- primary symptoms: joint pain (usage-related pain) and relieved by rest, stiffness, limitation of motion.
- OTHER: muscle weakness and poor balance, comorbidities like fibromyalgia.
- tenderness – joint-line tenderness suggests articular pathology, while tenderness away from the joint line suggests periarticular soft-tissue pathology.
- bony swelling
- joint deformity
- instability – common symptom in knee oa.
■ DIP (Heberden’s nodes = osteophytes → enlargement of joints)
■ PIP (Bouchard’s nodes)
■ CMC (usually thumb squaring)
■ 1st MCP (other MCPs are usually spared)
- hip: pain can radiate to the anterior thigh, but generally does not go below the knee
- knee (usually affected bilaterally)
- foot: common in first MTP and midfoot
- lumbar spine: very common, especially L4-L5, L5-S1
- cervical spine: C5-C6
- Generalized Osteoarthritis: 3+ joint groups
non-nodal generalized oa, which is more common in men
nodal generalized oa, which is more common in women
- RHEUMATOID ARTHRITIS (RA):
• swelling of the joints is hard and bony in oa; soft, warm, and tender joint swelling is typical of ra.
• stiffness of the joint is a very common feature of ra, but it is a relatively rare feature of oa.
- CRYSTALLINE ARTHRITIS – GOUT AND PSEUDOGOUT: presence of tophi, and the punched out juxta-articular gouty erosions are also useful in distinguishing oa from gout
- PSORIATIC ARTHRITIS: unlike hand oa, psoriatic arthritis may target just one finger, often as dactylitis, and characteristic nail changes are usually present.
- INFECTIOUS ARTHRITIS
- USG: useful for detecting synovial inflammation, effusion, and osteophytosis.
- SYNOVIAL FLUID: non-in ammatory
- The Radiographic Hallmarks of OA
• Joint space narrowing
• Subchondral sclerosis
• Subchondral cysts
■ normal CBC and ESR, CRP
■ negative RF and ANA
control pain and swelling,
improve the quality of life,
prevent progression of the process,
EXERCISE AND PHYSICAL THERAPY,
noninflammatory oa with acetaminophen,
nsaids if acetaminophen is inadequate or inflammatory oa is present,
topical nsaids or capsaicin as alternative to oral nsaids or acetaminophen,
intraarticular glucocorticoids if nsaids and apap are insufficient
- most common arthropathy (accounts for ~75% of all arthritis)
- increased prevalence with increasing age
thinning of the articular cartilage with age, reduced hydration.
chondrocalcinosis (abnormal calcification ): results from the accumulation of calcium pyrophosphate dihydrate (cpp) crystals
- JOINT INJURY - POSTTRAUMATIC
inflammatory mediators, including tnf-alpha and interleukin (il)-6, are present shortly after injury.
macrophages within adipose tissue are a source of proinflammatory cytokines, including il-6 and tnf-alpha.
adipocytes produce adipokines such as leptin. that promote the development of oa.
rare mutations in collagen types ii, ix, or xi, resulting in a severe destructive form of arthritis that affects multiple joints, can begin as early as adolescence.
- ANATOMIC FACTORS:
congenital acetabular dysplasia is associated with premature hip oa, requires joint replacement.
individuals who have a varus alignment (bow-legged) are at increased risk of medial tibial-femoral oa, while those with a valgus alignment (knocked-knee) are at risk for lateral tibial-femoral oa.
- LACK OF OSTEOPOROSIS,
- PREVIOUS INJURY,
- MUSCLE WEAKNESS/STRENGHT
- ENDOCRINE/METABOLIC GENETIC EFFECTS
- SPORT ACTIVITIES
- PRIMARY: idiopathic.
- SECONDARY: caused by alkaptonuria, congenital disorders of joints, diabetes, ehlers-danlos syndrome, hemochromatosis and wilson's disease, inflammatory diseases (such as perthes' disease), lyme disease, and all chronic forms of arthritis, injury, marfan syndrome, obesity, joint infection.
- EROSIVE – INFLAMMATORY: less common, and more aggressive inflammatory form which often affects the distal interphalangeal joints of the hand.
- progressive deterioration of articular cartilage and surrounding joint structures caused by genetic, metabolic, biochemical, and biomechanical factors with secondary components of inflammation