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OSTEOARTHRITIS
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THE PHYSIOLOGY OF SYNOVIAL JOINTS

Anatomy of the joint
Articular Cartilage Subchondral bone Synovium Joint capsule Tendon Cancellous bone Muscle

ARTICULAR CARTILAGE
Covers the bone ends in every diarthrodeal joint transmit load and movement from one skeletal segment to another increases the area of the articular surfaces Improve adaptability and stability component is mainly type II collagen

CAPSULE AND LIGAMENTS

Helps to provide sability Overstretched or torn unstable Non-pathological ligamentous laxity stability is maintained by highly developed muscle power&the articular cartilage is not necessarily damaged.

Synovium and synovial fluid

It covers the articular surface Produces synovial fluid Target tissue in joint infections & autoimmune disorders ( RA ) Synovial fluid nourishes the avascular articular cartilage Reducing friction during movement Also helps maintaining joint stability

JOINT LUBRICATION
Boundary layer lubrication Fluid film lubrication Lubrication between synovial folds

OSTEOARTHRITIS
Osteoarthritis (OA) is a chronic joint disorder of synovial joints in which there is progressive softening and disintegration of articular cartilage accompanied by new growth of cartilage and bone at the joint margins (osteophytes), cyst formation&schlerosis in the subchondral bone, mild synovitis and capsular fibrosis. Asymmetric distributed Localized only one part of a joint related to abnormal loading Unaccompanied systemic illness

 Not a purely degenerative disorder Dynamic phenomenon : destruction& repair Cartilage softening and disintegration accompanied from hyperactive new bone formation, osteophytosis and remodelling Final figure determined by the relative vigour of these opposing processes Secodary factor of progressing disorder : the appearance of calcium-containing crystals in the joint Ischaemic changes (especially in elderly people)

secondary factors : Joint instability Prolonged anti-inflammatory medication.

Etiology

Predispose factors
Age Cartilage matrix changes (ex.crystal deposition , ochronosis) Inheritance Previous trauma & inflammatory Increase mechanical stress in the articular surface Increase load

Pathogenesis
Early stages : increase water content & extractability matrix proteoglikan Later stages : loose proteoglikan&cartilage defects Chondrocytes damage release cell enzymes matrix breakdown Forces are increasingly concentrated in the subchondral bone focal trabecular degeneration & cyst formation, increased vascularity, reactive sclerosis in the zone of maximal loading Cartilage remain : regeneration, repair and remodelling

Pathology
The cardinal features
(1) progressive cartilage destruction (2) subarticular cyst formation (3) sclerosis of the surrounding bone (4) osteophyte formation (5) capsular fibrosis.

 MEN : WOMAN 1 : 1 Age > 65 : 50 % Most commonest : fingers, hip, knee, spine RISK FACTORS Joint dysplasia : congenital acetabular dyslasia, Perthes ds Trauma : Fractures involving the articular surface & cause joint instability secondary OA

PREVALENSI

 Occupation: knee-bending activities, heavy vibrating tools Bone density Obesity : increase joint loading Family history

Clinical Feature PAIN :

widespread , referred, insidiously, increases slowly, aggravated by exertion , relieved by rest. Late stage pain in bed at night. Pain caused by capsular fibrosis Mild synovial inflammation muscular fatigue bone pressure due to vascular congestion intraosseous hypertension

STIFFNESS
occurs after periods of inactivity Later become constant & progressive

SWELLING
intermittent /continuos

Clinical Feature

Deformity : result from capsular contracture or joint instability Loss of function A limp, difficulty climbing stairs, restriction of walking distance or progressive inability to perform everyday tasks.

Typically, the symptoms of OA follow an intermittent course, with periods of remission sometimes lasting for months.

SIGN

Joint swelling Crepitus Local tenderness Deformity Instability.

IMAGING
X-Ray cardinal signs are asymmetric loss of cartilage (narrowing of the joint space) sclerosis of the subchondral bone cysts close to the articular surface Osteophytes Late : joint displacement & bone destruction Radionuclide scanning shows increased activity e.c. increased vascularity & bone formation CT and MRI Arthroscopy : may show cartilage damage before x-ray changes appear

Arthrodesis (Bone or joint fusion surgery )

to relieve pain : hips, ankles, wrists, fingers, thumbs, or spine. While a fused joint loses flexibility, it can bear weight better, is more stable and is no longer painful. for a painful or unstable joint where stiffness does not seriously affect function Young, active, heavy pt with single joint involvement Complication : pain, pseudarthrosis formation
non-union Nerve injury infection

Arthroplasty
Hip replacement is a procedure in which the surgeon removes damaged or diseased parts of the patient's hip joint and replaces them with new artificial parts (called arthroplasty ) Consideration for oa: > 60 y.o significant pain, deformity, functional loss with restricted ROM / joint instability If all other tx ineffective, and pain is severe

EXCISION ARTHROPLASTY Sufficient bone is excised to create a gap at which movement can occur (e.g.Girdlestone's hip arthroplasty). a shaped 'spacer' can be inserted; this may be tissue from another part (e.g. tendon) or artificial material like Silastic. PARTIAL REPLACEMENT One articular component only is replaced The prosthesis is kept in position either by acrylic cement or by a cementless fit between implant and bone. TOTAL REPLACEMENT Both articular bone ends are replaced by prosthetic implants

Complication :
Osteolysis from acrylic bone cement debris, bone resorption and subsequent loosening or fracture,protusio acetabuli. Post operative sciatic nerve palsy. Chronic pain.

Thank you

HAEMOPHILIC ARTHROPATHY
Manifest:
ACUTE BLEEDING (JOINT, MUSCLE,NERVE) JOINT DEGENERATION

Pathology
Haemorrhage (joint) synovial inflamation synovium thick A vascular pannus on articular surface and eroded cartilage develop large cyst release cartilage degrading enzymes

 elbow joints contractures and knees - ankles deformities recurrent haemarthrosis chronic synovitis acute joints or muscles bleeding chronic arthritis joint contractures

Clinical features

most in : knees,ankles, elbow, shoulders and hips.

ACUTE BLEEDING ( JOINT, MUSCLE OR NERVE )

Feature : common in joint a joint may rapidly fill with blood with trivial injury . Pain, warmth, boggy swelling,tenderness and limited movement large soft-tissue haematoma Neurological disorder forearm /leg bleeding potentially rise to compartment syndrome

JOINT DEGENERATION The sequel to repeated bleeding. Chronic synovitis cartilage degeneration
Arnold and Hilgartner classification : Stage I - soft-tissue swelling; StageII - osteoporosis and epiphyseal overgrowth; Stage III- slight narrowing of the articular space and squaring of the bone ends; Stage IV- marked narrowing of the articular space; and Stage V-joint disintegration.

Treatment
THE ACUTE BLEED Patient : Recognize the early symptoms of bleeding counteract the haemorrhage as soon as Frozen cryoprecipitate Fresh-frozen plasma Avoid joint aspiration

CHRONIC ARTHROPATHY Prevent to contractures, stiffness and muscle weakness. Operative treatment :
tendon lengthening osteotomy arthrodesis Synovectomy total hip replacement

NEUROPATHIC JOINT DISEASE (CHARCOT'S DISEASE)

Charcot, in 1868, described a type of destructive arthropathy associated with disease of CNS arising from loss of pain sensibility and position sense. causes : neurosyphilis syringomyelia multiple sclerosis, myelomeningocele, spinal cord compression, peripheral neuritis, leprosy and congenital indifference to pain. The early changes are similar to those of OA However, it soon becomes apparent that this is a rapidly destructive process; the articular surface breaks up, fragments of bone and cartilage appear in the joint or embedded in the synovium and there is thickening of the synovial membrane and marked joint effusion. In the late stages, there is complete loss of articular cartilage, fragmentation of the subchondral bone and joint subluxation

Clinical features
complains : weakness, instability, swelling, laxity and progressive deformity of the joint X-rays articular space thinning Osteophyte formation. Joint swelling Intra articular calcification gross erosion of the articular surfaces joint displacement

Charcot's disease The vertebrae are distorted and dense, the buttocks show the radio-opaque remains of former injections; the knee,elbow and hip joints look grotesque. Morah'lf it's bizarre, do a WR'. Note also the happy smile (though not all Charcot joints are tabetic, nor are they always painless).

Treatment No way of halting the destructive process. Conservative treatment Splintage of the unstable joint. Analgesic medication. Weightbearing joints Arthrodesis