Oa Presentasi Baru

7/27/2019 Oa Presentasi Baru

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DEGENERATIVE JOINT DISEASE

By

Arianto Prabowo



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DEFINITION

• Morphologic, biochemical, molecular andbiomechanical changes of both cells and matrixwhich lead to softening, fibrillation, ulceration, andloss of articular cartilage, sclerosis and eburnation

of subchondral bone, osteophytes, andsubchondral cysts (American Academy of Orthopaedic Surgeons and the National Institutesof Health).

• A heterogenous group of conditions that lead to

joint symptoms and signs which are associatedwith defective integrity of articular cartilage, inaddition to related changes in the underlying boneat the joint margins (American College of Rheumatology [ACR]).



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EPIDEMIOLOGY

Prevalence

• >80% of all people over the age of 55 have

radiographic evidence of OA and 4% in

persons age 18-24.

• 10% to 30% of those affected have

significant pain and disability.

• below 45, men are affected more thanwomen , and in all of group, men = women.



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Risk Factors

• generalized predisposition

• mechanical factors



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General

• age

• obesity

• heredity

• hormonal variables• osteoporosis

• diabetes mellitus

• hypertension

• hyperuricemia• Age is the most powerful predictor of thedevelopment of OA.



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o r g a n i z a t i o n Mechanical factors

• trauma

• joint shape

• occupation: OA hip, spine and knee>> in coal miner

• sports


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o r g a n i z a t i o n PATHOGENESIS

• Genetic factor External

cause•

• Alteration of chondrocyte Mechanical stress

Release degradation enzymes

•

Alteration of cytokines alteration of • Proteoglycan matrix enzymes collagen matrix

•

• Mineralization alteration of cartilage

• Cartilage destruction• Synovitis

•

• OA symptom

•

•



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Matrix degeneration Cytokines : Il-1, TNF-

Enzymes : collagenolytic enzymes : collagenase 1(matrix

metalloproteinase-1(MMP-1)=fibroblast collagenase,

collagenase 2 (MMP-8)=neutrophil collagenase,

collagenase 3 (MMP-13) = collagenolytic activity

Nitric oxide

OA

Matrix synthesis

IGF-1 (Insulin GrowthFactor-1): cartilage

synthesis

TGF--: tissue growth

factor-beta



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o r g a n i

z a t i o n PATHOLOGY

• Not synonymous with aging – In aging : cartilage loses water

– In OA : cartilage absorbs water (cause unknown)

• The pathology of OA reflect both : – Damage to the joint

– Reaction to that damage

1. What happens to cartilage : – Cartilage becomes soft

– Cartilage proteoglycan framework breaks up

– Cartilage deforms/fibrillates/splits/peels off

– Underlying subchondral bone exposed



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2. what happens to subchondralbone – subjected to increased stress/force

– reacts by forming new bone “subchondral cysts” : exactmechanism unknown

thought to be related to increased joint fluid pressure



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o r g a n i

z a t i o nTheory formation of subchondral cyst



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3. What happens to surrounding soft tissues

• Synovium and joint capsule becomes inflamed

and swollen : - synovitis, capsulitis (bio-active

substances, joint detritus)• Inflamed synovium produces more joint fluid : -

effusion, Baker’s cyst

• Repeated episodes of inflammation result in

adhesions :• Joint pain



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TYPES AND CAUSE OF OSTEOARTHRITIS

Types of osteoarthritis :

• Primary• Secondary



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Primary OA

• Genetic predisposition (type II collagen)

• Need not necessarily affect weight-bearing

joints

• More in women

• Younger age group



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Secondary OA

• Secondary to any abnormality in joint that directlyor indirectly interferes with cartilage physiology

• e.g. – - physical trauma to joint : fracture, dislocation, meniscus

and ligament injury – - disease of joint : rheumatoid arthritis, gout, TB, septic

arthritis, etc

– - deformity of joint : congenital (SCFE, DDH), malunitedfracture, ligament laxity, epiphyseal disorders etc

– - obesity – - nutritional : RARE : Kashin-Beck disease (China :

fungus-infected wheat grain)



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CLINICAL FEATURES

Symptoms

• Joint pain

– deep, aching, poorly localized

– early, pain with use

– later, pain at rest

• Morning stiffness

– limited to involved joints – lasting less than 30 minutes

• Joint enlargement



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Symptoms

• Joint instability or buckling

• Weakness of hands• Giving way of weight-bearing joints

• Loss of function



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Signs

• Joint distribution

– predilection for DIPs, PIPs, first CMCs, spine,

hips, knees, and first MTP – usually spares MCPs, wrists, elbows, shoulders,

and ankles

• Bone enlargement of joint

• Crepitus on motion

• Pain with motion

• Limitation of range of motion



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Signs

• Malalignment and or joint deformity

• Typical hand deformities

Pattern of joint involvement• Axial : cervical and lumbar spine

• Peripheral : distal interphalangeal joint,

proximal interphalangeal joint, first

carpometacarpal joints, knees, hips



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RADIOGRAPHIC FEATURES

1 Radiographic criteria for Osteoarthritis (OA)

are as follows :

– Joint space narrowing secondary to degeneration

and disappearance of articular cartilage associatedwith subchondral sclerosis ( eburnation)

– Osteophyte formation at joint margins or sites of

ligamentous attachment

– Periarticular ossicles (often near DIP joints) – Subchondral bone cysts

– Altered shape of a bone end



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• Loss of joint and the presence of new bone

formation or osteophytes The cardinal

radiographic features

• The association between pain and the

radiographic features of OA is not constant, inthat many joint with pathologic or radiographic

evidence of this disease remain asymptomatic



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2. Radiographic grading has been

described using the above criteria :

• Grade 0 : no OA (no criteria present)

• Grade 1 : doubtful OA• Grade 2 : minimal OA

• Grade 3 : moderate OA

• Grade 4 : severe OA (four or more criteriapresent)


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• Plain film radiography has been the

mainstay of assessment of OA severity and

progression

• In the knee, medial compartment joint

space narrowing the most sensitiveindicator of disease progression

• Joint malalignment a sign of disease

progression



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Alternate Imaging Methods

• Such as CT, radionuclide imaging,ultrasound and MR imaging have been

proposed as methods to improve diagnostic

imaging of OA

• CT provides little advantage over

conventional X-ray or tomogram

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• Radionuclide imaging : inadequate,because it lack anatomic detail, and

the imaging finding are not specific

• Ultrasonic evaluation of cartilage isreliable, but it is of limited clinical use

because the weight -bearing areas are

inaccessible to interrogation

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• MR imaging show great promise as a

noninvasive means of assesing OA

– provides superb soft tissue contrast,

multiplanar and volumetric capabilities,

superior in plane resolution ( as low as 5 mm

in clinically employed sequences) and

sensitivity to early pathologic changes

– does not rely on ionizing radiation to create

images

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LABORATORY FEATURES

• Laboratory investigation do not have an important rolein the diagnosis of OA except to exclude other form of arthritis

• Typically the ESR is normal or slightly elevated in the

inflamatory stage• Aspiration and analysis of synovial fluid in

uncomplicated OA shows a noninflamatory fluid with aWBC number less than 2000/mm3 and the percentageof polymorphonuclear leucocytes below 25%. There istypicallly a predominance of mononuclear cells.Crystals may be observed including calciumpyrophosphate dehydrate (CPPD) and / or hydroxyapatite crystals.

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DIAGNOSIS

• Usually easily made from history & physical

examination

• Blood tests to differentiate from other types of

arthritis

– Total & differential white cell counts

– RH factor, LE cell, Uric acid,etc

• X-rays usually adequate to confirm diagnosis

• Occasionally MRI to exclude meniscal & other

lesions

• Occasionally arthroscopy to confirm early diagnosis

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TREATMENT

AIMS OF TREATMENT

1. To help the patient understand the

nature of the disease2. To provide psychological support

3. To alleviate pain

4. To suppress the inflamatory reaction(in the synovial membrane)

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5. To encourage the patient to remain as

physically active as possible in order to

maintain joint function and prevent

deformity6. To correct existing deformity

7. To improve function

8. To strengthen weak muscles9. To rehabilitate the individual patient

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METHODS OF TREATMENT

• Nonpharmacologic modalities

• Pharmacologic therapy

• Surgery

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Nonpharmacologic modalities

1. Patient education• Help patient understand their disease

• Make informed decision about therapy

• Adhere to recommend treatment plans

2. Self-management programs – eg Arthritis Foundation Self-Management Program

3. Personalized social support through telephonecontact

4. Weight reduction ( if overweight)• 5 kg decrease or more during the 10 years the studydecreased their risk of developing OA by more than 50%

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5. Aerobic exercise program

6. Physical therapy

– ROM exercises – Muscle-strengthening exercises

– Hot/cold therapies

– Transcutaneous electrical nerve stimulation (TENS)

7. Occupational therapy – Joint protection & energy conservation

– Assistive device for activities of daily living

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8. Assistive devices for ambulation – Ambulatory aids are used to increase stability and to

reduce or unload weigh-bearing joints

• Canes : the load on a WB joints can be reduced by using acane in the opposite hand

• Crutches : when more unweighting is required

• Walkers : these provide maximum stability but at the expenseof mobility and speed. Stairs and most outdoor environmentsare barriers to their use

9. Patellar taping

10. Appropriate foot wear

11. Lateral-wedged insoles (for genu varum)

bracing

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Pharmacologic therapy

Oral

• Analgesics – Simple : acetaminophen

– Other pure analgesics : tramadol

• Nonselective NSAID plus misoprostol or a protonpump inhibitor

• Non acetylated salicylate

• COX-2 specific inhibitor

• Structural Modifying Osteoarthritis Drug (SMOAD) – Diarchein (diacythylrhein)

• IL-1 & MMP inhibitor

– Avocado/soybean unsaponifiables : IL-1 inhibitor

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– Glucosamine sulfate (GS)

– Chondroitin sulfate (CS)• GS & CS, as chondroprotective agent :

1.Enhance cartilage cell macromolecular synthesis

2.Enhance the synthesis of hyaluronan

3.inhibit the enzymes that degrade cartilagecell macromolecular

4.Reduce joint pain reduce synovitis

– Hydroxy chloroquine, methotrexate (MTX)

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Topical

• Capsaicin

• Methylsalicylate

Intraarticular

• Corticosteroid : triamcinolone hexacetonide,methylprednisolone, prednisolone acetate

• Hyaluronic acid (hyaluronan)

• Orgotenin, yttrium-90, silicone, somatostatin,tenoxicam

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NSAID

• Chondroprotective : – Tiaprofenat

– Diclofenac – Piroxicam

– Tenidap

– Tolmetin

• Chondrodegenerative – Naproxen

– Aspirin

– Ibuprofen

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SURGERY

Indication :• Relief pain or severe disability after

failure of conservative measures to

reverse or alleviate the pathologicalprocess

• Correction of mechanical

derangement that may lead to OA

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Contraindication :

• Infection

• Poor vascular supply

• Emotional instability or occupational factors

that make surgical rehabilitation unlikely to

succeed

• Obesity (relative CI)• Serious medical illness (relative CI)

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Goal of Treatment :

To correct deformity

To relief pain

To improve activity daily living (ADL)

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o r g a n i z a t i o n SURGICAL MANAGEMENT OF ARTHRITIS

SURGERY :

Before making the decision of surgical intervention :

1. Weight the risk and benefit of each type of

procedures

2. Ability of patient to cooperate and to understand

the disease, possible outcome of the surgical

procedures

3. Cost and benefit of a procedure

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Surgery :

I. Arthroscopy - Debridement

II. Osteotomy

III. Arthroplasty

IV. Arthrodesis (fusion)

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Type of operation

• Arthroscopy1. Lavage & debridement of fibrillation

cartilage

2. Drilling, resection or abrasion of subchondral bone to growfibrocartilage on exposed subchondralbone

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DEBRIDEMENT

Indication Younger patient, nodeformity

Recovery period 3 weeks – 3 months

Improvement in Variablepain

Functional ModerateImprovement

Cost Modest Options if procedure Osteotomy, Arthrodesis,fails Total Joint Replacement

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ARTHROSCOPY




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• Technique of allo or autografting of

osteochondral Mosaic plasty

• Periosteal and perichondral resurfacing

(soft tissue arthroplasty) – One of way to harvest new cell in cartilage

defect (extrinsic repair )

• Cell transplantation

– Intrinsic repair

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Arthroscopic Mosaicplasty

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Open Mosaicplasty

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CHONDROCYTE TRANSPLANTATION

on





on





OSTEOTOMY :Operation to reduce weight of joint (osteotomy)

Osteotomy near joint

To correct biomechanics alignment which isaltered by the deformity or after minisectomy

Varus : high tibial osteotomyValgus : supracondylair femur osteotomy

on





OSTEOTOMY Indication Younger patient, mild

and moderate jointdeformity

Recovery period

3 mo’s for knee, 6 – 12 for hip

Improvement in pain Pain relief Functional Moderate

Improvement Cost Modest Options if procedure Arthrodesis, Total

fails Joint Replacement

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OSTEOTOMY




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ARTHROPLASTY :

Arthroplasty (reconstruction of a joint)

•Resection & interpositional arthroplasty

•Interpositional arthroplasty

•Artificial joint arthroplastyPartial

Total

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• Total Joint Replacement : T.K.R.

• - One of the most successful procedure

in orthopaedic surgery at the moment

introduced by Gunston in 1960

-

on





• Long term report : - relieve pain

- implant survival

• for 10 years 94%

• - As the last alternative, considered

when all other option have been

exhausted

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TOTAL JOINT REPLACEMENT

Indication : Significant pain,

loss deformity

Recovery period 3 – 6 mo

Functional improvement Significant Improvement in pain Significant

Cost Most expensive

Optional if procedure Arthrodesis

fails

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ARTHROPLASTY





on




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ARTHROPLASTY

on

ARTHROPLASTY




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on





ARTHRODESIS :- Arthrodesis (fusion of a joint)

•Although TKR give a great success,

arthrodesis which is now not muchdone – it is still use as a salvageoperation in TKR failure

- Also in active young adult patient

on SURGICAL MANAGEMENT OF ARTHRITIS





ARTHRODESIS :

Indication Young and active

(spinal arthrodesis)

Recovery period 3 – 6 Mo

Improvement in pain Significant

Functional Excellent

improvement

Cost

Modest Optional if procedure Joint replacement

fails

on





• There is still a place for fusionof the joint, although total jointreplacement has become thetreatment of choice for severeOA.

• OA in the single lowerextremity joint in a young,overweight, active patientswith severe joint destruction.

ARTHRODESIS (FUSION)

o n





Surgical intervention should be carefullycarried out :

1. Weight the advantage and

disadvantage2. Cost and benefit3. Patient tolerance4. Type of intervention

o n Treatment of OA in the future




o r g a n i z a t i o Treatment of OA in the future

• Biologic agent – Growth factor : IGF-1, ßFGF, TGF-ß

– Anticytokines :

• IL-4, IL-10, IL-13 inhibitor : as antiinflamatory

• Recombinant human IL-4 (rhIL-4) : to supress synthesis of TNF-, or IL-1 ß

• IL-13 : IL-1 ß, TNF- , dan stromelysin

• Gene therapy – Gene of TGF-ß, gene of IL-Ra

• Cytokine inhibitors : – IL-1 inhibition

– TNF- inhibitors :• Soluble TNF- receptors

• Anti TNF-

• Nitric oxide synthase inhibitors

• Metalloprotease inhibitors

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There is great potential for the effective

treatment of OA through :

• Primary• Secondary prevention strategy

• Tertiary

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• Primary prevention : – Elimination of risk factors

• Secondary prevention

– Structure modifying therapy : a new drugwhether act on symptoms or have structuremodifying properties, the later of which has noproven examples

• Tertiary prevention

– Treating pain and disability in establisheddisease

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The seven step arthritis cure

1. Consultation with an expert

2. Glucosamine and chondroitin sulfates

3. Improve the biomechanic stress to the joint

4. Exercise regularly

5. Eat a healthful diet (ACES)

6. Ideal body weight

7. Fight depression

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The seven step OA prevention program

1. Eat healthful joint preserving diet

2. Maintain the ideal BW

3. Exercise regularly

4. Prevent injuries

5. Ensure proper recovery optimize thebiomechanics to counteract stress to the joint

6. Consider use of glucosamine and chondroitinsulfates prophylactically

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