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Current Concept and Management of Osteoarthritis
Current Concept and Management of Osteoarthritis HANS WAINE, M.D. Associate Professor of Medicine, 'I'ufts University School of Medicine, Boston, M assachusetls
OS'l'EOARTHRITIS is the commonest disease of joints. It is identifiable by a consistent morphologic change: irregular adventitious growths of cartilage or bone at the articular margins. In these terms, osteoarthritis is not one clinical entity, but a syndrome of numerous and varied disorders. Idiopathic or primary osteoarthritis is the clinical phase of degenerative joint disease, a universal process associated with aging. Secondary osteoarthritis comprises t\\O groups of conditions: first, those in which antecedent degeneration of hyaline cartilage results from specifically catabolic factors such as those listed in Table 3; second, thm;p ill \I hich the structural changes of osteoarthritis follow upon pathogenic stimuli which are not necessarily degenerative, such as those listed in Table 4.
Table 1. Osteoarthritis Degenerative joint disease Hypertrophic (osteo) arthritis Senescent arthritis
Synonyms Arthritis deformans (Osteo) Arthronosis Arthrosis Osteochondrosis
The term primary generalized osteoarthritis has recently been applied to a clinical complex which will not be considered here because of its obscure nature and doubtful homogeneity.
Etiology The cause of degenerative joint disease, which is the first stage of primary osteoarthritis, is unknown. The progression of the disease correlates with advancing years, but the nature of the biologic defect in senescent cartilage has not been fully defined. Hereditary predisposition seems a likely factor and has a proved association with Heberden's nodes which are usually considered a manifestation of osteoarthritis.
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The disease of laboratory animals which closely resembles human osteoarthritis also is, in some species, genetically determined. The etiologic role of sex is not clear. Females develop some subjective and objective manifestations of osteoarthritis oftener than do males, in the human and in other species. However, there is also good evidence that the morphologic alterations of osteoarthritis are evenly distributed between men and women. Functional stresses, or normal wear and tear, are not the causes of degenerative joint disease, but, they surely contribute to the development of osteoarthritis. Pathogenesis (Figs. 1,2 and 3)
The earliest structural defects have been seen in the ground substance of articular cartilage. The ground substance first changes in the weightbearing portions of an articular surface from a pearl gray, glistening, smooth, optically refractory to a yellowish, dull, pitted, irregularly fibrillated substance. In physical terms, this degenerated cartilage llwks the resilience of the normal tissue. Pressure causes it to be displaced toward the margin of the joint. At an early stage of osteoarthritis, there develops a peripheral ridge which may later become ossified. Chemically, there is a change in the sulfated mucopolysaccharides of the matrix which not only supports but also nourishes the chondrocytes. The loss of ground substance from cartilage exposes its collagenous fibrils which have less tolerance for pressure than for tension. Degeneration is thus compounded by the attrition of weight bearing and the movement of rough surfaces against each other. In a mature person, the cartilaginous covering of the epiphyses, being avascular, devoid of nerves and sparsely supplied with cells, has limited ability for autogenous repair. In response to the degenerative process there may be some hyperplasia and proliferation of chondrocytes, but the catabolic forces tend to overbalance regeneration. Since the supply of nutriment to hyaline cartilage derives mainly from synovial fluid and by infusion as into an expanding sponge, the loss of resilience may further impair the metabolism of chondrocytes. As degeneration of cartilage involves more surface and penetrates to greater depth, the articular covering may be split and splintered. But the usual development of degenerative joint disease is so gradual over the course of decades, that clinical evidence will rarely be disturbing. Moreover, in the course of naturally evolving degenerative joint disease, there occur two major compensatory phenomena: the broadening of the surface by marginal osteophytes and the condensation of subchondral bone (the latter sometimes shoots a sprout of fibrous marrow into the decayed cartilage to make substitute fibrocartilage). The clinical correlations to this indolent process are noteworthy in the negative: absence of significant local and systemic inflammation and
Fig. 1. Photomicrograph of normal patellar cartilage from a young adult. Note the distinct zones from top to bottom: tangential, transitional, radial, calcified. Compare cellularity and compactness of matrix with Figure 2.
Fig. 2. Photomicrograph of degenerating patellar cartilage (6th decade). Note the dissolution and disintegration of the superficial zone, the deep clefts, the paucity of cells and the occasional cluster of proliferating chondrocytes.
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Fig. 3. Photomicrograph of metatarsophalangeal joint in sagittal section (7th decade). The articular cartilage of the proximal epiphyses is frayed and has been totally eroded on parts of both surfaces. The subchondral bone is thickened. On the palmar side (right) there is an articulating sesamoid bone. On the dorsal aspect (left) there is a large osteophyte. This osseous excrescence is partially covered by cartilage. A smaller osteophyte is present at the opposing articular margin. Such adventitious growths frequently develop at the juncture of synoviaJis and cartilage, and are typical of osteoarthritis. (Committee on Pathology. The Arthritis and Rheumatism Foundation.)
failure of ankyloses to develop except occasionally in sacroiliac and sternoclavicular joints. Epidemiology There is no reliable information on the incidence and prevalence of clinical osteoarthritis. Radiologic evidence may be found in about 50 per cent of the general population in the fifth decade of life. By anatomical and histological methods the disease can be shown to affect some individuals in their early twenties. After that age the incidence of morphologic changes rapidly rises to reach over 80 per cent at the age of 60 (Fig. 4). DIAGNOSIS
Symptoms alld Signs In peripheral osteoarthritis, the symptoms are ordinarily limited to the affected joints, possibly with regional radiation of pain. The classical symptoms are deep aching, pain on motion and crepitus. There may be a gradual enlargement of the articular margins by soft tissue and bone. An important sign is tenderness, usually palpable during the active stage at the articular margins near the insertions of tendons.
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Fig. 4. Correlation of osteoarthritis with age. The solid line shows the percentage of positive x-rays, the broken line shows the degree of histopathologic change, each by decades, in knee joints of 2 series of persons without known rheumatic disease. Note the earlier development of morphologic lesions and the steep rise in both radiologic and pathologic evidence during the fourth and fifth decades. (Compiled from Bennet, Waine and Bauer; and Soila and Pyykonen.)
The signs of inflammation are ordinarily lacking, but a Heberden's node may develop precipitously and appear so red, hot and tender as to suggest gouty or purulent arthritis. The distribution of joint involvement is not strictly diagnostic in that arthritis of the terminal interphalangeal joints may be other than osteoarthritis and in that osteoarthritis does at times affect the proximal interphalangeal joints (Bouchard's nodes). It is less common in the metacarpal phalangeal joints, in the elbows, wrists and ankles. Generally the articulations exposed to stress, including weight bearing, are affected earliest and more severely. The pain of osteoarthritis, in contradistinction to that of the inflammatory types of arthritis, disappears immediately on rest. In osteoarthritis one would not expect to find an effusion of a joint although rarely, as in an acute Heberden's node and after contributory severe trauma or strain, the synovial space may be distended. The indices of general health by history, physical examination and laboratory tests are not affected in osteoarthritis. Unlike inflammatory rheumatic diseases, osteoarthritis does not cause systemic manifestations such as fever, weight loss, malaise, fatigability, anemia and elevation of the sedimentation rate. It is ordinarily not difficult to recognize osteoarthritis, but there are three major pitfalls. One, in the diagnosis of early rheumatic disease one must often defer a definite conclusion to
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allow for observation during several weeks or months. The condition at any given time may be less diagnostic than its dynamics. Second, certain symptoms (chiefly pain) may appear to be referred from demonstrable osteoarthritic lesions when in fact they are caused by visceral or vascular or malignant disease. Third, and most common, pain may be attributed to osteoarthritis per se when in fact the clinical episode is due to one or more decompensating factors (such as malposture, osteoporosis, emotional tension) or due to complications of osteoarthritis (such as narrowed intervertebral foramina, herniated nuclei pulposi, periostitis). Next to the elimination of other arthritides, the identification of precipitating factors is the most important step in the diagnosis of osteoarthritis, because it is essential to the practical management of the disease. Whenever these factors are amenable to treatment, their correction will cause osteoarthritis to become compensated. In osteoarthritis of the spine (spondylosis) the local symptoms tend to be overshadowed by remote complaints due to involvement of various neural elements. This relation is usually recognized in patients with sciatica, radicular pain about the trunk and brachial neuralgia; and spondylosis may also cause rectal and genital symptoms. Osteoarthritis of the cervical spine may be manifested by pain or paresthesias referred to the occipital, pharyngeal, otic, retrobulbar or frontal areas. Dysphagia is occasionally due to anterior vertebral osteophytes. Rarely posterior hypertrophic excrescences have led to necrosis of the spinal cord, paralysis and death. In order to find tenderness one must palpate separately the accessible articulations of the spine. In patients with thick adipose and muscular tissues the examiner may have to use his knuckles to exert sufficient pressure. For the localization of active spinal lesions, perhaps first suggested by the distribution of referred pain, the observation of segmental muscle spasm and the determination of a sensory level of hyperesthesia may be helpful. Laboratory It is usually necessary to perform those laboratory tests which may indicate other types of arthritis, if only because there is no readily applicable specific test for osteoarthritis. If synovial fluid can be aspirated, it is viscous, yellowish, clear, nonclotting and contains well polymerized hyaluronic acid and up to 1000 or 1500 cells per cubic millimeter, predominantly of the mononuclear series. X-ray
X-rays show typical abnormalities in variable degrees: narrowing of the joint spaces, condensation of the bone-cartilage border, irregular outlines of the articular heads, osteophytes, or periarticular ossicles. The value of radiologic criteria, however, is limited by the following considerations: first, radiologic osteoarthritis may represent a reaction of
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articular tissues to damage other than primary degeneration of hyaline cartilage; second, in degenerative joint disease the x-rays may be negative during the active stage; third, positive x-rays frequently do not coincide with e1inic'ally aetive dii'icase. Differential Diagnosis
The distinction from rheumatoid arthritis and other inflammatory diseases of connective tissue may not be obvious during the early stage of articular symptoms. Under these conditions the following criteria will be useful. Osteoarthritis usually develops in one or a few joints, is not characterized by inflammation, and is not accompanied by signs and symptoms of systemic illness. Rheumatoid arthritis frequently begins with symptoms and signs of general illness and the articular manifestations are often those of a symmetrical polyarthritis. Rheumatoid patients usually have matutinal stiffness, relieved by exercising, whereas the pain of osteoarthritis is promptly brought on by functional stress. In contrast to ostcoarthritis, gouty and septic arthritis cause sudden and severe synovitis. Course
Whereas thc pathologic c:hangcR of degenerative joint disease advance with inereaRing age, these lesions do not as a rule cause significant symptoms and functional incapacity. The clinical course of symptomatic osteoarthritis depends largely on the degree to which precipitating factors such as injuriCf;, abnormalities of posture and of body mechanics, obesity, occupational strains and psychogenic tension can be corrected and controlled. The natural COUI'Ae of osteoarthritis is expected to be benign with the exception of some localization and complications as malum coxae senilis, compression or rupture of the intervertebral disks or obliteration of the intervcrtebral foramina. Osteoarthritis therefore is a diAease in which signs (marginal proliferations, crepitwl) often precede the onset of symptoms by months and years. Symptomatic or decompemlated ostcoarthritis tends to begin in the fourth or fifth decade of life. Unless the precipitating or contributory causes are severe, chronic and refractory, a symptomatic episode will respond to treatment within days, rather than months. TREATMENT
Objectives
Osteoarthritis, whether idiopathic or secondary, cannot be cured but it can be satisfactorily controlled in the majority of patients. The initial aim of therapy is the protection of articular surfaces. For the relief of strain, one should afford the affected joint the maximum of practicable
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rest and one should attempt to correct any precipitating factors. The ultimate purpose of therapy is restoration of function to a reasonable level of competency by graded exercises. Protective Measures
It is necessary to guard the acute lesion against the functional stresses of weight bearing and motion for a period of days and rarely, for a week or two. This is usually accomplished by bandages, braces, splints and by the use of mechanical supports in the form of canes, crutches or walking calipers for the lower extremities. For the cervical spine, collars of felt or leather or ambulatory head traction splints may be used. Other parts of the spine may be protected by strapping, by a canvas belt, or by braces, or corsets or casts made of plaster or plastic. For lesions of the lower extremities, curtailment of stair-climbing, walking and standing may be indicated. For lesions of the hips and spine, bed rest and traction may be required. Precipitating Factors (Table 2)
The majority of clinical episodes probably result from physical strain on joints in the course of occupational or recreational exercise. When symptoms have developed as a result of excessive lifting, walking, gripping, bending, carrying, or overhead manipulations, it is usually not difficult to recognize and curtail the precipitating event. Other occupational hazards, such as improper seating at work or crouching postures of dentists and barbers, or the use of pneumatic hammers and vibrating instruments often cause clinical osteoarthritis, and must then be obviated. Malposture is another common aggravator of osteoarthritis. Acute spondylosis will usually be relieved by bracing and splinting; and one must note the patients' position of sleep, because improper bed support will foster mal posture. Yet, a sudden change from a soft to a hard mattress or from a high to a low neck support during recumbency may aggravate strain and symptoms. With postural and mechanical defects of the lower extremities such as unequal length or pronated feet, a foot lift may eliminate the aggra va ting circumstance. In 0 ther deformi ties such as bowed or knock knees, one must usually depend on scheduled curtailment of walking, standing, lifting and climbing, or on mechanical supports to the extremities. Obesity likewise is a potent precipitating factor of osteoarthritis, Table 2.
Factors Which Commonly Precipitate Symptomatic Osteoarthritis (Primary)
Bruxism Emotional strain Malposture
Menopause Obesity Physical strain
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Table 3. Disorders Which May Cause Degeneration of Cartilage and Osteoarthritis (Secondary) Bruxism Congenital deformity Diabetes mellitus Dyschondroplasia Gout Granulomatous synovitis Hemophilia Hemosiderosis
Table 4.
Hurler's syndrome Hysteria Infectious arthritis Malalignment Muscular imbalance Obesity Ochronosis Parkinsonism
Pneumatic hammer disease Hheurnatoid arthritis Scurvy Subluxation Taboneuropathy Trauma Villonodular synovitis Wilson's disease
Disorders Which May Cause Osteoarthritis (Secondary) Without Antecedent Degeneration of Cartilage
Acromegaly Aseptic necrosis of bone Calcinosis Endarteritis Epiphysitis
Hyperparathyroidism Osteogensis imperfecta Osteomalacia Osteomyelitis Osteoporosis
Osteosarcoma Paget's disease Pulmonary osteoarthropathy Hickets Vitamin D intoxication
probably both due to a physical effect upon the weight-bearing joints and a metabolic factor acting on all joints. Clinical problems arise chiefly in the joints of the lower spine and of the lower extremities. With severe and chronic obesity ambulatory treatment of osteoarthritis usually fails. Symptoms of osteoarthritis may further be precipitated by excessive muscular tension as a result of emotional disturbances. Treatment of the primary cause or the provision of relaxing diversions or medications are then indicated. The menopause in females is statistically associated with the development of osteoarthritis and in some animal species estrogens have a retarding effect on the evolution of degenerative joint disease. It is not clear whether there is a specific relation between estrogen deficiency and osteoarthritis, though the symptoms of osteoarthritis in menopausal women often improve with gonadal therapy. There is a large group of patients in whom symptoms of osteoarthritis develop secondarily to other local or systemic diseases such as those listed in Tables ;) and 4. The means and effectiveness of therapy will then be determined by the tractability of the underlying cause. Modalities of Therpay
DRUGS. For routine medication, salicylates are unsurpassed, relieving pain and muscle spasm. Acetylsalicylic acid in scheduled doses amounting to 3 grams daily usually suffices. Some patients are more tolerant to salicyl salicylic acid or choline salicylate. Depending on the severity of precipitating factors, the acute attack may require the supplementation of salicylates by codeine 0.03 gram or dextro-propoxyphene (Darvon) 0.065 gram three times daily for a few days. In attacks which are com-
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plirated by nervous tension, the further addition of phenobarbital gram three times daily may bc indicated, or of meprobamate 0.4 gram three times daily which, apart from its tranquilizing effect, also exertf) spasmolytic action. When oHteoarthritis occurs in menopam,al patients, especially in associatiol1 with osteoporosis, the combined administration of estrogens and testosterone often aids in the control of symptoms and has moreover a demonstrated and specific benefit to connective tissue matrix. Unless otherwise contraindicated, 1 cc. of a long-acting mixture containing about 2 mg. of estradiol and 2 mg. of testosterone should be injected intramuscularly every three to four weeks for six to nine months. While there is no indication for systemic treatment with corti co steroids, the intra-articular injection of hydrocortisone in dmies of 10 to 30 mg. (or of a suitable analogue) will afford rapid relief in acute osteoarthritis precipitated by physical stress. The injection may be repeated once or twice. Such treatment will not benefit an acute Heberden's node. Other intra-articular injections as of procaine, physiologic salt solution, iodid('f) or formaldehyde are not indicated. In general, narcotics and analgeHie drugs of significant toxic potential should not be given to osteoarthriti(' patients whose pain will invariably respond to safe and harmless
o.m
mea~iUres.
PHYSICAL THERAPY. Physical therapy improves general hygiene, permits the patient to participate in treatment, and provides the physician with a convenient lever on management of a chronic ailment in which it is safer to change exercises than drugs. In the acute stage, heat from an infrared lamp or moist packs applied over the affeded joint for 45 minutes acts as a counterirritant. ExerciHe should be withheld until pain and muscle spasm have subsided, usually for four to seven days. Thereafter, graduated exerciHes have a tonic effect on musele, cartilage and bone. Exercise is the only means known by which a modest amount of repair can be induced in adult articular cartilage, and it serves to prevent and correct the loss of range due to adaptive shortening of tendons and intra-articular ligaments. Immediately following an acute attack, exercising may be advantageously combined with hydrotherapy and may require some assistance, but the aim should be to achieve active exercise as soon as possible and to progress to resistance exercises. ROENTGEN THERAPY. Ionizing radiation should not be mied routinely. It has analgesic effects, but the only valid indication in osteoarthritis is severe and inoperable malum coxae senilis in patients of advanced age, to whom 1000 I' in divided dOHes should be given over the hip joints. SURGERY. Osteoarthritis o('('a~iollally beeomeH a disablillg and rarely an ominous, even catastrophic illneHs. When it affeds the hip joints, it tends to be difficult to control. Over a period of a few years, symptoms may change from slight and intermittent to severe and constant pain
Current Concept and M anagernent of Osteoarthritis
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on weight bearing. Concomitantly, the ranges of internal rotation and extension deeline, straining the lumbosacral and sacroiliac joints even at rest in recumbency, and prohihiting adequate sleep. Inahility to walk and stand, limitation of perpelldi(~ular hip motion to 40 degrees and regular nocturnal pain then form the indicatiolls for arthroplasty. The results are usually good and at times brilliant, with anyone of several procedures, according to the preference of an orthopedic surgeon. Most candidates for hip arthroplasty need two or three weeks of preoperative treatment to the local lesion, preferably hy hydrokinetherapy twice daily, and systematic treatment with anabolic hormones, such as Norethandrolone, 10 mg. three times daily. It is generally agreed that the functional gain depends also on assiduous after-care by physical therapy. Orthopedic surgery will often be useful in advanced osteoarthritis of the knee joints, metatarsal phalangeal joints and articulations of the low back. In osteoarthritis of the cervical spine, complicated by pressure on nerve roots or cord, surgical intervention is urgently indicated when signs of early neuropathy increase despite stringent conservative treatment hy splinting and traction. CONCLUSION
Primary osteoarthritis is the elinical phase of d(~gnerative joint dil'lnal'ln, and like it, assoeiatnd with advancing age. Ordinarily, it is a benign but incurable disorder, without significant symptoms and disability. When osteoarthritis is active and severe, one I'IhouJd search for and try to correct precipitating and contributory faetorl'l. Secondary osteoarthritis results from known ehondro-catabolic agents (urates, sepsis) or llondegenerative stimuli (somatotropin, rickets), but the principles of diagnosi:-; and treatment are ::;imilar. There is no pnwticable routine diagnw,tic test. The morphological changes of osteoarthritis usually precede the elinical manifestation::;, whieh do not inelude Hymptoms and signs of systemic illness attributable to oHteoarthritis. Treatment aims to compensate for stress-indueed exacerbations by rest, physical modalities, salicylates and c:ontroJ of nonphysiologic pathogens. For the few disabling and rare catastrophic complications orthopedic surgery is a nccnssary and effective treatment. REFERENCES Amprino, R. and Bairati, A.: Studi sulle trasformation: delle cartilagini dell' nomo nell' acrescimento e nella senescenza. Ztschr. IIdlforsehung u. mikrosp. Anat. 20: 143, 1933. Bennet, G. A., Waine, H. and Bauer, W.: Changes in the Knee Joint at Various Ages. New York, Commonwealth Fund, 1942. Callendar, G. R. and Kelser, R. A.: Degenerative Arthritis-A Comparison of Pathological Changes in Man and Equines. Am. J. Path. 14: 680, 1938.
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Cecchi, E. and Bisogno, E. M.: Arthrotische Knopel unter dem Electronmikroscop. Ztschr. f. Rheumaforschung. 16: 12, 1957. Collins, D. H.: Pathology of Articular and Spinal Diseases. London, Arnold, 1949. Johnson, L. C.: Kinetics of Osteoarthritis. In Comparative Pathology of Arthritis and Rheumatism, New York, Paul B. Hoeber, 1959. Kellgren, J. H. and Moore, R.: Generalized Osteoarthritis and Heberden's Nodes. Brit. M. J. 1: 181, 1952. Mathew, B. F.: Composition of Articular Cartilagc in Osteoarthritis. Brit. M. J. 2: 660,1953. Saiif, J.: Effects of Exercise on Adult Articular Cartilage. Act. orthop. Scandinav. Suppl. VII. Copenhagen, Ejnar Munksgaard, 1950. Schmorl, G. and Junghams, H.: Human Spine in Health and Disease. First American Edition edited by Stefan P. Wilk and Lowell S. Goin. New York, Grune & Stratton, 1959. Soila, P. and Pyykonen: Tables of the Incidence of Osteochondrosis in Joints. Act. rheumat. scandinav. 6: 151, 1960. Silberberg, M. and Sil,;erberg, R.: Effects of Endocrine Secretions on Articular Tissues and Their Relation to Ageing Processes. In Rheumatic Diseases. Philadelphia, W. B. Saunders Co., 1952. Snapper, 1.: Bone Diseases in Medical Practice. New York, Grune & Stratton, 1957. Sokoloff, L.: Osteoarthritis in Laboratory Animals. In Comparative Pathology of Arthritis and Rheumatism. New York, Paul B. Hoeber, 1959. Steindler, A.: Postgraduate Lectures on Orthopedic Diagnosis and Indications. Springfield, Ill., Charles C Thomas, 1952. Stecher, R. M. and Hersh, A. H.: Heberden's Nodes; Mechanism of Inheritance in Hypertrophic Arthritis of Fingers. J. Clin. Invest. 23: 699, 1944. Waine, H.: The Nature of Degenerative Joint Disease. Ann. West. Med. & Surg. 2: 313, 1948. Waine, H.: Observations on Osteoarthritis. Arthritis & Rheum. 1: 454, 1958. 25 Bennet Street Boston 11, Massachusetts
OS'l'EOARTHRITIS is the commonest disease of joints. It is identifiable by a consistent morphologic change: irregular adventitious growths of cartilage or bone at the articular margins. In these terms, osteoarthritis is not one clinical entity, but a syndrome of numerous and varied disorders. Idiopathic or primary osteoarthritis is the clinical phase of degenerative joint disease, a universal process associated with aging. Secondary osteoarthritis comprises t\\O groups of conditions: first, those in which antecedent degeneration of hyaline cartilage results from specifically catabolic factors such as those listed in Table 3; second, thm;p ill \I hich the structural changes of osteoarthritis follow upon pathogenic stimuli which are not necessarily degenerative, such as those listed in Table 4.
Table 1. Osteoarthritis Degenerative joint disease Hypertrophic (osteo) arthritis Senescent arthritis
Synonyms Arthritis deformans (Osteo) Arthronosis Arthrosis Osteochondrosis
The term primary generalized osteoarthritis has recently been applied to a clinical complex which will not be considered here because of its obscure nature and doubtful homogeneity.
Etiology The cause of degenerative joint disease, which is the first stage of primary osteoarthritis, is unknown. The progression of the disease correlates with advancing years, but the nature of the biologic defect in senescent cartilage has not been fully defined. Hereditary predisposition seems a likely factor and has a proved association with Heberden's nodes which are usually considered a manifestation of osteoarthritis.
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The disease of laboratory animals which closely resembles human osteoarthritis also is, in some species, genetically determined. The etiologic role of sex is not clear. Females develop some subjective and objective manifestations of osteoarthritis oftener than do males, in the human and in other species. However, there is also good evidence that the morphologic alterations of osteoarthritis are evenly distributed between men and women. Functional stresses, or normal wear and tear, are not the causes of degenerative joint disease, but, they surely contribute to the development of osteoarthritis. Pathogenesis (Figs. 1,2 and 3)
The earliest structural defects have been seen in the ground substance of articular cartilage. The ground substance first changes in the weightbearing portions of an articular surface from a pearl gray, glistening, smooth, optically refractory to a yellowish, dull, pitted, irregularly fibrillated substance. In physical terms, this degenerated cartilage llwks the resilience of the normal tissue. Pressure causes it to be displaced toward the margin of the joint. At an early stage of osteoarthritis, there develops a peripheral ridge which may later become ossified. Chemically, there is a change in the sulfated mucopolysaccharides of the matrix which not only supports but also nourishes the chondrocytes. The loss of ground substance from cartilage exposes its collagenous fibrils which have less tolerance for pressure than for tension. Degeneration is thus compounded by the attrition of weight bearing and the movement of rough surfaces against each other. In a mature person, the cartilaginous covering of the epiphyses, being avascular, devoid of nerves and sparsely supplied with cells, has limited ability for autogenous repair. In response to the degenerative process there may be some hyperplasia and proliferation of chondrocytes, but the catabolic forces tend to overbalance regeneration. Since the supply of nutriment to hyaline cartilage derives mainly from synovial fluid and by infusion as into an expanding sponge, the loss of resilience may further impair the metabolism of chondrocytes. As degeneration of cartilage involves more surface and penetrates to greater depth, the articular covering may be split and splintered. But the usual development of degenerative joint disease is so gradual over the course of decades, that clinical evidence will rarely be disturbing. Moreover, in the course of naturally evolving degenerative joint disease, there occur two major compensatory phenomena: the broadening of the surface by marginal osteophytes and the condensation of subchondral bone (the latter sometimes shoots a sprout of fibrous marrow into the decayed cartilage to make substitute fibrocartilage). The clinical correlations to this indolent process are noteworthy in the negative: absence of significant local and systemic inflammation and
Fig. 1. Photomicrograph of normal patellar cartilage from a young adult. Note the distinct zones from top to bottom: tangential, transitional, radial, calcified. Compare cellularity and compactness of matrix with Figure 2.
Fig. 2. Photomicrograph of degenerating patellar cartilage (6th decade). Note the dissolution and disintegration of the superficial zone, the deep clefts, the paucity of cells and the occasional cluster of proliferating chondrocytes.
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Fig. 3. Photomicrograph of metatarsophalangeal joint in sagittal section (7th decade). The articular cartilage of the proximal epiphyses is frayed and has been totally eroded on parts of both surfaces. The subchondral bone is thickened. On the palmar side (right) there is an articulating sesamoid bone. On the dorsal aspect (left) there is a large osteophyte. This osseous excrescence is partially covered by cartilage. A smaller osteophyte is present at the opposing articular margin. Such adventitious growths frequently develop at the juncture of synoviaJis and cartilage, and are typical of osteoarthritis. (Committee on Pathology. The Arthritis and Rheumatism Foundation.)
failure of ankyloses to develop except occasionally in sacroiliac and sternoclavicular joints. Epidemiology There is no reliable information on the incidence and prevalence of clinical osteoarthritis. Radiologic evidence may be found in about 50 per cent of the general population in the fifth decade of life. By anatomical and histological methods the disease can be shown to affect some individuals in their early twenties. After that age the incidence of morphologic changes rapidly rises to reach over 80 per cent at the age of 60 (Fig. 4). DIAGNOSIS
Symptoms alld Signs In peripheral osteoarthritis, the symptoms are ordinarily limited to the affected joints, possibly with regional radiation of pain. The classical symptoms are deep aching, pain on motion and crepitus. There may be a gradual enlargement of the articular margins by soft tissue and bone. An important sign is tenderness, usually palpable during the active stage at the articular margins near the insertions of tendons.
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100 90 80 70 I-
z
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UJ Do
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10
20
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AGE
50
60
70
80
Fig. 4. Correlation of osteoarthritis with age. The solid line shows the percentage of positive x-rays, the broken line shows the degree of histopathologic change, each by decades, in knee joints of 2 series of persons without known rheumatic disease. Note the earlier development of morphologic lesions and the steep rise in both radiologic and pathologic evidence during the fourth and fifth decades. (Compiled from Bennet, Waine and Bauer; and Soila and Pyykonen.)
The signs of inflammation are ordinarily lacking, but a Heberden's node may develop precipitously and appear so red, hot and tender as to suggest gouty or purulent arthritis. The distribution of joint involvement is not strictly diagnostic in that arthritis of the terminal interphalangeal joints may be other than osteoarthritis and in that osteoarthritis does at times affect the proximal interphalangeal joints (Bouchard's nodes). It is less common in the metacarpal phalangeal joints, in the elbows, wrists and ankles. Generally the articulations exposed to stress, including weight bearing, are affected earliest and more severely. The pain of osteoarthritis, in contradistinction to that of the inflammatory types of arthritis, disappears immediately on rest. In osteoarthritis one would not expect to find an effusion of a joint although rarely, as in an acute Heberden's node and after contributory severe trauma or strain, the synovial space may be distended. The indices of general health by history, physical examination and laboratory tests are not affected in osteoarthritis. Unlike inflammatory rheumatic diseases, osteoarthritis does not cause systemic manifestations such as fever, weight loss, malaise, fatigability, anemia and elevation of the sedimentation rate. It is ordinarily not difficult to recognize osteoarthritis, but there are three major pitfalls. One, in the diagnosis of early rheumatic disease one must often defer a definite conclusion to
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allow for observation during several weeks or months. The condition at any given time may be less diagnostic than its dynamics. Second, certain symptoms (chiefly pain) may appear to be referred from demonstrable osteoarthritic lesions when in fact they are caused by visceral or vascular or malignant disease. Third, and most common, pain may be attributed to osteoarthritis per se when in fact the clinical episode is due to one or more decompensating factors (such as malposture, osteoporosis, emotional tension) or due to complications of osteoarthritis (such as narrowed intervertebral foramina, herniated nuclei pulposi, periostitis). Next to the elimination of other arthritides, the identification of precipitating factors is the most important step in the diagnosis of osteoarthritis, because it is essential to the practical management of the disease. Whenever these factors are amenable to treatment, their correction will cause osteoarthritis to become compensated. In osteoarthritis of the spine (spondylosis) the local symptoms tend to be overshadowed by remote complaints due to involvement of various neural elements. This relation is usually recognized in patients with sciatica, radicular pain about the trunk and brachial neuralgia; and spondylosis may also cause rectal and genital symptoms. Osteoarthritis of the cervical spine may be manifested by pain or paresthesias referred to the occipital, pharyngeal, otic, retrobulbar or frontal areas. Dysphagia is occasionally due to anterior vertebral osteophytes. Rarely posterior hypertrophic excrescences have led to necrosis of the spinal cord, paralysis and death. In order to find tenderness one must palpate separately the accessible articulations of the spine. In patients with thick adipose and muscular tissues the examiner may have to use his knuckles to exert sufficient pressure. For the localization of active spinal lesions, perhaps first suggested by the distribution of referred pain, the observation of segmental muscle spasm and the determination of a sensory level of hyperesthesia may be helpful. Laboratory It is usually necessary to perform those laboratory tests which may indicate other types of arthritis, if only because there is no readily applicable specific test for osteoarthritis. If synovial fluid can be aspirated, it is viscous, yellowish, clear, nonclotting and contains well polymerized hyaluronic acid and up to 1000 or 1500 cells per cubic millimeter, predominantly of the mononuclear series. X-ray
X-rays show typical abnormalities in variable degrees: narrowing of the joint spaces, condensation of the bone-cartilage border, irregular outlines of the articular heads, osteophytes, or periarticular ossicles. The value of radiologic criteria, however, is limited by the following considerations: first, radiologic osteoarthritis may represent a reaction of
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articular tissues to damage other than primary degeneration of hyaline cartilage; second, in degenerative joint disease the x-rays may be negative during the active stage; third, positive x-rays frequently do not coincide with e1inic'ally aetive dii'icase. Differential Diagnosis
The distinction from rheumatoid arthritis and other inflammatory diseases of connective tissue may not be obvious during the early stage of articular symptoms. Under these conditions the following criteria will be useful. Osteoarthritis usually develops in one or a few joints, is not characterized by inflammation, and is not accompanied by signs and symptoms of systemic illness. Rheumatoid arthritis frequently begins with symptoms and signs of general illness and the articular manifestations are often those of a symmetrical polyarthritis. Rheumatoid patients usually have matutinal stiffness, relieved by exercising, whereas the pain of osteoarthritis is promptly brought on by functional stress. In contrast to ostcoarthritis, gouty and septic arthritis cause sudden and severe synovitis. Course
Whereas thc pathologic c:hangcR of degenerative joint disease advance with inereaRing age, these lesions do not as a rule cause significant symptoms and functional incapacity. The clinical course of symptomatic osteoarthritis depends largely on the degree to which precipitating factors such as injuriCf;, abnormalities of posture and of body mechanics, obesity, occupational strains and psychogenic tension can be corrected and controlled. The natural COUI'Ae of osteoarthritis is expected to be benign with the exception of some localization and complications as malum coxae senilis, compression or rupture of the intervertebral disks or obliteration of the intervcrtebral foramina. Osteoarthritis therefore is a diAease in which signs (marginal proliferations, crepitwl) often precede the onset of symptoms by months and years. Symptomatic or decompemlated ostcoarthritis tends to begin in the fourth or fifth decade of life. Unless the precipitating or contributory causes are severe, chronic and refractory, a symptomatic episode will respond to treatment within days, rather than months. TREATMENT
Objectives
Osteoarthritis, whether idiopathic or secondary, cannot be cured but it can be satisfactorily controlled in the majority of patients. The initial aim of therapy is the protection of articular surfaces. For the relief of strain, one should afford the affected joint the maximum of practicable
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rest and one should attempt to correct any precipitating factors. The ultimate purpose of therapy is restoration of function to a reasonable level of competency by graded exercises. Protective Measures
It is necessary to guard the acute lesion against the functional stresses of weight bearing and motion for a period of days and rarely, for a week or two. This is usually accomplished by bandages, braces, splints and by the use of mechanical supports in the form of canes, crutches or walking calipers for the lower extremities. For the cervical spine, collars of felt or leather or ambulatory head traction splints may be used. Other parts of the spine may be protected by strapping, by a canvas belt, or by braces, or corsets or casts made of plaster or plastic. For lesions of the lower extremities, curtailment of stair-climbing, walking and standing may be indicated. For lesions of the hips and spine, bed rest and traction may be required. Precipitating Factors (Table 2)
The majority of clinical episodes probably result from physical strain on joints in the course of occupational or recreational exercise. When symptoms have developed as a result of excessive lifting, walking, gripping, bending, carrying, or overhead manipulations, it is usually not difficult to recognize and curtail the precipitating event. Other occupational hazards, such as improper seating at work or crouching postures of dentists and barbers, or the use of pneumatic hammers and vibrating instruments often cause clinical osteoarthritis, and must then be obviated. Malposture is another common aggravator of osteoarthritis. Acute spondylosis will usually be relieved by bracing and splinting; and one must note the patients' position of sleep, because improper bed support will foster mal posture. Yet, a sudden change from a soft to a hard mattress or from a high to a low neck support during recumbency may aggravate strain and symptoms. With postural and mechanical defects of the lower extremities such as unequal length or pronated feet, a foot lift may eliminate the aggra va ting circumstance. In 0 ther deformi ties such as bowed or knock knees, one must usually depend on scheduled curtailment of walking, standing, lifting and climbing, or on mechanical supports to the extremities. Obesity likewise is a potent precipitating factor of osteoarthritis, Table 2.
Factors Which Commonly Precipitate Symptomatic Osteoarthritis (Primary)
Bruxism Emotional strain Malposture
Menopause Obesity Physical strain
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Table 3. Disorders Which May Cause Degeneration of Cartilage and Osteoarthritis (Secondary) Bruxism Congenital deformity Diabetes mellitus Dyschondroplasia Gout Granulomatous synovitis Hemophilia Hemosiderosis
Table 4.
Hurler's syndrome Hysteria Infectious arthritis Malalignment Muscular imbalance Obesity Ochronosis Parkinsonism
Pneumatic hammer disease Hheurnatoid arthritis Scurvy Subluxation Taboneuropathy Trauma Villonodular synovitis Wilson's disease
Disorders Which May Cause Osteoarthritis (Secondary) Without Antecedent Degeneration of Cartilage
Acromegaly Aseptic necrosis of bone Calcinosis Endarteritis Epiphysitis
Hyperparathyroidism Osteogensis imperfecta Osteomalacia Osteomyelitis Osteoporosis
Osteosarcoma Paget's disease Pulmonary osteoarthropathy Hickets Vitamin D intoxication
probably both due to a physical effect upon the weight-bearing joints and a metabolic factor acting on all joints. Clinical problems arise chiefly in the joints of the lower spine and of the lower extremities. With severe and chronic obesity ambulatory treatment of osteoarthritis usually fails. Symptoms of osteoarthritis may further be precipitated by excessive muscular tension as a result of emotional disturbances. Treatment of the primary cause or the provision of relaxing diversions or medications are then indicated. The menopause in females is statistically associated with the development of osteoarthritis and in some animal species estrogens have a retarding effect on the evolution of degenerative joint disease. It is not clear whether there is a specific relation between estrogen deficiency and osteoarthritis, though the symptoms of osteoarthritis in menopausal women often improve with gonadal therapy. There is a large group of patients in whom symptoms of osteoarthritis develop secondarily to other local or systemic diseases such as those listed in Tables ;) and 4. The means and effectiveness of therapy will then be determined by the tractability of the underlying cause. Modalities of Therpay
DRUGS. For routine medication, salicylates are unsurpassed, relieving pain and muscle spasm. Acetylsalicylic acid in scheduled doses amounting to 3 grams daily usually suffices. Some patients are more tolerant to salicyl salicylic acid or choline salicylate. Depending on the severity of precipitating factors, the acute attack may require the supplementation of salicylates by codeine 0.03 gram or dextro-propoxyphene (Darvon) 0.065 gram three times daily for a few days. In attacks which are com-
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plirated by nervous tension, the further addition of phenobarbital gram three times daily may bc indicated, or of meprobamate 0.4 gram three times daily which, apart from its tranquilizing effect, also exertf) spasmolytic action. When oHteoarthritis occurs in menopam,al patients, especially in associatiol1 with osteoporosis, the combined administration of estrogens and testosterone often aids in the control of symptoms and has moreover a demonstrated and specific benefit to connective tissue matrix. Unless otherwise contraindicated, 1 cc. of a long-acting mixture containing about 2 mg. of estradiol and 2 mg. of testosterone should be injected intramuscularly every three to four weeks for six to nine months. While there is no indication for systemic treatment with corti co steroids, the intra-articular injection of hydrocortisone in dmies of 10 to 30 mg. (or of a suitable analogue) will afford rapid relief in acute osteoarthritis precipitated by physical stress. The injection may be repeated once or twice. Such treatment will not benefit an acute Heberden's node. Other intra-articular injections as of procaine, physiologic salt solution, iodid('f) or formaldehyde are not indicated. In general, narcotics and analgeHie drugs of significant toxic potential should not be given to osteoarthriti(' patients whose pain will invariably respond to safe and harmless
o.m
mea~iUres.
PHYSICAL THERAPY. Physical therapy improves general hygiene, permits the patient to participate in treatment, and provides the physician with a convenient lever on management of a chronic ailment in which it is safer to change exercises than drugs. In the acute stage, heat from an infrared lamp or moist packs applied over the affeded joint for 45 minutes acts as a counterirritant. ExerciHe should be withheld until pain and muscle spasm have subsided, usually for four to seven days. Thereafter, graduated exerciHes have a tonic effect on musele, cartilage and bone. Exercise is the only means known by which a modest amount of repair can be induced in adult articular cartilage, and it serves to prevent and correct the loss of range due to adaptive shortening of tendons and intra-articular ligaments. Immediately following an acute attack, exercising may be advantageously combined with hydrotherapy and may require some assistance, but the aim should be to achieve active exercise as soon as possible and to progress to resistance exercises. ROENTGEN THERAPY. Ionizing radiation should not be mied routinely. It has analgesic effects, but the only valid indication in osteoarthritis is severe and inoperable malum coxae senilis in patients of advanced age, to whom 1000 I' in divided dOHes should be given over the hip joints. SURGERY. Osteoarthritis o('('a~iollally beeomeH a disablillg and rarely an ominous, even catastrophic illneHs. When it affeds the hip joints, it tends to be difficult to control. Over a period of a few years, symptoms may change from slight and intermittent to severe and constant pain
Current Concept and M anagernent of Osteoarthritis
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on weight bearing. Concomitantly, the ranges of internal rotation and extension deeline, straining the lumbosacral and sacroiliac joints even at rest in recumbency, and prohihiting adequate sleep. Inahility to walk and stand, limitation of perpelldi(~ular hip motion to 40 degrees and regular nocturnal pain then form the indicatiolls for arthroplasty. The results are usually good and at times brilliant, with anyone of several procedures, according to the preference of an orthopedic surgeon. Most candidates for hip arthroplasty need two or three weeks of preoperative treatment to the local lesion, preferably hy hydrokinetherapy twice daily, and systematic treatment with anabolic hormones, such as Norethandrolone, 10 mg. three times daily. It is generally agreed that the functional gain depends also on assiduous after-care by physical therapy. Orthopedic surgery will often be useful in advanced osteoarthritis of the knee joints, metatarsal phalangeal joints and articulations of the low back. In osteoarthritis of the cervical spine, complicated by pressure on nerve roots or cord, surgical intervention is urgently indicated when signs of early neuropathy increase despite stringent conservative treatment hy splinting and traction. CONCLUSION
Primary osteoarthritis is the elinical phase of d(~gnerative joint dil'lnal'ln, and like it, assoeiatnd with advancing age. Ordinarily, it is a benign but incurable disorder, without significant symptoms and disability. When osteoarthritis is active and severe, one I'IhouJd search for and try to correct precipitating and contributory faetorl'l. Secondary osteoarthritis results from known ehondro-catabolic agents (urates, sepsis) or llondegenerative stimuli (somatotropin, rickets), but the principles of diagnosi:-; and treatment are ::;imilar. There is no pnwticable routine diagnw,tic test. The morphological changes of osteoarthritis usually precede the elinical manifestation::;, whieh do not inelude Hymptoms and signs of systemic illness attributable to oHteoarthritis. Treatment aims to compensate for stress-indueed exacerbations by rest, physical modalities, salicylates and c:ontroJ of nonphysiologic pathogens. For the few disabling and rare catastrophic complications orthopedic surgery is a nccnssary and effective treatment. REFERENCES Amprino, R. and Bairati, A.: Studi sulle trasformation: delle cartilagini dell' nomo nell' acrescimento e nella senescenza. Ztschr. IIdlforsehung u. mikrosp. Anat. 20: 143, 1933. Bennet, G. A., Waine, H. and Bauer, W.: Changes in the Knee Joint at Various Ages. New York, Commonwealth Fund, 1942. Callendar, G. R. and Kelser, R. A.: Degenerative Arthritis-A Comparison of Pathological Changes in Man and Equines. Am. J. Path. 14: 680, 1938.
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Cecchi, E. and Bisogno, E. M.: Arthrotische Knopel unter dem Electronmikroscop. Ztschr. f. Rheumaforschung. 16: 12, 1957. Collins, D. H.: Pathology of Articular and Spinal Diseases. London, Arnold, 1949. Johnson, L. C.: Kinetics of Osteoarthritis. In Comparative Pathology of Arthritis and Rheumatism, New York, Paul B. Hoeber, 1959. Kellgren, J. H. and Moore, R.: Generalized Osteoarthritis and Heberden's Nodes. Brit. M. J. 1: 181, 1952. Mathew, B. F.: Composition of Articular Cartilagc in Osteoarthritis. Brit. M. J. 2: 660,1953. Saiif, J.: Effects of Exercise on Adult Articular Cartilage. Act. orthop. Scandinav. Suppl. VII. Copenhagen, Ejnar Munksgaard, 1950. Schmorl, G. and Junghams, H.: Human Spine in Health and Disease. First American Edition edited by Stefan P. Wilk and Lowell S. Goin. New York, Grune & Stratton, 1959. Soila, P. and Pyykonen: Tables of the Incidence of Osteochondrosis in Joints. Act. rheumat. scandinav. 6: 151, 1960. Silberberg, M. and Sil,;erberg, R.: Effects of Endocrine Secretions on Articular Tissues and Their Relation to Ageing Processes. In Rheumatic Diseases. Philadelphia, W. B. Saunders Co., 1952. Snapper, 1.: Bone Diseases in Medical Practice. New York, Grune & Stratton, 1957. Sokoloff, L.: Osteoarthritis in Laboratory Animals. In Comparative Pathology of Arthritis and Rheumatism. New York, Paul B. Hoeber, 1959. Steindler, A.: Postgraduate Lectures on Orthopedic Diagnosis and Indications. Springfield, Ill., Charles C Thomas, 1952. Stecher, R. M. and Hersh, A. H.: Heberden's Nodes; Mechanism of Inheritance in Hypertrophic Arthritis of Fingers. J. Clin. Invest. 23: 699, 1944. Waine, H.: The Nature of Degenerative Joint Disease. Ann. West. Med. & Surg. 2: 313, 1948. Waine, H.: Observations on Osteoarthritis. Arthritis & Rheum. 1: 454, 1958. 25 Bennet Street Boston 11, Massachusetts