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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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• trauma
• joint shape
• occupation: OA hip, spine and knee>> in coal miner
• sports
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• 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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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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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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c o m p a n y n a m e
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
n
ARTHROSCOPY
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c o m p a n y n a m e
o r g a n i z a t i o n 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
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o r g a n i z a t i o n
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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
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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
on
OSTEOTOMY
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c o m p a n y n a m e
o r g a n i z a t i o n 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
-
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• 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
on
ARTHROPLASTY
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ARTHROPLASTY
on
ARTHROPLASTY
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c o m p a n y n a m e
o r g a n i z a t i o ARTHROPLASTY
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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
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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
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• 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)
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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
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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