Osteoarthritis

Author(s): Segun Dawodu, MD

Originally published:11/10/2011

Last updated:04/04/2017

1. DISEASE/DISORDER:

Definition

Osteoarthritis (OA) or degenerative joint disease (DJD) is a local joint disorder that involves a progressive wear and tear of the articular cartilage that lines the joint, cartilage fibrillations (cracks), inflammation of the synovial cells that line the joint, bone spurs (osteophytes), loss of joint space, and eventually wearing away and cyst formation in the subchondral bone.

Etiology

  1. Primary
    • Idiopathic (eg, aging persons, females)
    • Familial
  2. Secondary
    Due to prior joint trauma, such as a rotator cuff tear predisposing to glenohumeral osteoarthritis (aka rotator cuff arthropathy)

Predisposing factors include:

  1. Trauma/micro-trauma from chronic repetitive motion
  2. Infection
  3. Joint inflammatory conditions (eg, rheumatoid arthritis)
  4. Neuromuscular/neuropathic disorders (eg, Duchenne muscular dystrophy)
  5. Metabolic disorders (eg, osteoporosis)
  6.  Endocrine disorders (eg,acromegaly)
  7. Obesity
  8. Hemoglobinopathies (eg, sickle-cell disease)
  9. Bone disorders, other orthopedic disorders (eg, Paget disease, avascular necrosis)

Epidemiology including risk factors and primary prevention

  1. Frequency: More than 50% of adults over age 65 have OA. OA affects about 16-20 million people in the US, most commonly in the hands, knees and hips.
  2. Morbidity: Associated with pain, stiffness, decreased range of motion, loss of function and reduced endurance leading to weight gain. No direct mortality exists from OA per se but may occur from cardiovascular or metabolic complications associated with lack of exercise.
  3. No correlation based on race, except knee OA is more common in African-American women.
  4. 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.

Patho-anatomy/physiology

The usual mechanism begins with repetitive microtrauma caused by joint overload and excessive shear forces, causing micro then macroscopic injury to the articular cartilage,  associated inflammatory changes in the synovium and eventual joint space loss and eburnation of the subchondral bone.  Initially there is swelling of the cartilage from increased proteoglycan synthesis, release of cytokines interleukins and matrix metalloproteinases that cause-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 (fibrillations) leading to exposure of the subchondral bone, its microfracture, new bone formation, bone cysts from necrosis, and osteophyte formation. Other structures extrinsic to the joint like the , ligaments and surrounding neuromuscular structures may be affected, (eg, atrophy, contractures, nerve compression).

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

  1. Outerbridge stages grade chondral lesions and are based on arthroscopic findings:
    • 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
  2. Mild: Intermittent pain/mild discomfort with very little cartilage damage in line with Outerbridge grade 1.
  3. 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.
  4. 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.

Specific secondary or associated conditions and complications

  • Obesity
  • Falls
  • Chronic pain syndromes
  • Nerve irritation/damage, eg, cervical radiculopathy/myelopathy
  • Increased bursae formation
  • Psychologic – Fatigue, stress, pain related insomnia, anxiety, frustration and depression

2. ESSENTIALS OF ASSESSMENT

History

History of joint pain worse with activity  and relieved with rest but eventually becoming persistent; loss of motion; morning joint stiffness typically lasting less than 30 minutes; swelling; crepitus; weakness.

Physical examination

Look for loss of joint motion, crepitus, , joint deformities/malalignment, effusions, joint-line tenderness, antalgic gait, palpable/visible evidence of osteophytes, periarticular muscle spasms, muscle atrophy, Herberden nodes at the DIP joints and Bouchard nodes at the PIP joints of the hands. Wrists and MCPs should be spared and if involved point towards a systemic/inflammatory arthropathy

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.
  • Depression assessment should be performed when psychosocial stressors and chronic pain exist. The elderly are at particular risk.

Laboratory studies

Erythrocyte sedimentation rate (ESR) and  C-reactive protein (CRP) may be mildly elevated with  joint inflammatory states but large elevations may suggest a more systemic inflammatory condition.. Synovial fluid analysis is the test of choice and shows clear fluid with white blood cell count less than 2000/microliter with a mononuclear predominance.

Imaging

  • Plain x-rays are typically the initial study of choice but may be negative in early stage of the disease. Hallmarks include osteophyte formation, subchondral cysts, joint space narrowing and effusion. The Kellgren-Lawrence grading is commonly used
    • grade 0 – no radiographic features of OA
    • grade 1 – doubtful joint space narrowing and possible osteophytic lipping
    • grade 2 –  definite osteophytes and possible narrowing of joint space
    • grade 3 – multiple osteophytes, definite joint space narrowing, sclerosis and possible deformity of bone contour
    • grade 4 – large osteophytes, marked narrowing of joint space, severe sclerosis and definite deformity of bone contour
  • Magnetic resonance imaging (MRI): Provides greater resolution of cartilage and bone lesions, subchondral bone edema, bone infarcts, and related soft tissue and nerve lesions such as a pinched lumbar nerve root from facet joint osteoarthritis and hypertrophy. May be helpful if radiographs are normal.
  • Computerized tomography (CT): useful for delineating bony anatomy, fractures,  identifying small intra-articular bodies and for surgical planning.
  • Bone scans: differentiate OA from other causes of joint pain (eg, tumor, infection) or to determine symptomatic joints when multiple joints have OA (eg facet joint arthropathy).

Supplemental assessment tools

  • Musculoskeletal ultrasound: Can be used to evaluate joint space narrowing, osteophytes, effusion, associated soft tissue structures. Limited by inability to image through bone. Can be a cost effective screening tool.
  • Arthroscopy: considered the gold standard for visual direct inspection of the joint; can be used therapeutically to wash out intra-articular debris for pain relief.
  • Arthrocentesis: allows fluid analysis, gram stain, culture and birefringence under polarized light, etc. to evaluate for crystalline or inflammatory arthropathy
  • Diagnostic injection; Local anesthetic injection with or without corticosteroid can confirm an intra-articular source of pathology and possibly response to surgery, and can be therapeutic. Helpful in cases of referred pain .
  • Electrodiagnosis: can help to explore unexplained sensory symptoms or determine if weakness is pain limited or from nerve damage.
  • 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, pain alleviation, reduction of swelling, restoration of motion and functional rehabilitation leads to greater improvement/stabilization of function.
  • Weight loss can significantly reduce joint loads, particularly in the knee
  • Patients able to partake in regular exercises tend to show more functional improvement and ability to cope with the pain.

Environmental

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 regarding disease natural history, exercise programs, appropriate medication use, biopsychosocial techniques and regular follow-up with physicians, therapists and allied health professionals 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.

3. REHABILITATION MANAGEMENT AND TREATMENTS

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, psychologists, etc.

Patient & family education

Patient and family education includes 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.

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

  1. Early diagnosis and treatment is important
  2. Weight loss programs are key
  3. Exercise is vital
  4. Improved functional capacity as a goal of treatment rather than just pain
  5. Social and psychologic support is important
  6. Look for possible underlying medical problem that could cause joint pain superimposed on OA
  7. Vigilant monitoring of medication side-effects (eg, gastrointestinal bleeding from NSAIDs, allergic reactions)

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Emerging/unique interventions include

Doxycycline/tetracycline to decrease cartilage wear and tear; surgical innovation using chondroblasts/cartilage autografts or allografts grown in vitro and then transplanted into areas of worn cartilage; pulsed electromagnetic field stimulation; oral vitamin and antioxidant/anti-inflammatory supplements (Eg curcumin); platelet rich plasma (PRP) and bone or adipose derived stem cell injection treatments as anti-inflammatory and possible oscteochondral regenerative treatments.

  1. Pulsed electromagnetic field stimulation is approved by the US Food and Drug Administration.
  2. Hyaluronic acid  viscosupplements have cushioning, anti-inflammatory, pain relieving and viscoelastic properties, and may have disease-modifying characteristics
  3. Advances in acupuncture use toward pain control for OA.
  4. Use of doxycycline and tetracycline may decrease cartilage wear and tear.
  5. Autologous cartilage growth and transplant may enable cartilage replacement.
  6. Use of PRP and stem cells show mixed results in early clinical trials but are heterogenous in preparation and use. Further evidence is needed to support their widespread use.

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

The types and doses of oral supplements helpful to reduce OA burden is not clear (eg glucosamine, chondroitin, boswellia). The role of PRP and the optimal platelet concentration, presence of leukocytes, post PRP rehabilitation, anti-inflammatory vs regenerative effects need to be better elucidated. The benefits of stem cells and optimal harvest site (bone marrow vs adipose), adjuvants, dose (cell counts, volume, frequency), needs to be studied more. Advanced surgical cartilage replacement strategies need to be developed.

REFERENCES

Bibliography

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  3. D’Ambrosia RD. Epidemiology of osteoarthritis.Orthopedics.2005;28 (suppl 2):201-205.
  4. Kornaat PR, Bloem JL, Ceulemans RY, et al. Osteoarthritis of the knee: association between clinical features and MR imaging findings.Radiology.2006;239(3):811-817.
  5. Selfe TK, Taylor AG. Acupuncture and osteoarthritis of the knee: a review of randomized, controlled trials.Fam Community Health.2008;31(3):247-254.
  6. Creamer P, Hochberg C. Osteoarthritis.Lancet.1997;350(9076):503-508.
  7. Hathcock JN, Shao A. Risk assessment for glucosamine and chondroitin sulfate. Regul Toxicol Pharmacol.2007;47(1):78-83.
  8. 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.
  9. Diekman BO, Guilak F. Stem cell-based therapies for osteoarthritis: Challenges and opportunities. Current opinion in rheumatology. 2013;25(1):119-126. doi:10.1097/BOR.0b013e32835aa28d.

Original Version of the Topic 

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

Author Disclosure

Segun Dawodu, MD
Nothing to Disclose

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