OSTEOARTHRITIS Clinical Features and Diagnosis

Bantar Suntoko Rheumatology Division Dept of Internal medicine Medical Faculty of Diponegoro Kariadi Hospital Semarang
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INTRODUCTION

Bijlsma JWJ. Ann Rheum Dis 2005

INTRODUCTION(continue)

Osteoarthritis is a complex, and HETEROGENOUS PROCESS. TRIGGERED by diverse constitutional and environmental factors. Clinical presentation of OA is extremely variable in terms of : onset, pattern of involvement and severity.
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Equally variable are the prognosis and outcome in : different patients, and at different joint sites. Despite this heterogeneity a number of generalizations about OA can be made :
no primary extra-loco motor manifestations usually only one or a few joints are problematic slow evolution of symptoms and structural change strong age association uncommon before middle age

Definition: OA diseases are a result of both

mechanical and biologic event that destabilize the normal coupling of degradation and synthesis of articular cartilage,chondrocytes,extra cellular matrix,and subchondral bone

Manifest by morphologic,biochemical,molecular
and biomechanical changes of cells and matrix which lead to a softening, fibrillation, ulceration,loss of articular cartilage, sclerosis, eburnation of subchodral

bone, osteophytes,subchodral cyst

Classification of Osteoarthritis
(adapted from Altman et al )

Idiopathic Localized (eg,hands,feet,knees,hips and other joint Generalised (three or more joint groups listed above Secondary post traumatic congenital or developmental diseases localized ( eg hip dysplasia) generalized (eg,chondrodysplasia,inherited metabolic calsium deposition disease Other bone and joint disorders (eg,avascular
necrosis,RA,Pagets disease )
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single sites)

diseases(ochronosis,haemochromatosis)

Classification of Osteoarthritis (continue)

Other diseases

endocrine diseases
(eg,acromegaly,hyperparathyroidism )

Neuropathic ( Charcots disease) Miscellaneous

Risk factors
Genetic factor sex inherited disorders of type II collagen mutations in type II collagen gene other inherited disorders of bone and joints race, ethnicity Non genetic Environmental factors increasing age occupations and physical overweight demand of work depletion of female sex hormone major trauma to joints leisure previous joint surgery (menicectomy) and or sport activity

OA: disease of articular cartilage

Articular cartilage function :
1. Absorbing stress by deforming under mechanical load 2. Providing a smooth load bearing surface to permit low friction movement of the joint
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Joint degeneration cause OA Cartilage matrix disruption

Chondrocyte response to matrix disruption

increasing matrix synthesis it response may restore,maintain the tissue in altered state,or increase cartilage volume

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mechanical stress & enzymatic degradation collagen meshwork damage concentration agrecan & proteoglycan decrease water concentration increase matrix stiffness decrease and permeability increase

 Chondrocytes can sustain an increased

level of activity for years

Repair response

chondrocyte response decrease catabolic activity exceed than anabolic articular cartilage is loss leaving subchondral bone exposed chondrocyte proliferation increase matrix synthesis

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Sendi Normal dan Perubahannya Pada OA

Tulang subkhondral Tekstur tulang subkhondral normal

menebal dan ireguler,

tampak sklerostik dan pembentukan kista

Rawan sendi normal, tebal dan rata

Kapsul mengalami fibrosis, distorsi dan penebalan Fibrilasi, kerusakan dan berkurangnya volume rawan sendi

Ujung tulang rata Sinovium normal dengan selapis sel tunggal Kapsul sendi tebal

Sinovitis kronik
Pertumbuhan osteofit, dan penebalan jaringan ikat lunak
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Composition of cartilage
1.Extra cellular matrix 2.Intra cellular matrix proteoglican chondrocyte type II collagen MTP I,MTP 3,stromelisin water TGF ,TGF @, IL-1,
TNF @
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CLINICAL FEATURES

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Common symptoms and sign of OA

Symptoms Pain Stiffness Alteration in shape Functional impairment + anxiety, depression Signs Crepitus Restricted movement Tenderness - joint line - periarticular Bony swelling Deformity Muscle wasting / weakness + effusions, increased warmth + instability
OReilly S, Doherty M. in OA Oxford Press 1998

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The most frequent and important joint sites to be affected by OA include : - Knee - Hand - Hip and - Spinal facets joint

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PAIN
Origins of Joint Pain In Patients With OA Tissue Subchondral bone Osteophytes Ligaments Enthesis Mechanism of Pain Medullary hypertension, microfractures Stretching of nerve endings in periosteum Stretch Inflammation

Joint capsule
Periarticular muscle Synovium

Inflammation, distention
Spasm Inflammation
Brandt KD. Diagnosis and Nonsurgical Management of OA
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Possible causes of pain in OA : Potential sites and mechanisms of local pain generation in OA. Brandt KD et al. Oxford Med. Publ OA 1998

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- Distribution of OA of the knee joint. - OA of the knees can affect any combination of the three main compartments of each knee. - The most frequently involved are the medial tibiofemoral and and patello femoral
Huskisson EC et al. Ann Rheum Dis 1979 28

Distribution of OA of the hands

Swanson AB, Swanson G. Clin Rheum Dis 1985 29

Laboratory examination
X RAY:

marginal osteophyte asymmetrical joint space narrowing subchondral bone sclerosis subchodral cyts formation deformity of bone ends

Laboratory test:normal

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DIAGNOSIS

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ESSENTIALS OF DIAGNOSIS

Joint pain brought on and exacerbated by activity and relieved with rest. Stiffness that is self-limited upon awakening in the morning or when rising from a seated position after an extended period of inactivity. Absence of prominent constitusional symptoms. Examination notable for increased bony prominence at the joint margins, crepitance or a grating sensation upon joint manipulation, and little if any associated joint effusion. Diagnosis supported by radiographic features of joint space narrowing and spur (or osteophyte) formation.
33 Gelber AC, Current Rheum Diagnosis and Treatment 2004

Plain radiographic features of Osteoarthritis

The plain radiograph remains a key investigation in the clinical management of OA. It is particularly helpful for : 1) diagnosis showing characteristic structural changes typical of OA and absence of features of alternative arthropathies (for example, inflammatory erosive disease); 2) assessment of the severity of structural change; 3) identification of associated chondrocalcinosis.34

In interpreting the radiograph a number of important caveats need to be remembered, most importantly :
1) the common discordance between symptoms, disability, and degree of structural OA change for determination of symptom causation, the radiograph is no substitute for a thorough history and examination; 2) requirement of optimal views and techniques for example, in certain joints the assessment of joint space narrowing requires stressed (loaded) views; 3) lack of specificity of individual radiographic features;

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4) difficulties with quantification of OA changes the radiograph is relatively insensitive for detection of early OA and minor progression of cartilage and bone change (as may be required for intervention studies; 5) a static, not dynamic, assessment the radiograph provides an anatomical record of prior OA changes; scintigraphy and magnetic resonance imaging (MRI) are more informative of current dynamic, physiological change.
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RADIOGRAPHY

Diagnosis of OA is usually based on clinical and radiographic features. Disparity between the severity of radiographic findings and severity of symptoms or functional impairment in OA is common.

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The grading scale which has been employed for assessment of the severity of OA : Kellgren and Lawrence (K & L) scale.

Grade Grade 0 Grade I Grade II Grade III Grade IV None

OA Severity

Radiographic Findings No features of OA Minute osteophyte, doubtful significance Defenite osteophyte, unimpaired joint space Moderate diminution of joint space Joint space greatly impaired with sclerosis of subchondral bone

Doubtful Minimal Moderate Severe

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Misinterpretation of joint pain in patients with radiographic evidence of OA

The source of the pain is not osteoarthritis but - Some other type of arthritis - Pathologic changes in the adjacent bone (tumor, osteomyelitis, metabolic bone disease, etc) - Mechanical injury, pathologic fracture. - Referred pain of neuritis, neuropathy, or radiculopathy (eg, L4 radiculopathy may cause pain in the knee or greater trochanter) - Other neurologic disorders causing stiffness of joints (Parkinsons disease, upper motor neuron damage, etc) - Soft tissue rheumatism independent of osteoarthritis (OA) (eg, de Quervains tenosynovitis) The source of the pain is osteoarthritis but not at the joint suspected, for example : - OA of the hip causing pain localized to the knee - OA of the cervical apophyseal joints (C4-5) causing pain in the shoulder - OA of the acromioclavicular joint causing pain in the shoulder - OA of the lumbar apophyseal joints causing pain in the hip, knee, or ankle The pain is caused by secondary soft tissue rheumatism, for example : - Ligamentous instability (especially of the knee) - Enthesopathy - Bursitis 39

distribusi

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Osteoartritis sendi lutut

Femorotibial
Gr.1-2 Gr. 3 Gr.4

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Osteoartritis sendi lutut Kista subkondral

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Osteoartritis sendi lutut

patellofemoral

Loose bodies

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Osteoartritis sendi bahu

AC

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Osteoartritis sendi-sendi tangan

Metacarpal trapezoid Kista

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Osteoartritis sendi-sendi tangan

Herbeden

Bouchard

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Osteoartritis tulang belakang

Facet joint Diskus intervertebralis

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Osteoartritis tulang belakang

OA Facet joint

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Osteoartritis tulang belakang OA Facet joint For. Luschka osteopfit

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Osteoartritis tulang belakang OA Facet joint

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Osteoartritis tulang belakang

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Osteoartritis tulang belakang

Costovertebral

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Osteoartritis tulang belakang Spondilosis

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Osteoartritis tulang belakang

Spondilosis

Spondilolisthesis
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Main objectives in the management OA

Reduce symptoms: pain Minimize functional disability Limit progression of the structure changes

Comprehensive and individualized

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Non Pharmacologic therapy

Patient education: weigh loss ( if overweight ) Physical therapy: ROM exercises Quadriceps strengthening exercises Assistive devices for ambulation

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Pharmacologic therapy
Oral
Acetaminopen:should not exceed 4 g/day Cox-2 specific inhibitor Non selective NSAIDs plus misoprostol or proton pump inhibitor Opiad analgesic (eg, codein,propoxyphene,oxycodone)

Injection: Steroid intra articular

Hyaluronan acid Topical: Capsaicin Methyl salicylate cream

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Another therapy
Tidal lavage Surgical Acupuncture ? Agent under investigation
glukosamine and chodroitin sulfate DMOADs Autologous chondrocyte transplatation Autologous osteochondral plug

(mosaicplasty) mesenchymal stem cell

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Role of glucosamine and chondroitin sulfate

glucosamine:source crab,lobster,shrimp shell:
and proteoglicans stimulate synoviocytes mild anti inflammation
stimulate chondrocyte production collagen

chondroitin sulfate:source bovine trachea

inhibit degradatative enzymes add to GAG pool prevention of synovial thrombusi

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Hurley et al

Quadriceps weakness is common among patients with knee OA,cause 1.decrease stability of the knee joints 2.reduce the shock-attenuating capacity of muscle 3.decrease in sensory dysfungtion ( propioception )
Hurley et al.Rheum Dis clin north Am 1999;25:283-98
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Physiotherapist or occupational therapist Make individualized assessment: range of motion muscle strengthening endurance aerobic capacity function use of external device
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Risk factor for upper GI adverse event

Age > 65 years old Comorbid medical condition Oral glucocorticoid History of peptic ulcer disease History of GI bleeding Anti coagulant Smoking Alcohol consumption
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Risk factors renal failure using NSAIDs

Age > 65 years old Hypertension CHF Concomitant use of diuretics Concomitant ACE inhibitor Existing renal insuficiency

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Exercise makes people happy; it helps me to stop thinking of the meaningless.

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Thank You

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