acid-containing protein (BGLAP), is a noncollagenous protein found in bone and dentin.

Because it has gla domains, its synthesis is vitamin K dependent. Osteocalcin is secreted solely by osteoblasts In bone mineralization and calcium ion homeostasis.

Osteonectin - is a glycoprotein in the bone that binds calcium. It is secreted by osteoblasts during bone formation, initiating mineralization and promoting mineral crystal formation.

Osteonectin also increases the production and activity of matrix metalloproteinases, a function important to invading cancer cells within bone.

Osteopontin (OPN) - also known as bone sialoprotein I (BSP-1 or BNSP) –plays role in mineralization and bone remodelling.

What is alveolar bone ???

Alveolar bone is defined as the parts of maxilla and mandible that form and support the socket of teeth.

CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY- Jan Lindhe pg:34

Together with the root cementum and periodontal ligament, the alveolar bone constitutes the attachment apparatus of the teeth.

Forms when tooth erupts to provide osseous attachment to the forming PDL, disappears gradually after tooth is lost.

Develops and undergo remodeling with tooth formation, hence tooth-dependent bony structures.

Size, shape, location and function of teeth determine their morphology.

IS THERE ANY DIFFERENCE BETWEEN NORMAL BONE AND ALVEOLAR PROCESS /BONE ????

DEVELOPMENT OF ALVEOLAR PROCESS………

DEVELOPMENT OF ALVEOLAR PROCESS .

Meckel’s cartilage

For its development & maintenance

Morphology of Alv. Bone depends on

Size

Shape

position of teeth

If teeth are lost, Alv bone undergoes atrophy

If teeth congenitally missing – Alv. Bone not developed

                                                                                                   

  The alveolar process is composed of two parts. They are

(1)Alveolar bone proper(2)Supporting alveolar bone

STRUCTURE OF ALVEOLAR PROCESS :

Jaw bones

Basal boneAlveolar process

Alveolar bone proper

Supporting alveolar

bone

Cortical plates buccal ,lingual

Spongy bone

1 Alveolar bone proper : It consists of a thin lamella of bone that surrounds the root of the tooth and give attachment to principle fibers of the periodontal ligament.

Anatomically called as – Histologically called as – Radiologically called as - -         It is perforated by many openings that carry nerves and blood vessels in to the periodontal ligament therefore it is called cribriform plate. -

Histologic section showing foramen in alveolar bone proper (cribriform plate)

C

A

B

A-Periodontal ligamentB-CementumC-Foramen in alv. Bone proper

-         Consist of lamellated bone and bundle bone.

The bundle bone is that bone in which the principal fibers of the periodontal ligament are anchored.

The term “bundle bone” was chosen because the bundles of the principal fibers continue in to bone as sharpey’s fibers.

Bundle bone

2.supporting alveolar bone : : It is that part of the bone which surrounds the alveolar bone proper and gives supports to the socket. -     It consists of two parts : a    Cortical plates b    Spongy bone :

a.   CORTICAL PLATES : (1.5-3mm thick in posterior tooth region and thickness varies in anterior region ) -         It consists of compact bone and form the outer and inner plates of the alveolar processes. -         It is continuous with the bony maxilla and mandible and is much thicker in the mandible than in the maxilla. They are thickest in the mandibular premolar and molar regions especially on the buccal side. -         In the maxilla the outer cortical plate is perforated by many small openings through which blood and lymph vessels pass. In the mandible it is dense.

b.   SPONGY BONE :

-         It fills the area between cortical plates and the alveolar bone proper.

-         In the region of the anterior teeth of both jaws the supporting bone is usually thin, so no spongy bone is found here.

-     Roentgenograms permits the classification of the spongiosa of the alveolar process in to two main types.

Type : I :- interdental and interradicular trabecular are regular and horizontal in a ladder like arrangement.

More common in mandible.

Type : II :- shows irregularly arranged, numerous delicate interdental and interradicular trabecular.

More common in maxilla. Type-II

Type-I

Roentgenographic features

Figure shows Haversian system

Histology of Alveolar bone :

The interdental and interradicular septa contain the perforating canals of Zuckerkandl and Hirschfeld (Nutrient canals),which house the interdental and interradicular arteries ,veins ,lymph vessels and nerves.

Nutrient canal

Tooth

         The shape of the outlines of the crest of the alveolar septa in the roentgenogram is dependent on the position of the adjacent teeth.

1.5-2mm – always maintained through out the life and is constant.

Diagram of relation between CE junction of adjacent teeth shape of crest of alveolar septa

CREST OF ALVEOLAR BONE :

In

Health

Nerve Supply of Alveolar Bone

Blood Supply of Alveolar Bone

Lymphatic Drainage of Alveolar Bone

Osteoprogenitor cells :Undifferentiated mesenchymal cells and

hemotopoetic stem cells – under certain circumstances they divide and transform in to osteoblasts and osteoclasts.

y

RUNX2 is a key transcription factor associated with osteoblast differentiation.

β-catenin is a subunit of the cadherin protein complex and acts as an intracellular signal transducer in the Wnt signaling pathway.

colony stimulating factor 1 (CSF1), also known as macrophage colony-stimulating factor (M-CSF), is a secreted cytokine which influences hematopoietic stem cells to differentiate into macrophages or other related cell types

RANKLMember of the tumor necrosis factor (TNF) cytokine family.

Also known as – Tumor necrosis factor ligand superfamily member 11 (TNFSF11), TNF-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL), and osteoclast differentiation factor (ODF)

Bone marrow expresses low levels of RANKL, it plays a critical role for adequate bone metabolism, this surface-bound molecule (also known as CD254) found on osteoblasts serves to activate osteoclasts, which are critically involved in bone resorption.

Osteoclastic activity is triggered via the osteoblasts' surface-bound RANKL activating the osteoclasts' surface-bound receptor activator of nuclear factor kappa-B (RANK).

stimulation of osteoclast diffrentiation and bone resorption (lacey et.al 1998 ,kong et al 1999 )

Anti-RANKL antibody - Denosumab

RANK Member of the tumor necrosis factor receptor (TNFR) cytokine family

Also known as TRANCE Receptor or TNFRSF11A

RANK is the receptor for RANK-Ligand (RANKL) and part of the RANK/RANKL/OPG signaling pathway that regulates osteoclast differentiation and activation

RANKL binds to RANK, which then binds to TRAF6

TRAF6 stimulates the activation of the c-jun N-terminal kinase (JNK) and nuclear factor kappa-b (NF-kB) pathways

which trigger differentiation and activation of osteoclasts.

OSTEOPROTEGERIN Osteoprotegerin is a cytokine receptor, and a member of the

tumor necrosis factor (TNF) receptor superfamily.

Also known as osteoclastogenesis inhibitory factor (OCIF), or tumor necrosis factor receptor superfamily member 11B (TNFRSF11B).

Acts as a decoy and blocks the binding of RANKL to RANK and thus prevents Osteoclastogenesis

Osteoblasts : Derived from……. multipotent UNDIFFERENTIATED mesenchymal cells or alternatively from perivascular cells (PERICYTES).

Secretes both “collagenous(type 1 collagen) and non collagenous” bone matrix – OSTEOID .

Osteoblasts exhibit high level of alkaline phosphatase on their outer plasma membrane - believed to contribute - initiation of bone mineralization.

During osteogenesis osteoblasts secrete GF

OSTEOGENIC LINE OF CELLS :

TGF-β

BMP

PDG-F

IGF’S

2,7 -osteoinductive

FUNCTIONS :

Regulation of osteoclasts and deposition of bone matrix ( MACKIE 2003)

Bone remodeling and mineral metabolism Mineralization of new bone

Secrete type I collagen ,type V collagen, osteonectin, osteopontin ,RANKL, osteoprotegerin, growth factors

Osteocalcin and CBFA1

Express alkaline phosphatase

Recognize resorptive signal and transmit to osteoclast.

CBFA-1 – regulate the expression of osteoprotegerin.

OSTEOCYTES : (NERVE CELLS OF BONE ) Most abundant bone cells .

Communicate with each other and with other cells on surface of the bone via dendritic process encapsulated in canaliculi

Play role in calcium homeostasis

Exchange of metabolic and biochemical messages occurs between blood stream and canaliculi

Acts as mechanosensors instructing osteoclasts where to resorb and osteoblasts where and when to form (BOULPAEP AND BORON 2005 : MANOLAGAS 2000 )

Osteoclasts : (2-10 or as many as 50 nuclei)

Generally occur in clusters. They have prominent mitochondria, lysozomes, vacuoles and few endoplasmic reticulum.

Activity is controlled by PTH

They are found against the bone surface, occupying shallow depressions called Howship’s lacunaesurfaces or in deep resorption cavities called cutting cones.

Sequence of events;

Removal of mineral/inorganic Matrix

Degradation of org. matrix

Morphologic Characteristics

Ruffled/ Striated border

Clear zone

MORPHOLOGY : 40 to 100 microns in diameter

15 to 20 closely packed nuclei

Variable in shape

BONE LINING CELLS :

Similar to osteocytes – i.e., osteoblasts that do not get embedded in newly formed bone ,gets adhered to the outer surface of the bone

…..when bone formation halts.

Bone modeling and remodelling ….( does both same???)

  In the haversian canals, closest to the surface, osteoclasts differentiate and resorb the haversian lamellae and part of circumferential lamellae which is replaced by proliferating loose connective tissue. This area of resorption is called the cutting cone or the resorption tunnel.

Light micrograph of bone turnover. A, Cutting cone in cross section. Large multinucleated osteoclasts resorb an old osteon. B, Filling cone in cross section. Uninucleated osteoblasts ring the partially formed osteon.

Bone remodelingREMODELING involves the removal of discrete packets of old bone ,replacement of these packets with newly synthesised protenaceous matrix and subsequent mineralization of the matrixto form new bone . ( fernandez –tresguerres –hernandez et.al 2006 )

Remodeling of boneBone multicellular unit(BMU): local groups of osteoblasts and osteoclasts involved in bone remodelling is called bone

multicellular units (BMU).

  - each unit is organized into "cutting cone" of osteoclasts reabsorbing bone followed by trail

of osteoblasts reforming the bone to fill defect Osteoclast recruitmentResorptionOsteoblast recruitmentOriginationOsteiod formation MineralizationMineral maturationQuiescence: osteoblasts become resting bone lining cells on the newly formed bone surface

Osteoblast

Osteoclast progenitor cellMature osteoclast

RANKL+RANK

Bone resorption

RANKL+RAaNK

OPG

RANKL

RANK RANK

If OPG+RANKL=inhibit osteoclast genesis

BONE COUPLING:

New bone formation occurs at bone resorption sites in each cycle of bone remodeling to maintain the microarchitecture required for bone's mechanical properties. This is achieved through different levels of cellular communication. In bone matrix, TGF-β1, and probably IGF-1, act as the primary coupling factors and are released in response to osteoclastic bone resorption. These factors induce the migration of osteoblastic cells so that the new bone formation is spatiotemporally coupled with resorption through this mode of matricellular signaling. Negishi-Koga et al now reveal that Sema4D secreted from osteoclasts regulates osteoblast differentiation; Sema4D activates downstream of RhoA by binding to Plexin-B. RhoA also mediates the actions of both TGF-β1 and IGF-1. Thus, the matricellular signaling of TGF-β1 and IGF-1 is integrated with Sema4D–Plexin-B1–mediated osteoclast-osteoblast communication through RhoA. RANK-RANKL mediates communication to induce differentiation of osteoclast progenitors. Osteoclastic production of Sema4D is stimulated by increased osteoblastic RANKL. Sema4D then inhibits osteoblast differentiation to balance the supply of osteoclasts and osteoblasts, thus functioning in a negative-feedback loop.

Factors regulating Bone Formation1. Platlet derived growth factor2. Heparin binding growth factor3. Insulin like growth factor4. Transforming growth factor 5. Bone morphogenic protein

Factors regulating Bone Resorption1. IL 12. IL 63. TNF & Lymphotoxins4. Gamma interferon5. Colony stimulating factors6. Prostaglandin & other Arachidonic Acid

metabolites

Regulation of Bone by systemic hormones1. Parathyroid hormone2. 1,25 Dihydroxy vit D33. Calcitonin4. Estrogen

AT MICROSCOPIC LEVEL :4 types of bones are seen ….

Phase I bone/Woven bone

Composite bone

Phase II bone/lamellar bone/Mature load bearing bone

Bundle bone

Plays main role in healing

It forms very quickly(30-60mm/day) And resorbs very quickly

Forms very slowly (0.6-1mm/day)

AGE CHANGES :

Changes in the alveolar bone with aging are similar to those occurring in the reminder of the skeletal system.

More irregular periodontal surface of bone Less regular insertion of collagen fibers Osteoporosis Decreased vascularity.

Conditions involving loss of alveolar bone :The various causes of alveolar bone loss are:

I. Extension of gingival inflammation II. Trauma from occlusion III. Systemic factors

I. PeriodontitisII. Periodontal abscessIII. Food impactionIV. Overhanging restorationV. Adjacent tooth extractionVI. Ill-fitting prosthesis

BONE DISTRUCTION CAUSED BY EXTENTION OF BONE DISTRUCTION CAUSED BY EXTENTION OF GINGIVAL INFLAMMATION :GINGIVAL INFLAMMATION :

Most common cause of bone loss in periodontal disease is extension of inflammation from marginal gingiva into supporting periodontal tissues.

Spread of inflammation from gingiva directly to PDL is less frequent.

The transition from gingivitis to periodontitis is

associated with changes in compostion of bacterial

plaque.

In advanced stages number of motile organisms and

spirochetes increases.

Radius of action of plaque

Garant &Cho suggest that bacterial plaque can induce bone loss within range of 1.5 to 2.5 mm.

Page and Schroeder on the basis of waerhaug’s measurements made on human autopsy specimens, postulated that there is range of effectiveness of about 1.5 to 2.5mm within which bacterial plaque can induce loss of bone. This is known as radius of action.

Rate of bone loss

In study of Srilankan labourers with no oral hygiene & no dental care Loe & associates found the rate of bone loss to average about 0.2mm a year for facial surfaces & about 0.3mm a year for proximal surfaces.

Bone Destruction Pattern in Periodontal Disease

Horizontal bone loss Most common pattern of bone loss in

periodontal disease. Bone is reduced in height but margin remain

almost perpendicular to tooth surface not necessarily equal degree around same tooth

Bone deformities

Careful probing & surgical exposure required to determine exact dimension of the defect

Vertical / Angular bone defect.

walls remain intact.Three wall defect

Two wall defect

One wall defect

Combined defect

These defects are classified on bases of No. of osseous wallspresent :

No.of walls in the apical portion of the defect is greater than its occlusal portion .

Crater:Concavities in the crest of interdental bone

Most common osseous Defect -35.2 %

Most common inMandible – 62%

Bulbous bone contour (Exostosis) :

Bony enlargements caused by adaptation to function or buttressing bone formation etc.

More frequently found in maxilla.

Reverse Architecture

Caused because of loss of interdental, facial&/lingual wall without concomitant loss of radicular bone

-Maxilla

Ledges :Plateau like bone margins caused by

resorption of thickened bony plates .

Bone Destruction caused by Trauma from Occlusion Def:” when occlusal forces exceeds the adaptive capacity of the

tissue , tissue injury results k/a Trauma from occlusion

Primary trauma from occlusion: Alteration in occlusal forces in Normal periodontioum with normal height of bone

Secondary trauma from occlusion : Due to reduced ability of tissues to resist forces;in cases of :Normal periodontium with reduced height of bone &Marginal periodontitis with reduced height of bone

Studies related to TFO

Miyata T,Kobayashi Y, Araki H, et al;The influence of controlled occlusal overload on periimplant tissue; A histologic study in monkey ;2000.

Isidor F; Loss of ossiointegraion by occlusal load of oral implants;A clinical & radiographic study in monkeys;1996.

Harrel SK ,Nunn ME, The effect of occlusal discrepancies on peridontitis; 2001.

Bone Destruction by Systemic Disease Vit-D deficiency Diabetes Hyperparathyroidism Leukemia Paget’s disease Fibous dysplasia Histiocytosis ,X , Osteomyelitis Central giant cell granuloma Aneurysmal bone cyst

Vitamin D deficiency:

Vitamin D or calciferol - absorption of calcium from the gastrointestinal tract and the maintenance of the calcium phosphorous balance.

Experimental studies in animals showed that in osteomalacia, there is rapid, generalized severe osteoclastic resorption of alveolar bone, proliferation of fibroblasts that replace bone and marrow, and new bone formation around the remnants of unresorbed bony trabeculae.

Radiologically there is generalized partial to complete loss of lamina dura and reduced density of supporting bone, loss of trabeculae. Increased radiolucence of trabecular interstices and increased prominence of remaining trabeculae.

BOTH DEFICIENCY AND EXCESS…..???? Vitamin D at normal physiologic levels act on intestinal mucosa and the renal

distal tubule to increase the absorption of Calcium. This Calcium will then be available for use in mineralizing new bone formation.

Therefore, when you have Vitamin D deficiency you will develop rickets (in children) or osteopenia (in adults).

The issue, is that if you have too much of Vitamin D (Vitamin D excess) then at that time it will work on the nuclear receptors in the osteoblasts and promote bone resorption. – they bind to vitd receptor on osteoblasts and stimuates the expression of RANK-L - which in turn induces osteoclastogenesis

Therefore, both deficiency and excess of Vitamin D can cause osteopenia and bone resorption.

- From kaplans Textbook of physiology

Alveolar Bone Loss Progression in Diabetes:

  Taylor et al suggested that poorer glycemic control leads to both an

increased risk for alveolar bone loss and more severe progression.

Factors potentially contributing to development of periodontal disease as per the Position Paper on Diabetes and Periodontal Diseases published in the August 1999.

1. Polymorphonuclear Leukocyte Function. 2. Collagen Metabolism and Advanced Glycation End products.

HYPERGLYCEMIA –ACTIVATES OSTEOCLASTS …BUT HOW????? Hyperglycemia induces - production of macrophage colony stimulating

factor(M-CSF), Tumor Necrosis Factor –α and Rank L, all of which are osteoblast derived activators of osteoclast proliferation and differentiation.

Further suppression of osteoblast proliferation takes place by decreasing osteocalcin and osteopontin expressions.

Bone quality is also reduced as a result of advanced glycation end products, which eventually results in fractures.

Hyperparathyroidism : Oral changes include malocclusion and tooth mobility, radiographic

evidence of alveolar osteoporosis with closely meshed trabeculae, widening of the lamina dura, and radiolucent cyst like spaces.

Bone cysts become filled with fibrous tissue with abundant hemosiderin-

laden macrophages and giant cells. They have been called brown tumors, although they are not really tumors but reparative giant cell granulomas.

This disease is called osteitis fibrosa cystica or Von Recklinghausen’s

disease. Other diseases in which it may occur are Paget’s disease, fibrous

dysplasia, and osteomalacia.

Hematological disorders:

In leukemia , the presence of infiltrate in marrow spaces and the periodontal ligament results in osteoporosis of alveolar bone with destruction of the supporting bone and disappearance of periodontal fibers. (the malignant T-lymphocytes produced an osteoclast-activating-factor-like substance that caused osteoclast proliferation and hypercalcemia.)

 

In Sickle cell anemia generalized osteoporosis of the jaws, with a peculiar stepladder alignment of the trabeculae of interdental septa and pallor and yellowish discoloration of oral mucosa.

Pagets disease :In pagets disease - Osteoclasts and osteoclast

precursors contain paramyxoviral transcripts and appear hyperresponsive to 1,25-(OH)2D3 and RANK ligand (RANKL).

Osteoclasts in Paget's disease are increased both in number and size

BONE REGENERATION :Osteogenesis is the ability of the graft to produce new bone, and this process is

dependent on the presence of live bone cells in the graft.

Osteoconduction is the physical property of the graft to serve as a scaffold for viable bone healing. Osteoconduction allows for the ingrowth of neovasculature and the infiltration of osteogenic precursor cells into the graft site.

Osteoinduction is the ability of graft material to induce stem cells to differentiate into mature bone cells. This process is typically associated with the presence of bone growth factors within the graft material or as a supplement to the bone graft.

BONE GRAFTS :

Is there any relation between bisphosponates and osteoradionecrosis of jaw ??????

References:

Orban’s oral Histology &Embryology.

Fundaments of periodontics second edition by Thomos G. wilson’jr DDS ;Knneth S. Kornman’DDS,pHd

Clinical periodontology 12th edition by Neeman ,Takei,carranza

Journal of clinical periodontology Vol;27jan-May-2000;j-272

the dental clinics of North America;Advances in periodontics part -1 by david C. vandersall Vol-42,No.2, Apr.1998

Contemporary Periodontics by Robert J. Jenco; Henry M>.Goldman ;D.Walter Cohen

Clinical Dentistry in Health & Dease,vol-2 The Mouth & Perioral tissue Crispian scully

Periodontal Diseae Clinical ,Radiologic, Histopathologic features by Glickman –pSumlow

di Fiore’ s atlas of Hitology

Presented by Dr.s.Gnana sekar,GDC ,VJD.

Dr.Narendra dev(HOD &Prof)

Dr.S.V.Madhuri (ASSO. Prof)

Dr.B.Lahari (ASSIS.Prof)

Guided by