| What is OA? | Result of both mechanical and biological events destabilize normal coupling of degradation and synthesis of articular cartilage and subchondral bone, involves all tissues of diarthrodial joint, changes in cells and matrix lead to softening, fibrillation, ulceration, and loss of articular cartilage, sclerosis and eburnation of subchondral bone.
It is characterized by joint pain, tenderness, limitation of motion, crepitus, occasional effusion, local inflammation.
Most common chronic joint disorder, burden and healthcare expenditure enormous, 4th leading cause of years lived with disability, increasing due to obesity and overall aging of population, disease of whole joint organ, optimal management risk strat and early dx on clinical grounds. |
| How is the anatomy of joints? | Cartilage facilitates joint function and protects underlying bone by distributing large loads, maintaining low contact stress, reducing friction at the joint.
Articular cartilage composition (chondrocytes [maintain matrix] and matrix [collagen II, proteoglycans, give compressibility and elasticity, aggrecan main proteoglycan, central core of GAG chondriton sulfate and keratane sulfate which assocciated with hyaluronic acid, collagen network provides stability and resistance against force] it is 2% cells, 70% liquid and 20% solid)
Synovial fluid, synoviocytes, manufactured HA GAG, supply nutrients to avascular articular cartilage, provides viscosity to absorb shock from slow movement, and elasticity to absorb shock from rapid movement.) |
| How is the pathology of OA? | Damage to articular cartilage, osteophyte formation at joint margin, subchondral bone sclerosis, synovial capsule thickening, lead to joint degeneration and associated symptoms (pain, tenderness, stiffness, loss of function, disability) |
| How is the ethiopathogenesis of OA? | Stage I proteolytic breakdown of cartilage matrix, Stage 2 fibrillation and erosion of cartilage surface develop, with release of proteoglycans and collagen fragments into synovial fluid, Stage 3 breakdown products of cartilage induce chronic inflammatory response in synovium which leads to further breakdown of cartilage. |
| How is molecular pathogenesis of OA? | Progressive loss of homeostasis in joint organs involving cartilage, bone, synovium, ligaments and muscles.
Changes in ECM synthesis, produce pro-inflammatory cytokines, tissue destructive enzymes, bone remodeling, angiogenesis driven by GF, synovitis by immune cells and pro-inflammatory cytokines, adipokines and sex hormones also play a role. |
| What are the molecular changes in OA causing pathogenesis? | Changes in cartilage matrix composition and properties (early disease water increases cause edema and softening, type II collagen synthesis decreases by MMP1&3, proteoglycan decrease, leads to increased water retention, accumulation of advanced glycation end products (AGE) lead to protein modification, bind to RAGE on chondrocytes leads to catabolic activity and more collagenase, leads to irreversible collagen damage)
Changes in catabolism (MMP, matrix degrading enzymes, ADAMTS, aggrecanases)
Activation of skeletal developmental pathways (TGFb, BMPs, Wnt signals, that stimulate chondrocyte hypertrophy, lead to osteophyte formation and fibrosis, activation and suppression of Wnt lead to OA.) |
| How is synovitis and pro-inflammatory molecules? | Products of cartilage breakdown are released into the synovial fluid and are phagocytosed by synovial cells, amplifying synovial inflammation
activated synovial cells in the inflamed synovium produce catabolic and proinflammatory mediators that lead to excess production of the proteolytic enzymes responsible for cartilage breakdown, creating a positive feedback loop
In addition to these effects on cartilage inflammation and breakdown, the inflamed synovium contributes to the formation of osteophytes via BMP |
| What are systemic mediators of OA? | Estrogens (Chondrocytes receptors, trigger GF, in menopause decrease GF)
Obesity (adipokines mediators of inflammation) |
| How is epidemiology of OA? | United States and international statistics
On the basis of the radiographic criteria for osteoarthritis, more 50% of adults older than 65 years are affected by the disease
the most common articular disease
Age-related demographics
Symptoms typically do not become noticeable until after the age of 50 years
The prevalence of the disease increases dramatically among persons older than 50 years, likely because of age-related alterations in collagen and proteoglycans that decrease the tensile strength of the joint cartilage and because of a diminished nutrient supply
to the cartilage.
Sex-related demographics
Women>men specially DIPs, knees, erosive OA
Race-related demographics |
| What are risk factors of OA? | Obesity/metabolic disorder (main reversible cause, knee, hip and hand OA)
Dietary intake and nutrients (antioxidants, vit C lower risk, vitD promising nutriment of OA)
Age, Sex and Ethnicity (age best risk factor, women greater risk hand and knee OA)
Sex Hormones (more in women menopause, estrogen)
Occupational factors
Joint Deformity/Laxity Joint Deformity
Acute Injury and Joint loading (secondary OA especially ACL meniscus)
Repetitive activities with joint overuse, Muscle weakness, genetics (Collagen II genes, matrix protein genes, vit D, estrogen receptors) |
| How is hx of pt with OA? | slow progression occurring over several years or decades.
patients can become less and less active and thus more susceptible to morbidities related to decreasing physical activity
(including potential weight gain).
Early in the disease, joints may appear normal
gait may be antalgic if weight-bearing joints are involved (mechanical pain)
Pain is usually the initial source of morbidity in osteoarthritis, with the disease’s primary symptom being deep, achy joint
pain exacerbated by extensive use
reduced range of motion and crepitus
Stiffness during rest (gelling) usually lasting for less than 30 minutes
Initially, pain can be relieved by rest and may respond to simple analgesics
joints may become unstable, pain may become more prominent (even during rest) and may not respond to medications |
| How is PE of pt with OA? | Reduced range of motion and crepitus are frequently present
Malalignment with a bony enlargement may occur
Limitation of joint motion or muscle atrophy around a more severely affected joint may occur.
Osteoarthritis of the hand most often affects the distal interphalangeal (DIP) joints but also typically involves the
proximal interphalangeal (PIP) joints and the joints at the base of the thumb
Heberden nodes, which represent palpable osteophytes in the DIP joints, are more characteristic in women than
in men
Bouchard nodes at PIP joints
Inflammatory changes are typically absent or at least not pronounced. |
| How is prognosis of OA? | The prognosis in patients with osteoarthritis depends on the joints involved and on the severity of the condition
No proven disease-modifying or structure-modifying drugs for osteoarthritis
A systematic review found the following clinical features to be associated with more rapid progression of knee
osteoarthritis:
Older age
Higher BMI
Varus deformity
Multiple involved joints |
| How is imaging for OA? | Four Key X-ray Changes (LOSS)
L – Loss of Joint Space
O – Osteophytes
S – Subarticular Sclerosis (increased density of the bone
along the joint line)
S – Subchondral Cysts (fluid filled holes in the bone, aka
geodes)
X-ray changes do not necessarily correlate with symptoms.
Significant changes might me found incidentally on someone
without symptoms. Equally, someone with severe symptoms
of osteoarthritis may have only mild changes on an X-ray |
| How is Kellgren and Lawrence staging system of knee OA? | . |
| How is Knee OA clinical subset? | medial tibiofemoral +++ lateral tibiofemoral, patellofemoral compartments
Xray: PA, lat, schuss
Baker cyst
A popliteal cyst communicating with the joint space is common
The cyst may rupture into the posterior calf muscles, mimicking venous thrombosis and should be considered in ‘doppler negative’ leg swelling in the acute setting |
| How is hand OA clinical subset? | Women > men mainly postpmenopausal
Genetics, obesity,
PIP, DIP, cmc,
Heberden nodes, bouchard nodes
If MCP check inflammatory or hemochromatosis
Generalised OA?
Erosive OA
Xray: Seagull erosion, saw tooth deformity
DD: PsA |
| How is hip OA clinical subset? | Women = men
Uni or bilateral
Xray: AP, Lesquenne
Lesquenne view:
anteroposterior view centred on one hip and a false profile incidence
corresponding to an oblique view which seems especially of interest in case of superolateral space narrowing OA
The superior-external pole is most often involved (superior lateral, superior-intermediate and superior-medial) |
| How is spine OA clinical subset? | Posterior facet articulations intervertebral fibrocartilaginous discs vertebral bodies Osteophytes of the vertebrae can narrow the foramina and compress nerve roots
Symptoms include: back pain a radicular pain with specific topography, especially when it is associated to disc herniation, ligamentous hypertrophy, spondylolisthesis or foraminal narrowing from apophyseal joint subluxation |
| What is diffuse idiopathic skeletal hyperostosis (DISH)? | Bony hardening of ligaments in areas where they attach to your spine, asymptomatic, mechanical pain most common mild to moderate upper back pain, maybe neck and lower back, can be progressive worsens causes serious complications.
Presentation (stiffness, pain, loss of ROM, dysphagia)
Risk factors (male sex, older age (over 50), T2DM and other conditions) |
| What are complications of DISH? | • Disability
• Difficulty swallowing. Bone spurs in the neck can put pressure on your esophagus. The pressure from bone spurs can also cause a hoarse voice or sleep apnea
• Spinal fracture |
