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Osteoarthritis of the Hand:
INTRODUCTION Osteoarthritis, a disease characterized by degeneration and functional loss of joints throughout the body, is the most prevalent joint disorder affecting the population.1 This disease tends to affect older individuals due to biomechanical wear-and-tear imparted on joints over the years. Since the average age of the population is increasing, osteoarthritis is of growing significance.1 The hand plays a vital role in daily function. As a result, osteoarthritis of these joints can be especially debilitating. Occupations that involve extensive repetitive motion and overuse of the hands have a much higher prevalence of osteoarthritis.6 85% of adults aged 75-79 have the disease.2 Women are more commonly affected than men. This difference is often attributed to the decrease in estrogen production following menopause.2 There is no direct evidence showing race to be a risk factor for osteoarthritis.6 Given the prevalence of this debilitating disease, it is crucial to identify the population at risk and detect the condition early. This allows for maximal treatment and maintenance of hand function.
PATHOPHYSIOLOGY AND MECHANISM OF DISEASE Osteoarthritis is characterized by gradual erosion of the articular cartilage in the involved joint.3 It is separated into primary and secondary categories based largely on etiology.3 In the case of primary degenerative joint disease, there appears to be no direct initiating event. The onset is related to a combination of biochemical, inflammatory, and immunologic factors.6 Typically, these factors induce degenerative changes over a number of years.3 Secondary osteoarthritis is characterized by numerous risk factors that predispose an individual to developing osteoarthritis of the hand.3 Common predisposing factors include previous and/or repeated traumatic injury, malformation of the bony structure secondary to birth defect or improper development, ligamentous laxity, obesity, and genetic factors.3,6 Normal joints of the hand are enclosed in a fibrous capsule lubricated by synovial fluid.4 A small amount of elastic cartilage serves to cushion and protect joints from mechanical stress.4 This cartilage matrix is composed of collagen for tensile strength, and water-bound proteoglycans for a cushioning effect.7 Healthy intraarticular cartilage is sustained by continuous breakdown and regeneration of its components.7 Repetitive mechanical stress of the hand results in destruction and deterioration of the cartilage matrix within the joints.3 Cartilage producing cells (chondrocytes) are unable to synthesize new cartilage at a rate commensurate with surrounding cartilage destruction.7 The depletion of cartilage causes friction as the bones of the joint lose their cushion and rub against one another. This weakens bones and as a result, micro fractures develop.3 Synovial fluid may leak into the cracks created by these fractures, become walled-off, and form cysts.3 Pieces of bone appropriately named “loose bodies” appear in the joint space.3 These “loose bodies” have the potential to compress and irritate other structures within the joint cavity.6 Finally, synthesis of new bone in response to intraarticular bone destruction often leads to osteophyte formation.6 Osteophyte formation within confined spaces has the potential to compress and irritate surrounding structures.6
CLINICAL MANIFESTATIONS Osteoarthritis of the hand most commonly effects middle-aged or elderly individuals.1 As discussed earlier, primary osteoarthritis commonly presents in patients with an occupational history involving years of extensive, repetitive biomechanical stress of the hands. Secondary degeneration of hand joints is attributed to predisposing factors such as injury to the hands, musculoskeletal malformations, and obesity. Genetic predispositions play a role in the pathogenesis of both primary and secondary joint degeneration within the hand. The most common manifestations of osteoarthritis of the hand involves the distal interphalangeal joints (DIP), the carpometacarpal joint (CMC) of the thumb, and less commonly, the proximal interphalangeal joint (PIP).2 Thumb CMC joint degeneration is increasingly prevalent in obese patients.7 The wrist is usually not affected. Early in the disease process, pain is isolated to activities involving the hand. Resting the affected hand usually alleviates the pain. Pain experienced at rest, or throughout the night, usually signals the onset of advanced disease.1 Morning pain is common and is usually less than 30 minutes in duration.1 As osteoarthritis progresses, stiffness of the affected joints and loss of strength are common.2 Inflammation and swelling of the hand may be present. This is less common, and usually only occurs in advanced stages of the disease.1 As disease progresses, synovial fluid cysts develop within the eroded bone. This clinical finding is more common in women than men. Nodes form within the distal interphalangeal joints (DIP) and are known as Heberden’s Nodes. Nodes formed within the proximal interphalangeal joints are known as Bouchard’s Nodes.3 Another sign of advanced disease is non-symmetrical angulations of affected fingers. This results in limited range-of-motion and crepitus (a dry, crackling sound upon passive movement).3
TREATMENT Before formulating any treatment plan, you should consult your doctor. Treatment of hand osteoarthritis involves the alleviation of pain, swelling, and prevention of further joint deterioration.2 Initial treatment often involves physical and occupational therapy and aims to strengthen the muscles of the hand and improve function. Simple methods of pain control might be utilized during these sessions (i.e.: ice, heat). Taking glucosamine and chondrotin sulfate may help to replenish cartilage and reduce symptoms. If pain is resistant, oral medications may be recommended. Tylenol is usually well tolerated and often a safe choice for patients of advanced age. Nonsteroidal anti-inflammatory drugs (NSAIDS) have proven effective in the alleviation of both pain and inflammation but should be used only after discussion with your doctor. Medications such as motrin, ibuprofen, and aleve should not be used in individuals of advanced age or with a history of peptic ulcer, kidney disease, asthma or hemophilia. If your symptoms are resistant to conservative treatments, a more invasive approach may be warranted. Intraarticular injections of glucocorticoids (steroids) are effective in the alleviation of inflammation and pain.2 Although occasional steroid injections are safe and well tolerated, frequent use can lead to systemic adverse effects. Side effects may include muscle wasting, redistribution of fat from the extremities to the trunk, hyperglycemia (high blood-glucose levels), suppression of the immune system, and insomnia.5 Finally, operative treatment may be indicated when medical and pharmacological management fails to prevent loss of hand function.2 Arthrodesis (fusion of the joint in a functional position) or arthroplasty (joint replacement) are surgical treatments that usually yield excellent results.2
SUMMARY Hand osteoarthritis is a prevalent disease characterized by the erosion and destruction of the joints of the hand. This degenerative process occurs due to years of overuse and mechanical stress. The resultant clinical findings include pain, weakness, inflammation, and structural deformities. Several treatment modalities exist to treat the pain and functional loss associated with osteoarthritis. Failure of these treatments may be an indication for surgical repair of the involved joints. In conjunction with your doctor, an effective and appropriate treatment plan can be formulated to maximize your function and reduce your pain.
Authors: Jason P. Welter, B.S., New York College of Osteopathic Medicine, Old Westbury, NY Elise Weiss, M.D., New York-Presbyterian Hospital, The University Hospital of Columbia and Cornell, New York City, NY
REFERENCES
1) Manek NJ, Lane NE. Osteoarthritis: Current Concepts in Diagnosis and Management. American Family Physician 2000; 61: 1-3 2) Garcia-Moral C. Interphalangeal Joint Arthritis. www.emedicine.com/orthoped/topic406.htm2005: 2-6 3) Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease 7th Edition 2005: 1304-1305 4) Moore KL, Dalley AF. Clinically Oriented Anatomy, 4th Edition 1999: 809. 5) Katzung BG. Basic and Clinical Pharmacology, 9th Edition 2004: 651. 6) Power-Pak C.E. www.powerpak.com/print.asp?page=courses/3089/lesson.htm2005: 1-24 7) Bernstein J. Musculoskeletal Medicine 2003: 105-108.
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