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98 Osteoarthritis

Osteoarthritis (OA) is the most common rheumatic disorder afflicting humankind and vertebrates in general. The most common alternative terms, osteo­arthrosis and degenerative joint disease, are used because of divergent concepts of the nature and cause of the disorder.

One school maintains that OA is a family of systemic inflammatory disorders with similar clinical and pathological end results. An­other supports the use of the term “osteoarthrosis” because inflammation is not present. Still another uses the term “degenerative joint disease” because it is held that aging and “wear and tear” are responsi­ble for its occurrence.

William Heberden, an eighteenth-century En­glish physician, gained immortality by describing what we now term Heberden’s nodes, a common heri­table form of osteoarthritis, especially common in women. In his Commentaries, he writes:

What are those little hard knots, about the size of a small pea, which are frequently seen upon the fingers, particu­larly a little below the top, near the joint? They have no connection with the gout, being found in persons who never had it: They continue for life; and being hardly ever attended with pain, or disposed to become sores, are rather unsightly, than inconvenient, though they must be some little hindrance to the free use of the fingers (Heberden 1802)

Modem research provides new data for a compre­hensive definition encompassing clinical, biochemi­cal, and anatomic features (Denko 1989). OA is a multifactorial systemic inflammatory disorder with clinical symptoms of pain and stiffness in movable joints, showing radiographic evidence of cartilage loss and bony overgrowth. The anatomic changes - cartilage loss and a kind of bony overgrowth and spurs-may occur physiologically without clinical symptoms. Osteoarthritis is classified as primary (id­iopathic) when there is no known predisposing fac­tor; or secondary, when there is a clearly defined, underlying condition contributing to its etiology, such as trauma, metabolic diseases, or gout.

Several symptom complexes are grouped as variant subsets such as generalized osteoarthritis or erosive inflam­matory osteoarthritis.

Distribution and Incidence

Osteoarthritis spares no race or geographic area. In the majority of patients, especially the younger group, the disease is mild and does not cause signifi­cant disability. However, in patients in the older age group it is more severe and often produces disability with loss of time from work and thus economic loss. The disease occurs with increased severity and fre­quency in older populations as a result of prolonged exposure to pathophysiological processes responsible for its development.

OA occurs with more frequency and more severity in women than in men. There is a sex difference in distribution of the joints involved. Lower spine and hip disease are more common in men, whereas cervi­cal spine and finger arthritis are more common in women. The most commonly affected joints are the distal Interphalangealjoints (Heberdens nodes)-, the proximal Interphalangeal joints of the fingers {Bou­chard’s nodes)-, the first metatarsophalangeal {bun­ion) joints of the feet; and the spine, the hips, and the knees (Peyron 1984).

Studies of the incidence of osteoarthritis produce divergent data because of differences in definition and diagnostic techniques. For example, when the definition includes only pathological anatomic changes (cartilage loss and bony growth), investiga­tors find evidence for the disorder in 90 percent of persons over age 40. Only about 30 percent of persons with radiographic changes of degenerative joint disease complain of pain in relevant joints (Moskowitz 1984). The frequency and severity of symptoms of the illness increase with age so that osteoarthritis is a major cause of symptomatic arthritis in the middle-aged and elderly population.

Epidemiology

The first epidemiological studies on osteoarthritis were reported about 60 years ago in England, using only questionnaires and clinical examination to evaluate incapacity and invalidism due to the dis­ease.

These methods, however, lacked diagnostic reli­ability, and classification of the disease was difficult. Later, use of roentgenograms to detect changes al­lowed for the classification of OA ranging from mild to severe, depending on the loss of cartilage and the presence of bony overgrowth. The cartilage loss is seen as joint space narrowing, whereas bony over­growth can be one or more of the following: osteo­phytes, bony ebumation, or increased bone density. Early physical findings such as Heberden’s nodes may precede radiographic changes.

Various surveys have explored demographic fac­tors associated with osteoarthritis. A study of skeletal remains of contemporary white and black Americans, twelfth-century Native Americans, and protohistoric Alaskan Eskimos showed that those who underwent the heaviest mechanical stresses suffered the most severe joint involvement (Denko 1989). Climate does not influence the prevalence of GA. In two groups of Native Americans of the same ethnic descent but with one living in a cold mountain region and the other in a hot desert, no differences were found in radiographs of the hands and feet. Hereditary predisposition to Heberden’s nodes have been found in half of the observed cases. The remaining cases are thought to be traumatic.

Differences in patterns of affected joints occur in different ethnic groups. Heberden’s nodes are rare in blacks, as is nonnodal generalized osteoarthritis. Oc­cupational factors may play a role in the incidence, especially in males. Studies from Great Britain, United States, and France show osteoarthritis to be a major cause of incapacity, economic loss, and social disadvantage in persons over the age of 50. Hip disease is more common in white populations than in blacks and Native Americans. Asian populations have a low incidence of hip disease, but incidence of OA of the fingers in Asia is high, as is the incidence in Europeans. Knee disease shows less difference among ethnic groups, being similarly prevalent in whites and blacks in South Africa and Jamaica (Peyron 1984).

Protective factors are few, including mainly the absence of mechanical stress such as that resulting from motor impairment, hemiplegia, or poliomyeli­tis. Predisposition to osteoarthritis occurs in indi­viduals who have pseudogout (calcium pyrophos­phate deposition disease). Deposits of urate crystals such as that occurring in gout also predispose the individual to osteoarthritis.

Etiology

The popular concept that osteoarthritis is a single disease resulting from attrition of cartilage due to age and wear-and-tear is not tenable in light of mod­ern experimental studies. Osteoarthritis can be re­garded as the result of aberrations in a complex pattern of biological reactions whose failure leads to anatomic changes in joint structure and function. One or more biological feedback loops may lead to malfunction of the complex system. Biological modi­fiers induce variable effects, depending on the target mechanism. A recent hypothesis proposes that OA is a multifactorial metabolic inflammatory disorder in which too little cartilage and too much bone are synthesized because of impaired liver function in processing growth hormone and insulin. Hepatic dys­function results in altered neuropeptide levels: too little insulin-like growth factor-1, which is required for cartilage growth, and too much insulin, which accelerates bony growth and osteophyte formation (Denko, Boja, and Moskowitz 1987).

Clinical Manifestations

Osteoarthritis usually has an insidious onset depend­ing on the specific joints afflicted and the patient’s tolerance to pain. The characteristic symptoms are pain and stiffness localized to the involved joints. In early disease the pain occurs with use of the joint; later pain occurs during rest. Morning stiffness is usually of short duration, less than 30 minutes. Fre­quently it is related to changes in the weather. The affected joint creaks on movement, and its motion is reduced.

The affected joint is enlarged, owing to bony over­growth and to synovitis with accumulation of fluid.

It is tender and painful. Late in the disease, subluxa­tion and muscle atrophy occur. Rarely is there ankylosis or fusion with complete loss of motion.

Radiographic examination shows cartilage loss, causing joint-space narrowing with bony overgrowth. The bony changes include eburnation in the sub­chondral region as well as spur development around the margin of the joint. Subchondral erosions are com­mon, as are subchondral cysts. Osteophytes usually form as these changes occur.

In a related disorder, excessive osteophytes occur along the anterior and anterolateral surfaces of the vertebrae and bridge the disk spaces. These patients are diagnosed as having diffuse idiopathic skeletal hyperostosis (DISH), a disorder different from osteo­arthritis in its biochemical changes.

History and Geography

Since prehistory, vertebrates have presumably suf­fered from osteoarthritis. Bones of dinosaurs show bony spurs and ankylosed spinal segments that are markers of the disease. The same changes occurred in prehistoric humankind as well as in animals, modern and ancient, such as horses and dogs (Roth­schild 1989). Clinical descriptions of arthritis date back to the fifth century B.C., to Hippocrates, who described the Scythians as having markedly lax or hypermobile joints:

I will give you strong proof of the hypermobility (laxity) of their constitutions. You will find the greater part of the Scythians, and all the Nomades, with marks of the cautery on their shoulders, arms, wrists, breasts, hip-joints, and loins, and that for no other reason but the hypermobility and flabbiness of their constitution, for they can neither strain with their bows, nor launch the javelin from their shoulder owing to their laxity and atony: but when they are burnt, much of the laxity in their joints is dried up, and they become braced, better fed, and their joints get into a more suitable condition.... They afterwards be­came lame and stiff at the hip joint, such of them, at least, as are severely attacked with it.

(Adams 1891)

The disorder was attributed to divine retribution for the destruction of the Temple of Ashkelon which the Scythians wrought during an invasion of Pales­tine. D. G. Rokhlin (1965) has illustrated severe shoulder OA, deforming arthrosis, in a Scythian skeleton derived from this Hippocratic period (fifth to third century B.C.). Evidently, shoulder OA was com­mon among the Scythians despite their treatment.

Over the centuries, the names of disorders encom­passing OA have changed and have included terms such as “rheumatism” and “lumbago,” which are no longer scientifically used. Today we can recognize dozens of forms and subsets of OA.

The prevalence of OA and the pattern of joint involvement show wide geographic differences. Fac­tors influencing the prevalence of osteoarthritis are very complex. Climate is often blamed for rheumatic troubles. Sixteen worldwide population samples- 13,200 Caucasians, blacks, and Native Americans aged 35 and over - were examined with X-rays, all of which were read by one observer. The following observations resulted, in part. OA was most preva­lent in the north of England, where 67 percent of men and 73 percent of women had OA. The lowest incidence was in Nigeria and Liberia. Prevalence of OA was also low in Soweto, South Africa, and in Piestany, Czechoslovakia.

The incidence of OA also varied with the specific joint being studied. For exmple, OA of the hips was common in males over 55 in the north of England; 22 to 25 percent were affected. These men were mainly coal miners and shepherds. In contrast, only 1 to 3 percent of black men, and only 2 to 4 percent of the black women, were affected in Jamaica, Liberia, Nige­ria, and South Africa. Data on Heberden’s nodes in 10 of the population samples revealed the highest frequency - 32 percent - in the population of Wat­ford, England; 30 percent in the Blackfeet Indians of Montana; and 26 percent in the people of Azmoos, Switzerland. All the black populations had low preva­lence, as did inhabitants of Oberholen, Germany. The Pima Indians of Arizona had an 11 percent incidence in the women, whereas in the men 20 percent were affected, a reversal of the normal sex distribution. (For more examples see Lawrence and Sebo 1980.)

Factors influencing the prevalence of osteoarth­ritis in populations include heredity, occupation, and possibly diet and resultant body build. Comparison of figures for populations living in very different parts of the world indicates no correlation with latitude, longitude, or any type of climate. Comparison was made Ofradiographs of hands and feet for 17 different European, African, and American groups of individu­als living from 54o north to 26o south. Nine were white, four black, and four Native American. Eleven of the population groups lived in rural areas, six in urban areas. No significant differences were found among the different groups in the prevalence of osteoarthritis. A survey in Sweden showed that the highest incidence of OA was in the southeast and cen­tral northern regions of the country and seemed to correlate more closely with the occupations of the pa­tients than with climatic conditions. More workers in farming and forestry had the disease than did work­ers in other occupations (Peyron 1984).

Charles W. Denko

Bibliography

Adams, F. 1891. The genuine works of Hippocrates. New York.

Denko1 Charles W. 1989. Osteoarthritis: A metabolic disor­der. In New developments in antirheumatic therapy, Inflammation and drug therapy series, Vol. 3, ed. Kim D. Rainsford and G. D. Velo, 29-35. Lancashire, U.K.

Denko, Charles W., B. Boja, and R. W. Moskowitz. 1987. Serum levels of insulin and insulin-like growth factor-1 (IGF-I). In osteoarthritis (OA). Arthritis and Rheumatism 30 (Supplement, ab): 29.

Heberden, William. 1802. Commentaries on the history and cure of disease. Reprinted under the auspices of the Library of the New York Academy of Medicine. New York, 1962.

Howell, D. S. 1984. Etiopathogenesis of osteoarthritis. In Osteoarthritis: Diagnosis and management, ed. R. W. Moskowitz et al., 129-46. Philadelphia.

Lawrence, J. S., and M. Sebo. 1980. The geography of osteoarthrosis. In The Oetiopathogenesis of osteoarth­rosis, ed. G. Nuki, 155-83. Kent, U.K.

Moskowitz, Roland W 1984. Osteoarthritis: Symptoms and signs. In Osteoarthritis: Diagnosis and manage­ment, ed. R. W. Moskowitz, D. S. Howell, and V. M. Goldberg, 149-54. Philadelphia.

Peyron, Jacques G. 1984. The epidemiology of osteoarth­ritis. In Osteoarthritis: Diagnosis and management, ed. Roland W. Moskowitz et al., 9-27. Philadelphia.

Rokhlin, D. G. 1965. Paleolithic and Mesolithic osseous finds [in Russian]. In Diseases of ancient man, Chap­ter 5, 216—43. Moscow-Leningrad.

Rothschild, Bruce M. 1989. Skeletal paleopathology of rheu­matic diseases: The subprimate connection. In Arthri­tis and allied conditions: A textbook of rheumatology, Ilth edition, ed. Daniel J. McCarty, 3-7. Philadelphia.

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Source: Kiple Kenneth F. (Editor). The Cambridge World History of Human Disease. Cambridge University Press,1993. — 1200 p.. 1993

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