Rheumatology: Osteoarthritis Flashcards
OA
One of the most common types of arthritis accounting for 30% of physician visits.
Associated with aging and in 1990 affected 21 million people in the US or 12% of the population.
A slowly progressive musculoskeletal disorder most often affects the hands, spine, knees and hips.
A disease with many names: degenerative joint disease, degenerative disc disease, hypertrophic arthritis, osteoarthosis.
A group of overlapping disorders of various etiologies arising from a combination of systemic factors and local factors that gradually converge to produce a condition with definable morphologic and clinical outcomes
OA Risk Factors
Obesity Heredity Age Joint trauma Abnormal joint mechanics Smoking Different types of work Disability Distress Psychosocial and Socioeconomic
Joint Shape & Function
Distributes load and keeps it stable
Medial compartment of the knee gets compressed more often especially in obese people
Flat feet can affect the distribution of weight along with fractures
Idiopathic OA
Idiopathic OA: can be a localized or generalized form of the disease.
Localized OA most commonly affects the hands, feet, knee, hip, and spine. Can affect the shoulder, TMJ, sacroiliac, ankle, and wrist joints (rare).
Generalized OA consists of involvement of three or more joint sites
Secondary OA
Posttraumatic: acute (e.g., fracture through joint), repetitive (e.g., occupational injury), postoperative (e.g., meniscectomy)
Postinflammatory: infection, inflammatory arthropathies (e.g., RA)
Skeletal Failure: osteonecrosis, osteochondritis, Paget’s disease
Dysplastic: chondrodysplasias, epiphyseal dysplasias, congenital dislocation of the hip, developmental disorders, leg-length inequality, endocrine and metabolic, acromegaly, ochronosis, hemochromatosis, crystal deposition disorders
Connective Tissue: hypermobility syndromes and mucopolysaccharidoses
Signs and Symptoms of OA
Symptoms: pain, stiffness, swelling, altered function, weakness, deformity, grinding or clicking, instability
Signs: altered gait, tenderness, enlargement, crepitus, limitation of motion, deformity
Lab work up shows a noninflammatory synovial fluid and workup. The typical synovial fluid shows: Clear fluid, WBC
Pathophysiology of OA
OA anatomically shows patchy cartilage damage and bone hypertrophy.
OA is associated with aging but bone and cartilage changes are distinctly different.
Chondrocyte function and cartilage matrix biology is regulated by hormones, cytokines and growth factors
Chondrocyte clusters and start to die and develop osteophytes
Proinflammatory cytokines including IL-1 likely play an important role in OA pathogenesis
RA vs. OA
RA inflammation is at a much higher level with eroding bones
MMPs and Force Distribution
MMP= matrix metalloproteases causes cartilage breakdown
Cells congregate and then breakdown
If the knee doesn’t align properly, it will change the way it functions and can develop OA and just a matter of time because changing force distribution
Fragmented matrix components from activated proteases may enhance the catabolic signaling.
Crystals deposited in cartilage may contribute to the changes in OA.
Signs of inflammation are common and may influence the course of disease.
Biomechanical factors are essential in the pathogenesis of OA.
Genetics can play a large role as well
Pathology of OA
Early degenerative changes are present in this articular cartilage.
-Small tangential clefts are seen on the surface of the already altered hyaline cartilage.
-A deeper vertical cleft has appeared, and the splitting process of fibrillation is already under way.
-Clumping of chondrocytes is present.
(hematoxylin-eosin, medium power)
OA vs. Aging
Cartilage Hydration: OA increases, aging decreases
Proteoglycan Concentration: OA increases, aging has no change
Collagen Concentration: OA decreases, aging has no change
Chondrocyte Proliferation: OA increases, aging has no change
Metabolic Activity: OA decreases, aging has no change
Subchondral Bone Thickness: OA decreases
Heberden’s vs. Bouchard’s Nodes
Heberden’s in DIPs
Bouchard’s in PIPs
Work Up
ESR, CBC, LFT, BMP, CRP
Rheumatoid factor titers: Not needed unless there is evidence of an inflammatory arthritis.
Evaluation of synovial fluid: if the joint is swollen and you can tap it then send the fluid to the lab and do not forget to order the crystals.
Xray the affected joints
The work up is very important when atypical joints (wrists, MCPs, elbows, shoulders, ankles, 2-5th MTPs) are involved.
If your patient has OA in one of these areas go looking for a secondary cause
Radiographic Findings
No ankylosis though alignment can be abnormal
Bone mineralization is normal
Subchondral sclerosis, cysts and/or osteophytes (spurs)
Cartilage space narrowing
No calcification in the cartilage *
Typical deformities and distribution
No erosions * (erosive OA shows gull wings)
Vacuum sign in the spine
Note: when doing xrays looking for OA always order standing or weight bearing films because shows the functional space the patient actually has
Management of OA
Weight loss Ambulatory aids – canes, walkers Exercise!!!!! Spints or Braces Parafin baths for hands/feet Topical rubs TENS Heat/Cold Meditation, biofeedback Traction OMM
