Diseases Of The Joints

Diseases of the Joints

OSTEOARTHRITIS (DEGENERATIVE JOINT :(DISEASE, OSTEOARTHROSIS Adegenerative disease of the articular cartilage .rather than an inflammation of bones & joints .It is the commonest chronic joint disease It affectsmainly the large weight bearing joints , particularly the hip and knee, and the joints of .the cervical & lower lumbar vertebrae It is.mainly a disease of the elderly

:Pathology The earliest change is loss of proteoglycan from .1 the superficial zone of the articular cartilage, followed by disruption of the smooth surface of the cartilage, then fissuring & finally completeloss of the articular cartilage with exposure of the underlying bone which becomes thickened, hard, .(smooth & polished (eburnation Cartilage cells at the periphery of the articular .2 cartilage proliferate to form small cartilagenous nodules that change into “osteophytes” by .endochondral ossification Osteophytes may cause deformity, limitation of .movement and pressure effects A reactive inflammation develops in the synovium .3 .& peri-articular tissues, ending in fibrosis

:Clinical Features Pain and stiffness of the affected joints .1 A characteristic limp in osteoarthritis of .2 the hip joint Decreased cerebral blood flow due to .3 compression of the vertebral arteries by osteophytes

:Etiology & Pathogenesis Poorly understood and probably multifactorial. One or more of :the following factors may be involved An alteration in the biochemical composition of the articular .1 cartilage which may be genetically determined Exaggerated wear & tear of the articular cartilage in old age .2 Local ischemia due to severe atherosclerosis in old age .3 (Continuous overload on joints by increased weight (obesity .4 Continuous overuse of joints e.g. knees & ankles in foot .5 ball players & metatarso-phalangeal joints in ballet dancers Secondary response to previous joint injury by repeated .6 (trauma or arthritis (septic or rheumatoid

:RHEUMATOID ARTHRITIS A chronic, slowly progressive, systemic autoimmune inflammatory disease mainly affecting the joints, particularly thesmall .joints of the hands and feet It is commoner infemales and usually occurs between20-50 yrs of age

:Etiology and pathogenesis Rheumatoid arthritis results from an autoimmune reaction that develops in genetically predisposed individuals upon exposure to an appropriate antigenic stimulus, which may :be either An .1infective agent such as EBV or human parvovirus An .2endogenous antigen : IgG or type II collagen The antigen is taken up by macrophages and synovial lining cells that process it and present it to T-lymphocytes which then proliferate and activate B- lymphocytes that transform into plasma cells which secrete immunoglobulins including .rheumatoid factors Also, activated macrophages release factors that lead to destruction of articular cartilage and proliferation of .endothelial cells

:Articular Lesions Inflammation & hyperplasia of the .1 :synovium The inflamed synovium isgrossly thickened, villous .& congested Microscopically:, it shows the following a) Heavy infiltration by lymphocytes & plasma cells b) Increased vascularity c) Hyperplasia of the synovial lining cells d) Accumulation of fibrin on the surface of the synovium The synovial fluid is increased and shows .2 .increased fibrinogen and neutrophils

:Pannus formation .3 Granulation tissue known as “pannus” extends from the inflamed synovium over the surface of the articular cartilage eroding & destroying it as it .progresses The articular cartilage is eventually replaced by fibrous tissue following fibrosis of the pannus on .the articular surface If granulation tissue from both articular surfaces becomes adherent, subsequent fibrosis of the granulation tissue will lead to obliteration of the joint cavity by fibrous adhesions between the (two articular surfaces (fibrous ankylosis

An inflammatory reaction .4 similar to that occuring in the joint also occursin the synovial sheaths around the tendons, ending in their destruction & fibrosis

:Extra-articular lesions :Rheumatoid factors .1 IgM, IgG or IgA antibodies present in the serum and synovial fluid of 85% of rheumatoid .arthritis patients They can be detected by a special agglutination test . known as theF2 latex fixation test Seropositive patients have a worse prognosis than seronegative patients

:Rheumatoid nodules .2 Occur in 20 -35% of rheumatoid arthritis patients typically in the subcutaneous tissue over the elbows .and rarely in the viscera Microscopically, each consists of a central area of fibrinoid necrosis surrounded by pallisaded histiocytes, lymphocytes and plasma cells

Ulnar deviation of the .3 wrist due to disuse atrophy of small muscles of hands and fingers

Arteritis .4 due to immune .complex deposition It may lead to hemorrhages in nail folds, peripheral neuropathy, visceral infarcts andgangrene of digits

:Cardiac lesions .5 a) Rheumatoid nodules in the conducting system which may lead to heart block b) Coronary arteritis which may lead to myocardial infarction c) Myocarditis and endocarditis

:Pulmonary lesions .6 (a) Large rheumatoid nodules (Caplan’s syndrome b) Diffuse interstitial fibrosis :Serosal inflammation .7 a) Pericarditis b) Pleurisy

Splenomegaly with hypersplenism and .8 granulocytopenia in some patients (Felty’s (syndome in adults andStill’s disease in children Enlargement and decreased secretion of .9 salivary and lacrimal glands in some patients, particularly middle aged females (Sjogren’s (syndrome Enlargement of lymph nodes due to .10 reactive follicular hyperplasia Secondary amyloidosis .11 in 20% of patients

:GOUT AND GOUTY ARTHRITIS Gout is a disease resulting from hyperuricemia i.e. increase of serum ureate concentration above 7 mg/dl in adult males & 6 mg/dl in adult females

:Causes Primary gout .1in which the hyperuricemia is not a .consequence of another disease It usually occurs in middle aged males, often giving a .positive family hisory The hyperuricemia results from increased production or decreased excretion of uric acid or both probably .due to specific enzymatic disorders Secondary gout .2which develops in the course of another disease e.g. leukemia, chronic renal failure, hyperparathyroidism, or drug therapy e.g. diuretics

:Pathology Lesions result from deposition of ureate crystals in various tissues, particularly articular and peri-articular tissues as :well as the subcutaneous tissue Deposition of ureate in the synovium and peri-articular tissue results in an inflammatory reaction which is first .acute then becomes chronic ending in fibrous ankylosis Deposition of ureate in subcutaneous tissue leads to the formation of multiple firm nodules known as “tophi” that .develop most commonly on the ears, fingers & elbows Microscopically, tophi consist of needle shaped ureate crystals surrounded by macrophages, lymphocytes & foreign body .giant cells

:Clinical Features Acute arthritis .1 with pain, swelling and redness of the affected joints. The first attack usually occurs in the .metatarsophalangeal joint of the big toe Chronic arthritis .2 following repeated attacks of acute arthritis. it may lead to deformity and limitation of .movement Gout nephropathy .3 due to deposition of ureate crystals in .the renal medulla and the formation of uric acid stones It may lead to.)chonic renal failure & death ) 20% of patients