Osteoarthritis, Causes, Features, Diagnosis and Treatment
Osteoarthritis by far is the most common form of arthritis in the elderly. Its also known as osteoarthrosis and degenerative joint disease, characterized by a slowly progressive deterioration of a joint in which there is;
- Localized loss of cartilage
- Subchondral sclerosis
- Cyst formation
- Capsular and synovial thickening.
Osteoarthritis is a dynamic condition, characterized by both reparative and degradative processes.
Osteoarthritis has been divided into two main types:
- A) The primary or idiopathic form
Divided into subsets depending on clinical features
- B) Secondary osteoarthritis
In which some underlying condition is present. eg
- Childhood anatomic abnormalities (e.g., DDH, slipped femoral epiphyses)
- Inheritable metabolic disorders ( alkaptonuria, Wilson's disease, hemochromatosis)
- Neuropathic arthropathy (Charcot's joints)
- Hemophilic arthropathy
- Acromegalic arthropathy
- Paget's disease
- Noninfectious inflammatory arthritis (e.g., rheumatoid arthritis, spondyloarthropathies)
- Gout, calcium pyrophosphate deposition disease (pseudogout)
- Septic or tuberculous arthritis
Diabetic patients have a higher incidence of osteoarthritis than nondiabetics.
- Estimates of radiographic evidence of OA - range from 33% to almost 90% in those people over the age of 65
- Over the age 40 (for symptomatic disease)
- Leading cause of disability in those over age 65
Until middle age, osteoarthritis occurs with the same frequency in men and women, but after the age of 50 symptomatic Osteoarthritis is more common in women, and this difference in prevalence widens with increasing age.
Women are also more likely to have multiple joint involvements.
Genetic factors play a role in the development of Heberden's nodes. The genetic mechanism appears to involve a single autosomal gene, sex influenced, dominant in women and recessive in men
Characterized by the onset of primary generalized osteoarthritis at a young age
Aging alone does not cause osteoarthritis, but matrix alterations that occur with aging may facilitate the process.
Trauma, especially in the form of excessive repetitive impulse loading over many years, is likely to be an important risk factor. Certain occupations are associated with a high incidence of osteoarthritis in specific joints that are otherwise rarely involved in osteoarthritis. A single severe insult to a joint may lead to osteoarthritis many years later.
Chronic malalignment and ligamentous instability (either congenital or secondary to joint injury) resulting in abnormal biomechanical forces are important factors in the development of osteoarthritis. Eventually, chondrocytes react to trauma by enhancing the enzymatic breakdown of the cartilage matrix while mounting an insufficient repair response.
Pathophysiology Of osteoarthritis
Biomechanical and metabolic changes in cartilage, such as decreased total proteoglycan content, shortening of the glycosaminoglycan branches, and a decrease in the length of the subunit core protein. As the disease advances, the hyaluronate binding region becomes defective, resulting in a lack of aggregation.
he total content of collagen in cartilage does not change in osteoarthritis. However, the collagen fibers are less uniform in size and the weave is looser. Eventually, the supporting collagen network is disrupted, allowing the proteoglycan molecules to expand and imbibe water.
This exposure of water-binding proteoglycans explains the increased water content in osteoarthritic cartilage and its swelling when immersed in water.
Synthesis and release of degradative enzymes, including acid cathepsins, neutral proteases, sugar-splitting enzymes, and sulfatases.
Collagenase enzyme activity, which is difficult to demonstrate in normal cartilage, was positively correlated with the severity of human osteoarthritic lesions based on histologic criteria.
Concurrently with this accelerated breakdown of cartilage matrix, the chondrocyte increases its synthesis of proteoglycan, type II collagen, and hyaluronic acid, in an attempt to reverse the depletion of matrix constituents
The products of regenerating cartilage appear to differ slightly in structure and function from their normal counterparts.
Eventually, the disease progresses to a stage where tissue changes are so severe that the chondrocyte "fails," and synthesis of matrix constituents diminishes.
Immunological factors are all implicated in the pathogenesis of osteoarthritis. Interleukin-1 and tumor necrosis factor, enhance the enzymatic degradation of cartilage matrix and that a number of growth factors stimulate matrix formation
Focal, chronic synovitis, characterized by lymphocyte and mononuclear cell infiltration, is frequently seen in osteoarthritis.
This is probably due to the secretion of inflammatory mediators initiated by the release of hydroxyapatite or calcium pyrophosphate crystals or by cartilage breakdown components, and/or the presence of immune complexes in the surface of the cartilage.
Risk factors Of osteoarthritis
- Age over 50
- Obesity (weight-bearing joints)
- Prolonged occupational or sports stress
- Injury to a joint
Distinguish from other types of arthritis by absent systemic findings, minimal articular inflammation, and distribution of involved joints (e.g., distal and proximal interphalangeal joints, not wrist and metacarpophalangeal joints)
In the spine, distinguish from osteoporosis, metastatic disease, multiple myeloma, other bone diseases.
Neurologic complications of osteoarthritis of the cervical spine may be confused with amyotrophic lateral sclerosis, spinal cord tumors, and basilar artery disease
Not helpful (sedimentation rate not increased)
Disorders that may alter lab results:
In secondary OA, the underlying disorder may have abnormal lab results, e.g., hemochromatosis - abnormal iron studies
Synovial fluid may have a slightly increased white blood cell count, predominantly mononuclear
Calcium pyrophosphate dihydrate and/or apatite crystals may occasionally be seen in effusions and require polarized light microscopy or special techniques to see
Subchondral bone trabecular microfractures
Degradation response produced by the release of proteolytic enzymes, collagenolytic enzymes, prostaglandins, and immune responses
X-rays usually normal early; later often show
- Narrowed joint space
- Osteophyte formation
- subchondral bony sclerosis
- cyst formation
- Erosions may occur on the surface of distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints when OA is associated with inflammation (erosive osteoarthritis).
In advanced cases, there is gross deformity and subluxation.
Osteoporosis is not a feature of osteoarthritis
May be helpful to distinguish between OA and chronic inflammatory arthritides
OA - cell count usually < 500 cells/mm3, predominantly mononuclear =-Inflammatory - cell count usually > 2000 cells/mm3, predominantly neutrophils
Signs and symptoms of osteoarthritis
The joints commonly affected in osteoarthritis are the
- Distal and proximal interphalangeal joints of the hands
- First carpometacarpal join
- The first metatarsophalangeal joint
- The hip and the knee,
For reasons that are unclear, the wrist, elbow, shoulder, and ankle are spared, except with previous trauma or congenital anomaly.
1) Pain on motion and later also at rest; 2)limitation of motion due to the incongruity of joint surfaces, muscle or capsular contracture
2)Stiffness (especially morning and after sitting so-called gelling) of less than 30 minutes duration
3)Joint enlargement (e.g., Heberden's nodes of distal interphalangeal joints)
Heberden's nodes are characterized by bony enlargement of the dorsolateral and dorsomedial aspects of the distal interphalangeal joints of the fingers.
Flexor and lateral deviation of the distal phalanx are common.
Similar nodes at the proximal interphalangeal joints are known as Bouchard's nodes.
Heberden's nodes are prevalent in the elderly. They may be single, but they usually are multiple. In most patients they develop slowly over months or years, giving rise to little or no pain. In a few patients, they evolve rapidly with the involvement of the first carpometacarpal joint is common and is frequently symptomatic.
Marked osteophytosis at this site leads to a characteristic squaring appearance of the hands.
5)Tenderness usually absent; may be associated with synovitis, with tenderness along joint margins
6)Crepitation as a late sign
- Local pain and stiffness with osteoarthritis of the spine, with radicular pain (if there is compression of a nerve
Management Of osteoarthritis
Enhancement and preservation of functional ability, such as walking, dressing, and living independently.
The principal aims on
- Protecting joints from excessive loading
- Maintaining joint motion and stability
- Reducing symptoms of pain and stiffness.
Erosive inflammatory osteoarthritis is a variant of osteoarthritis of the hands. This entity, which most often affects postmenopausal women, involves the distal and proximal interphalangeal joints and less often the metacarpophalangeal joints. Painful inflammatory episodes eventually lead to joint deformities and sometimes to ankylosis.
After years of intermittent acute flares, the joints become quiescent. The clinical picture may be confused with rheumatoid arthritis
1)The reassurance of absence of generalized systemic disease, with recognition of potential disability from osteoarthritis
2)Weight reduction if obese
3)General fitness program
4) Heat (local, tub baths, etc.)
5) Physical therapy to maintain or regain joint motion and muscle strength. Quadriceps strengthening exercises can relieve the pain and disability of the knee.
6)Project joints from overuse eg.., cane, crutches, walker, neck collar, elastic knee support
Biomechanical Approaches to Therapy
1. Patients with obesity lose weight Correction of excessive and harmful loading becomes a high priority.
2 Reducing the load in affected joints include the use of
- walking aids
- wedged insoles that change the angle of the legs,
- heel lift if one leg is shorter than the other
- Occupational therapy to modify activities of daily living can reduce unnecessary overloading of the joints of the upper and lower extremities.
A structured exercise program does not appear to accelerate joint destruction and is believed to be important in the maintenance of normal cartilage. Aerobic, low-impact exercises in patients with symptomatic osteoarthritis of the weight-bearing joints improved their aerobic capacity, endurance, ability to walk, and sense of well-being, without increasing their joint symptoms.
Several short periods of walking, interspersed with rest periods, are preferable to sustained walking for the patient with osteoarthritis of the hip or the knee.
A body-toning exercise program such as regular swimming or riding stationary bicycles is well tolerated. Strenuous exercises and stair climbing should be avoided whenever possible.
Specific exercises to improve the strength of muscle groups include isometric, isokinetic, and isotonic exercises.
Use of NSAIDs
Arthroscopic Joint Debridement
Flaps of undermined cartilage and frayed cartilage can cause pain and muscle spasm if they become caught in the joint
In the early stages of osteoarthritis of the hip and knee, the weight-bearing areas of the joint are primarily affected.
Osteotomies are used to redirect the weight to areas of cartilage that have remained relatively intact
Joint fusion involves removing the joint and holding the bones on either side of the joint together so that they heal to form one long bone. Joint fusion has always been the most effective way to permanently eliminate the pain
Total Joint Arthroplasty
Total joint arthroplasties are procedures that replace the articular surfaces of joints with one or more artificial substances including metal, ultra-high-density polyethylene, ceramic, and Silastic.
Arthroplasties of the hip and knee should not be considered unless the joint is irreversibly damaged, with areas of full-thickness loss of cartilage,