From Robbins & Cotran,
Osteoarthritis
††† Degenerative joint disease.
††† Most common type of joint disease.
††† One of the most disabling conditions in developed nations.
††† Secondary only to cardiovascular disease in causing long-term disability.
††† Characterized by progressive erosion of articular cartilage.
††† Considered to be an intrinsic disease of articular cartilage in which biochemical & metabolic alterations result in its breakdown, irregardless of presence of inflammatory cells.
Classification
††† Primary osteoarthritis appears to be idiopathic as an aging phenomenon.
††† Usually oligoarticular but may be generalized.
††† Secondary osteoarthritis appears in younger individuals with some predisposing conditions - e.g. previous macrotraumatic/repeated microtraumatic injuries to a joint, a congenital development deformity of a joint(s), some underlying systemic disease (diabetes, ochronosis, hemochromatosis, marked obesity) etc.
††† Often involves one or several predisposed joints.
††† Gender has some influence on distribution.
††† The knees & hands are more commonly affected in women.
††† The hips are more commonly affected in men.
Pathogenesis
††† Normal articular cartilage is located at the ends of the bones - bathed in synovial fluid, in ensures virtually friction-free movements within the joint; in weight-bearing joints, it spreads the load across the joint surface in a manner that allows the underlying bones to absorb shock & weight without being crushed.
††† These functions require the cartilage to be elastic & possess high tensile strength - these attributes are provided by type-II collagen & proteoglycans, both secreted by chondrocytes as major components of the cartilage.
††† In adult bones, turnover of cartilage is maintained by chondrocytes (both synthesis & degradation) - in osteoarthritis this process is disturbed.
††† Aging & mechanical effects is a most important influence.
††† Evidence includes increasing frequency of osteoarthritis with advancing age; its occurence with weight-bearing joints; & an increase in the frequency of the disease in conditions that predispose the joints to abnormal mechanical stress - e.g. obesity & previous joint deformity.
††† Genetic factors also play a role, especially in cases involving the hands & hips.
††† Specific genes have not yet been identified, but there are suggestions linking to chromosomes 2 & 11.
††† The risk of osteoarthritis is increased in direct proportion to bone density & associated with high levels of estrogens.
††† Osteoarthritis is characterized by significant changes in both the composition & mechanical properties of cartilage.
††† Early in the course of the disease, the degenerating cartilage contains increased water & decreased concentration of proteoglycans.
††† There appears to be a weakening of the collagen network, presumably caused by decreased local synthesis of type-II collagen, & increasing breakdown of preexisting collagen.
††† The levels of certain molecular messengers (e.g. IL-1, TNF & NO) are increased & appear to be responsible for some of the changes in the composition of the cartillage.
††† Apoptosis is increased, likely responsible for the decreasing number of chondrocytes.
††† Cumulatively, these changes tend to reduce the tensile strength & the resilience of the articular cartilage.
††† In response to the regressive changes, chondrocytes in the deeper layers proliferate & attempt to repair the damage by producing new collagen & proteoglycans.
††† While initially effective, molecular signals causing chondrocyte loss & changes in the extracellular matrix eventually predominate - the reasons for this phenomenon remain unclear.
Morphology
††† In early stages, the chondrocytes proliferate, accompanied by biochemical changes as water content of the matrix increases & concentration of proteoglycans decreases.
††† Degradation of the superficial cartilage layers causes vertical & horizontal fibrillation & cracking of the matrix.
††† Gross examination at this stage reveals a granular articular surface that is abnormally soft.
††† Eventually, full-thickness portions of the cartilage are sloughed, & the exposed subchondral bone plate becomes the new articular surface.
††† Friction smoothes & burnishes the exposed bone, giving it the appearance of polish ivory (bone eburnation).
††† Rebuttressing & scelrosis of the underlying cancellous bones follow.
††† Small fractures through the articulating bone are common, & the dislodged pieces of cartilage & subchondral bone tumble into the joint & form loose bodies (joint mice).
††† Synovial fluid is forced into the fracture gaps, & this loculated fluid collection increases in size, forming fibrous walled cysts.
††† Mushroom-shaped osteophytes (bony outgrowths) develop at the margins of the articular surface & are capped by fibrocartilage & hyaline cartilage that gradually ossify.
††† The synovium shows minor alterations, but is congested & fibrotic with scattered inflammatory cells.
Clinical Course
††† Osteoarthritis is an insidious disease - primary osteoarhritis is usually asymptomatic until patients are in their fifties.
††† If a young patient develops osteoarthritis, a search for underlying causes should be made.
††† Characteristic symptoms include: deep, achy pain that worsens with use; morning stiffness; crepitus; & limitation of range of movement.
††† Impingement on spinal foramina by osteophytes results in cervical & lumbar nerve root compression with radicular pain, muscle spasms, muscle atrophy, & neurological deficits.
††† Typically, only one or few joints are affected.
††† Joints commonly involved include the hips, knees, lower lumbar & cervical vertebrae, proximal & distal interphalangeal joints of the fingers, first carpometacarpal joints, & first tarsometatarsal joints of the feet.
††† Characteristic in women, but not in men, are Heberden nodes in the fingers, representing prominent osteophytes at the distal interphalangeal joints.
††† The wrists, elbows & shoulders are usually spared.
Osteoarthritis
††† Degenerative joint disease.
††† Most common type of joint disease.
††† One of the most disabling conditions in developed nations.
††† Secondary only to cardiovascular disease in causing long-term disability.
††† Characterized by progressive erosion of articular cartilage.
††† Considered to be an intrinsic disease of articular cartilage in which biochemical & metabolic alterations result in its breakdown, irregardless of presence of inflammatory cells.
Classification
††† Primary osteoarthritis appears to be idiopathic as an aging phenomenon.
††† Usually oligoarticular but may be generalized.
††† Secondary osteoarthritis appears in younger individuals with some predisposing conditions - e.g. previous macrotraumatic/repeated microtraumatic injuries to a joint, a congenital development deformity of a joint(s), some underlying systemic disease (diabetes, ochronosis, hemochromatosis, marked obesity) etc.
††† Often involves one or several predisposed joints.
††† Gender has some influence on distribution.
††† The knees & hands are more commonly affected in women.
††† The hips are more commonly affected in men.
Pathogenesis
††† Normal articular cartilage is located at the ends of the bones - bathed in synovial fluid, in ensures virtually friction-free movements within the joint; in weight-bearing joints, it spreads the load across the joint surface in a manner that allows the underlying bones to absorb shock & weight without being crushed.
††† These functions require the cartilage to be elastic & possess high tensile strength - these attributes are provided by type-II collagen & proteoglycans, both secreted by chondrocytes as major components of the cartilage.
††† In adult bones, turnover of cartilage is maintained by chondrocytes (both synthesis & degradation) - in osteoarthritis this process is disturbed.
††† Aging & mechanical effects is a most important influence.
††† Evidence includes increasing frequency of osteoarthritis with advancing age; its occurence with weight-bearing joints; & an increase in the frequency of the disease in conditions that predispose the joints to abnormal mechanical stress - e.g. obesity & previous joint deformity.
††† Genetic factors also play a role, especially in cases involving the hands & hips.
††† Specific genes have not yet been identified, but there are suggestions linking to chromosomes 2 & 11.
††† The risk of osteoarthritis is increased in direct proportion to bone density & associated with high levels of estrogens.
††† Osteoarthritis is characterized by significant changes in both the composition & mechanical properties of cartilage.
††† Early in the course of the disease, the degenerating cartilage contains increased water & decreased concentration of proteoglycans.
††† There appears to be a weakening of the collagen network, presumably caused by decreased local synthesis of type-II collagen, & increasing breakdown of preexisting collagen.
††† The levels of certain molecular messengers (e.g. IL-1, TNF & NO) are increased & appear to be responsible for some of the changes in the composition of the cartillage.
††† Apoptosis is increased, likely responsible for the decreasing number of chondrocytes.
††† Cumulatively, these changes tend to reduce the tensile strength & the resilience of the articular cartilage.
††† In response to the regressive changes, chondrocytes in the deeper layers proliferate & attempt to repair the damage by producing new collagen & proteoglycans.
††† While initially effective, molecular signals causing chondrocyte loss & changes in the extracellular matrix eventually predominate - the reasons for this phenomenon remain unclear.
Morphology
††† In early stages, the chondrocytes proliferate, accompanied by biochemical changes as water content of the matrix increases & concentration of proteoglycans decreases.
††† Degradation of the superficial cartilage layers causes vertical & horizontal fibrillation & cracking of the matrix.
††† Gross examination at this stage reveals a granular articular surface that is abnormally soft.
††† Eventually, full-thickness portions of the cartilage are sloughed, & the exposed subchondral bone plate becomes the new articular surface.
††† Friction smoothes & burnishes the exposed bone, giving it the appearance of polish ivory (bone eburnation).
††† Rebuttressing & scelrosis of the underlying cancellous bones follow.
††† Small fractures through the articulating bone are common, & the dislodged pieces of cartilage & subchondral bone tumble into the joint & form loose bodies (joint mice).
††† Synovial fluid is forced into the fracture gaps, & this loculated fluid collection increases in size, forming fibrous walled cysts.
††† Mushroom-shaped osteophytes (bony outgrowths) develop at the margins of the articular surface & are capped by fibrocartilage & hyaline cartilage that gradually ossify.
††† The synovium shows minor alterations, but is congested & fibrotic with scattered inflammatory cells.
Clinical Course
††† Osteoarthritis is an insidious disease - primary osteoarhritis is usually asymptomatic until patients are in their fifties.
††† If a young patient develops osteoarthritis, a search for underlying causes should be made.
††† Characteristic symptoms include: deep, achy pain that worsens with use; morning stiffness; crepitus; & limitation of range of movement.
††† Impingement on spinal foramina by osteophytes results in cervical & lumbar nerve root compression with radicular pain, muscle spasms, muscle atrophy, & neurological deficits.
††† Typically, only one or few joints are affected.
††† Joints commonly involved include the hips, knees, lower lumbar & cervical vertebrae, proximal & distal interphalangeal joints of the fingers, first carpometacarpal joints, & first tarsometatarsal joints of the feet.
††† Characteristic in women, but not in men, are Heberden nodes in the fingers, representing prominent osteophytes at the distal interphalangeal joints.
††† The wrists, elbows & shoulders are usually spared.
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