Osteoarthritis: Cause, Diagnosis and Treatment
It is the progressive, degenerative joint disease characterized by the loss of cartilage, resulting from bone spurs formation (osteophytes), pain, limitation of motion, deformity, and progressive disability.
Ageing, obesity, muscle weakness, joint abrasion, metabolic endocrine disease, congenital
Pathogenesis of Osteoarthritis
Damage to articular cartilage due to injury (inflammation, trauma, excess joint loading due to obesity) $\longrightarrow$ Activation of IL-1, TNF-$\alpha$ $\longrightarrow$ Activation of inducible nitric oxide (NO) synthase $\longrightarrow$ Production of NO $\longrightarrow$ Increased metabolic activity of chondrocytes $\longrightarrow$ Increased synthesis of matrix constituents and cartilage swelling $\longrightarrow$ Increased synthesis of matrix metalloproteinases (MMPs) 1, 3, 13, and 28 Collagen destruction (faster than synthesis) followed by net loss of cartilage followed by the destruction of articular cartilage and formation of osteophytes in the subchondral areas and at the margin of the joints $\longrightarrow$ Decreased space of the joint cavity and restricted joint movement.
[The pain in case of OA arises from the activation of nociceptive nerve endings in the joints by mechanical and chemical irritants].
Commonly affected joints: Mainly weight bearing diarthrodial joints of the peripheral and axial skeleton (knees hips). [In case of OA large joints are 1st affected where as in case of RA small joints are 1st affected].
Characteristic osteophytes and joint space reduction.
Blood: ESR is normal (except in case of the injury is induced by inflammation where ESR is slightly elevated).
Synovial fluid: Viscosity is high with a mild leukocytosis (less than 2,000 white blood cells/ $mm^3$) with predominantly mononuclear cells.
Osteoarthritis treatment algorithm pdf
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