Friday, November 12, 2010



A degenerative joint disorder in which there is progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis.


Still obscure
Increased frequency with age but not an expression of senescence
Progression of cartilage lesions probable requires stiffened subchondral bone
Cartilage aging ® splitting and flaking of the surface and decreased cellularity, decreased proteoglycan ground substance and loss of elasticity with a decrease in breaking strength
Mechanical changes in subchondral bone ® stiffer and transmits more load to the cartilage
May be biological change secondary to a disturbance in lubrication of the joint and hence nutrition of cartilage
Two forms of degeneration:

Limited cartilage loss seen mainly away from load bearing areas and probably due to wear and tear.
Progressive cartilage destruction always maximal in the major load bearing area and associated with symptomatic OA

Hereditary aspects of OA:

Joint congruity, CSH / CDH / DDH, Perthes, SFCE
Gait and posture
Joint / ligament laxity
Pagets, inflammatory arthropathies


People > 60 years old ® moderate to severe OA in 8%
25% of females and 16% of males have symptomatic OA
80% people > 80 years have radiological evidence of OA
Male = Female incidence but females more symptomatic
The hip, knee and spine most commonly affected
OA of the hip more common in males than females and often unilateral, 20% eventually ® involvement of the other side


Primary Osteoarthritis: (When no cause is obvious)

Poly-arthritis affecting finger joints, (chiefly distal, thumb (basal), big toe (MTP) and often also the knees and facet joint of the spine
Usually starts in the hands but many joints become involved
Stiffness and deformity may be marked but pain usually mild or in time becomes painless
Mainly affects post menopausal women and has a marked familial incidence
Heberdens nodular arthropathy ® distal IP joint of the hands only
Sometimes, particularly in men the DIP joint changes are absent but other joints symmetrically involved and spinal changes pronounced
Primary generalised OA is associated with increased incidence of CTS and tenosynovitis
The arthropathy of the individual joints has the same pathology as mono-articular OA
Differentiate spinal changes from DISH, and distal IP joint changes from psoriatic arthropathy and gout

Secondary Osteoarthritis: (When it follows a demonstrable abnormality)

Secondary OA estimated to account for 80% of osteoarthritis
Articular degeneration results from a disparity in the stress applied to articular cartilage and the ability of the cartilage to withstand that stress.
Solomon (1976); Aetiology of OA

Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of articular cartilage due to defective subchondral bone

Classification of cartilage degeneration: (Jackson)
Class 1: Softening of articular cartilage
Class 2: Fibrillation and fissuring of articular cartilage
Class 3: Partial thickness cartilage loss, clefts and chondral flaps
Class 4: Full thickness cartilage loss with bone exposed


Usually history of previous injury or pathology evident
History of intermittent disability
Usually present with pain
May experience decreased pain as the disease ® decreased ROM
Often worse on rising from bed and at the end of the day, aggravated by activity
Exaggerated by extremes of movement
Early ® relieved by rest, later ® pain at rest

Source of pain Helal (1965)

Capsular; due to stretch at extremes of movement
Muscular: following effort
Venous congestion: ® rest pain?

Movement may be associated with crepitus
Joint effusion or osteophytes may be evident
Muscle wasting may also be a feature
Deformity may precede the development of OA, but may also result from secondary muscle imbalance, capsular contracture or joint instability.
In the hip abduction, extension and internal rotation are affected first
Hip pain referred to the knee due to the fact that the obturator nerve supplies both joints (the sciatic and femoral do as well)


Joint space narrowing
Sub-articular sclerosis
Bone cysts
Bone density is either normal or increased
There may be evidence of other pathology eg, old trauma, congenital anomalies, RA, chondrocalcinosis etc
Rapid and severe joint changes may occur, especially in patients taking analgesics and NSAIDs



Capsular ligament is supplied by both myelinated and non-myelinated nerves, the synovial layer by only non-myelinated nerves


Secrete Hyaluronate (+ lubricin)

Two cell types
Type A: phagocytosis
Type B: secretory role
Complete absence of a basement membrane
Regulates movement of solutes, electrolytes and proteins
Synovial fluid a dialyslate of plasma and hyaluronate but has less high molecular weight proteins (eg fibrinogen) and more low molecular weight protein (eg albumin)
Cartilage is connective tissue derived from the mesenchyme
Articular cartilage is avascular, aneural and alymphatic, and a small number of chondrocytes are surrounded by a large quantity of extracellular matrix
The structure of this intercellular matrix determines the type of cartilage

Normal cartil

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