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Bones are joined together by joints, which allow varying degrees of movement between the adjacent bone ends; some joints permit considerable movement, others allowing only limited movement.
The most important type of joint that permits considerable movement is the synovial joint. Excessive movement at the joint is limited by a strong joint capsule and an enclosing ligament, assisted by attached muscles and tendons.
In joints in which there is only limited movement the bones are joined by fibrous or cartilaginous tissue, e.g. the fibrocollagenous and cartilaginous intervertebral discs between adjacent vertebral bodies.

Inflammatory disease of joints, which is grouped under the terms arthritis and synovitis, has four main causes: degenerative, e.g. osteoarthritis; autoimmune, e.g. rheumatoid arthritis, SLE, rheumatic fever; crystal depositions, e.g. gout and other crystalline arthropathies; and infective, e.g. tuberculous arthritis.

Osteoarthritis is a common and important degenerative disease with both destructive and reparative components

Osteoarthritis may arise as a primary disorder, as well as arising secondary to other joint malfunctions (particularly abnormal loading or structural deformities). The pathological changes involve cartilage, bone, synovium and joint capsule, with secondary effects on muscle. Main factors in development of osteoarthritis are ageing, abnormal load on joints, crystal deposition, and inflammation of joints.

In general, osteoarthritis affects joints that are constantly exposed to wear and tear. It is an important component of occupational joint disease, e.g. osteoarthritis of the fingers in typists, and of the knee in professional footballers. 

Previous abnormality of the joint predisposes to the early development of severe osteoarthritis (sometimes called 'secondary osteoarthritis'), causes include:

  Congenital abnormality of joints.

Trauma to joints (including trauma resulting from lack of sensory innervation).

Inflammatory joint disease.

Avascular necrosis of bone.

In a normal synovial joint the distance between the bone ends seen on radiography is maintained by the thickness of articular cartilage.
The early change in osteoarthritis is destruction of articular cartilage, which splits (fibrillation), becomes eroded and leads to narrowing of the joint space on radiography. There is inflammation and thickening of the joint capsule and synovium.
With time, there is thickening of sub-articular bone caused by constant friction of the two naked bone surfaces, leading to a highly polished bony articular surface (eburnation). Small cysts develop in the bone beneath the abnormal articular surface. Osteophytes form around the periphery of the joint by irregular outgrowths of bone. There may be reactive thickening of the synovium due to inflammation caused by bone and cartilage debris. Inflammatory changes are also often seen. Atrophy of muscle is caused by disuse following immobility of the diseased joint.
In osteoarthritis of the hands, osteophytes on the interphalangeal joints of the fingers are termed 'Heberden's nodes' and appear as small nodules.

Rheumatoid arthritis is a common and important cause of inflammatory joint disease, although it is but one manifestation of a generalized systemic disorder (Rheumatoid arthritis). It is characterized by the presence of a circulating autoantibody, 'rheumatoid factor' (seropositive arthritis), which distinguishes this form of disease from several other inflammatory joint diseases (seronegative arthritis).

Rheumatoid arthritis mainly affects peripheral synovial joints such as the fingers and wrists, but can also affect the knees and more proximal joints. Women are affected two to three times more commonly than men, and the usual age of onset is between 35 and 45 years. The affected joints become swollen, painful and warm, often with redness of the overlying skin.

In long-standing chronic disease the articular cartilage may be largely destroyed and replaced by fibrous pannus; the underlying bone shows osteolytic erosions, and the synovium lining the joint capsule is greatly thickened and chronically inflamed. The loss of articular surface can lead to the development of secondary osteoarthritic changes, particularly in weight-bearing joints such as the knee. Unlike most other autoimmune arthropathies, rheumatoid arthritis is chronic and progressive. It usually leads to eventual joint deformity, with secondary features (e.g. muscle wasting) due to disuse of the disorganized joint.

The early pathological change in rheumatoid arthritis is rheumatoid synovitis. The synovium is swollen and shows a villous pattern. There is a great increase in chronic inflammatory cells (mainly lymphocytes and plasma cells) in the synovial stroma, often with an exudate comprising fluid, which produces an effusion in the joint space, and fibrin which is deposited on the synovial surface. Soft tissue swelling from synovial inflammation can be marked.
With time, there is articular cartilage destruction; vascular granulation tissue grows across the surface of the cartilage (pannus) from the edges of the joint, and the articular surface shows loss of cartilage beneath the extending pannus, most marked at the joint margins.
The inflammatory pannus causes focal destruction of bone. At the edges of the joint there is osteolytic destruction of bone, responsible for 'erosions' seen on radiographs. This phase is associated with joint deformity.
The characteristic deformity and soft tissue swelling associated with long-standing rheumatoid disease of the hands.
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