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Disease/ Disorder


Osteoarthritis (OA) is a disease mostly affecting the articular cartilage, the entire joint including the synovium and the subchondral bone. The reference to it as a degenerative joint disease is no longer appropriate as it is not only due to “wear and tear” but may also be due to abnormal mechanics, inflammation, post-surgery, etc.1 OA can be primary or secondary.


  • Primary
    • Idiopathic (eg, aging persons, females)
    • Familial
  • Secondary

Predisposing factors include:

  • Trauma/micro-trauma from chronic repetitive motion
  • Infection
  • Joint inflammatory conditions (eg, rheumatoid arthritis)
  • Neuromuscular/neuropathic disorders (eg, Duchenne muscular dystrophy)
  • Metabolic disorders (eg, osteoporosis)
  • Endocrine disorders (eg, acromegaly)
  • Obesity
  • Hemoglobinopathies (eg, sickle-cell disease)
  • Bone disorders, other orthopedic disorders (eg, Paget disease, avascular necrosis)

Epidemiology including risk factors and primary prevention

  • Frequency: More than 50% of adults over age 65 have OA. OA affects more than 30 million people in the US.2
  • Morbidity: Associated with pain, loss of function and reduced endurance leading to weight gain. No direct mortality exists from OA per se but may occur from complications associated with of lack of exercise.
  • No correlation based on race, except knee OA is more common in African-American women.
  • Equally prevalent in men and women before age 55 but increases in women thereafter with higher rates in knees in women, and hips in men. It is the most common joint disorder worldwide affecting 10% of men and 18% of women over 60 years old.3,4


The usual mechanism is repetitive microtrauma and direct damage with the associated immune changes in the articular cartilage of predominantly the weight-bearing joints, such as the knees. Initially there is swelling of the cartilage from increased proteoglycans synthesis, release of cytokines, and metalloproteinases -associated inflammation. Hypertrophic repair of the cartilage can progressively occur for years. Reduced joint space from cartilage loss occurs with decreased proteoglycan synthesis and diminished cartilage elasticity, formation of clefts and fibrillations leading to exposure of the subchondral bone, its microfracture, new bone formation, bone cysts from necrosis, and osteophytes formation. Other joint structures like the synovium, ligaments and surrounding neuromuscular structures may be affected, (eg, atrophy, contractures).

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  • Mild: Intermittent pain/mild discomfort with very little cartilage damage in line with Outerbridge grade 1.
  • Moderate: Increased pain, associated swelling/effusion, crepitus and early wasting of muscles with more extensive damage to the articular cartilage and evidence of inflammation in line with Outerbridge grades 2 overlapping with 3.
  • Severe: Along with the moderate features, cartilage becomes extensively denuded, subchondral bone is exposed and severe muscle wasting occurs. The joint may be deformed secondary to severe wear of the cartilage, soft tissues and subchondral bone, eg, genu varum deformity, in line with Outerbridge grades 3/4.
  • Outerbridge stages based on arthroscopic findings are:6
    • Grade 1- softening and swelling
    • Grade 2- fragmentation and fissuring of less than 0.5 inches
    • Grade 3-fragmentation and fissuring at or greater than 0.5 inches
    • Grade 4- erosion down to the subchondral bone

Specific secondary or associated conditions and complications

  • Obesity7
  • Falls
  • Chronic pain syndromes
  • Nerve irritations/damage, eg, cervical radiculopathy/myelopathy
  • Increased bursae formation
  • Fatigue, stress and frustration/depression

Essentials of Assessment


History for joint pain/discomfort with activities and relieved with rest but becoming persistent; morning joint stiffness, swelling, weakness.

Physical examination

Physical examination for muscle atrophy, joint deformities/malalignment, effusions, joint-line tenderness, crepitus, antalgic gait, palpable/visible evidence of osteophytes, limited range of motion with stiffness/periarticular muscle spasms, Heberden nodes at the distal interphalangeal (DIP) joints and Bouchard nodes at the proximal interphalangeal (PIP) joints of the hands.

Functional assessment

  • Mobility assessment: Observe walking distance, and whether pain control and endurance can be improved with assistive devices. Gait analysis in hip/knee/spinal OA may be required.
  • Self-care assessment for activities of daily living.
  • Full assessment for depression when psychosocial stressors and chronic pain exist.

Laboratory studies

Erythrocyte sedimentation rate (ESR) may be elevated in generalized or in erosive inflammatory OA. C-reactive protein (CRP) may be elevated in associated inflammation. Synovial fluid analysis shows clear fluid with white blood cell count 2000/microliter with mononuclear predominance.


  • Plain x-ray shows arthritis well but may be negative at the early stage of the disease. The Kellgren-Lawrence grading is
    • Osteophytes
    • Joint space narrowing
    • Subchondral sclerosis
    • Subchondral cyst formations
  • Magnetic resonance imaging (MRI): Required if there is difficulty in diagnosis using x-ray (eg, osteonecrosis of hips/knees); MRI can best image soft-tissue injuries.
  • Computerized tomography (CT): useful in advanced OA to define small intra-articular bodies.
  • Bone scans: differentiate from other causes of joint pain (eg, osteomyelitis, tumours).
  • Ultrasound imaging: It can be used to assess and monitor cartilage degeneration and also enable non-radiation image assisted intra-articular injections.

Supplemental assessment tools

  • Arthroscopy: for visual inspection of the joint and washing out intra-articular debris for pain relief.
  • Arthrocentesis: allows fluid analysis, gram stain, culture and birefringence under polarized light, etc. Steroid injection trial could be diagnostic if pain relief occurs.
  • Electrodiagnosis: to explore unexplained sensory symptoms or weakness.
  • Goniometry: to define extent and progress of any restriction of joint mobility.
  • Pain assessment tools: to define level of pain initially, and as an outcome of treatment

Early predictions of outcomes

  • Early diagnosis and pain alleviation and rehabilitation leads to greater improvement/stabilization of function.
  • History of trauma affecting the joint’s articular surface leads more often to posttraumatic OA than does history of non-traumatized joints.
  • Patients able to partake in regular exercises tend to show more functional improvement and ability to cope with the pain.


High pressure density and cold tends to increase pain intensity. Depending on the joints affected, patients find it difficult to negotiate uneven terrain during community ambulation and outdoor activities.

Social role and social support system

Pain and functional compromise can challenge social integration. Assistive devices may increase a feeling of “standing out”. Patient education in exercise programs, medication use and regular follow-up with physicians may reduce these helpless feelings.

Professional Issues

Medicolegal pitfalls exist from the prolonged use of nonsteroidal anti-inflammatory drugs (NSAIDs). Complications include associated gastrointestinal, cardiovascular, renal and hepatic side-effects and have resulted in legal action. Physicians also need to rule out systemic or malignant causes of pain, even when OA may be a main or partial contributor. Other issues include frequency of steroid injection administration, the cost-benefit to the patient paying out of pocket for procedures such as platelet rich plasma (PRP) and other regenerative medicine options, acupuncture, and massage therapy.8

Rehabilitation Management and Treatments9

Coordination of care

The ideal approach to treatment should be a coordinated and integrated multidisciplinary approach involving physiatrists, rheumatologists, orthopedists, pain physicians, physical therapists, occupational therapists, social workers, etc.

Patient & family education

Patient and family education include such issues as life style changes towards weight reduction, regular exercise, judicious use of pain medications and joint protection/energy conservation techniques.

Emerging/unique interventions

Impairment-based measurement

  • Functional capacity evaluation/vocational assessment assess ability to cope and adapt to work demands and environment.
  • Refer to the Imaging section.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

  • Early diagnosis and treatment
  • Weight loss programs
  • Exercise prescription as part of treatment
  • Improved functional capacity as a goal of treatment
  • Muscle strengthening and stretching around diseased joints as a goal of treatment
  • Look for possible underlying medical problem that could cause joint pain superimposed on OA
  • Vigilant monitoring of medication side-effects (eg, gastrointestinal bleeding from NSAIDs, allergic reactions)

Cutting Edge/ Emerging and Unique Concepts and Practice

Emerging/unique interventions include doxycycline/tetracycline to decrease cartilage wear and tear; surgical innovation using chondroblasts/cartilages from patient’s own cartilage, which is cultured and then used for replacement of worn joint cartilage; pulsed electromagnetic field stimulation; regular intake of vitamins C and D as preventive; platelet rich plasma (PRP) and stem cells as future replacement. Some recent studies have no shown clear-cut benefit from these interventions; insurance companies may be reluctant to authorize them.

  • Pulsed electromagnetic field stimulation is approved by the US Food and Drug Administration.
  • Hyaluronidase enzymes and viscosupplement may have disease-modifying characteristics.
  • Advances in acupuncture use toward pain control for OA.
  • Use of doxycycline and tetracycline may decrease cartilage wear and tear.
  • Autologous cartilage growth and transplant may enable cartilage replacement.
  • Use of PRP and stem cells, although now commonly used, require more evidence to support their use.

Gaps in the Evidence- Based Knowledge

These gaps include lack of preponderant evidence to support use of hyaluronic acid, chondroitin sulfate and glucosamine as oral supplements with no long-term benefit.10 The same applies to PRP and stem-cells with some suggesting that these interventions may show medium-term benefits.11,12


  1. Poole AR. An introduction to the pathophysiology of osteoarthritis. Front Biosci. 1999 Oct 15. 4:D662-70.
  2. Osteoarthritis Fact Sheet. Centers for Disease Control and Prevention. Available at https://www.cdc.gov/arthritis/basics/osteoarthritis.htm. January 10, 2019; Accessed: March 27, 2021.
  3. Woolf AD, Pfleger B. Burden of major musculoskeletal conditions. Bull World Health Organ 2003; 81: 646–56.
  4. Pereira D, Peleteiro B, Araújo J, Branco J, Santos RA, Ramos E. The effect of osteoarthritis definition on prevalence and incidence estimates: a systematic review. Osteoarthritis Cartilage. 2011 Nov. 19(11):1270-85.
  5. Glyn-Jones S, Palmer AJ, Agricola R, Price AJ, Vincent TL, Weinans H, Carr AJ. Osteoarthritis. Lancet. 2015 Jul 25;386(9991):376-87. doi: 10.1016/S0140-6736(14)60802-3. Epub 2015 Mar 4. PMID: 25748615.
  6. Rodríguez-Merchán EC, Gómez-Cardero P. The outerbridge classification predicts the need for patellar resurfacing in TKA. Clin Orthop Relat Res. 2010 May;468(5):1254-7. doi: 10.1007/s11999-009-1123-0. PMID: 19844770; PMCID: PMC2853678.
  7. Felson DT, Zhang Y, Anthony JM, et al. Weight loss reduces the risk for symptomatic knee osteoarthritis in women. The Framingham Study.Ann Intern Med.1992;116(7):535-539.
  8. Selfe TK, Taylor AG.Acupuncture and osteoarthritis of the knee: a review of randomized, controlled trials.Fam Community Health.2008;31(3):247-254.
  9. American College of Rheumatology Subcommittee on Osteoarthritis Guidelines. Recommendations for the medical management of osteoarthritis of the hip and knee: 2000 update. Arthritis Rheum.2000;43(9):1905-1915.
  10. Hathcock JN, Shao A.Risk assessment for glucosamine and chondroitin sulfate.Regul Toxicol Pharmacol.2007;47(1):78-83.
  11. A Pas HI, Winters M, Haisma HJ, Koenis MJ, Tol JL, Moen MH. Stem cell injections in knee osteoarthritis: a systematic review of the literature. Br J Sports Med. 2017 Aug. 51 (15):1125-1133.
  12. Cui GH, Wang YY, Li CJ, Shi CH, Wang WS. Efficacy of mesenchymal stem cells in treating patients with osteoarthritis of the knee: A meta-analysis. Exp Ther Med. 2016 Nov. 12 (5):3390-3400

Original Version of the Topic 

Segun Dawodu, MD. Osteoarthritis. 01/24/2013.

Previous Revision(s) of the Topic 

Segun Dawodu, MD. Osteoarthritis. 4/4/2017.

Author Disclosure

Segun Dawodu, MD
Nothing to Disclose