1977, British Journal of Radiology, 50, 81-83
VOLUME 50 NUMBER 590
FEBRUARY 1977
The British Journal of Radiology Radiology now Osteoarthrosis of the hip: one disease or many?* Osteoarthrosis of the hip is a common disorder. In Kellgren's (1961) population study, approximately 20% of people over the age of 55 years showed evidence of osteoarthrosis of the hip. The morbidity in the middle-aged white subject is considerable (Sze, 1963), but surveys of prevalence and morbidity are bedevilled by the lack of internationally recognized clinical criteria, and imprecision in radiological interpretation. Though the disease is so common, aetiology and pathogenesis are ill understood. This is reflected in nomenclature. Osteoarthritis is a well-established name, but there is no suggestion that the disorder is primarily inflammatory in nature, and osteoarthrosis is preferred by many. Degenerative disease of the hip is an unwieldy term and covers such a broad spectrum that its precise meaning is uncertain. A disease is generally authenticated by the establishment of a specific natural history and characteristic pathological changes. Traditionally, osteoarthrosis has been separated into primary and secondary types; the term secondary osteoarthrosis is applied where change is superimposed on a preceding abnormality of the hip. Secondary osteoarthrosis therefore follows local trauma, dysplasia, aseptic necrosis, inflammatory arthritis, etc. If it is assumed that the normal hip is ideally suited for load-bearing, then even slight alteration in the convex-concave surfaces may result in inequable distribution of compression forces over the articular surface (Bullough et al., 1973; Goodfellow and O'Connor, 1975). Further studies are proceeding, but at present the relevance of altered local stress is not proven. Of great interest is the suggestion that minor joint dysplasia or deformity may predispose to degenerative change. It is possible, radiologically, to recognize the shallow sloping dysplastic acetabulum, and although it is not proven that such patients form *Reprints from Dr. D. J. Stoker, Institute of Orthopaedics, Royal National Orthopaedic Hospital, 234 Great Portland Street, London WIN 6AD. 81
part of the spectrum of congenital dislocation per se, alterations in joint mechanics may result in osteoarthrosis. Murray (1965), postulating that minor anatomical abnormalities may lead to so-called primary osteoarthrosis, has drawn particular attention to the "tilt deformity" in certain femoral heads affected by degenerative change. In this group of patients, the femoral head bears a resemblance to the slipped femoral capital epiphysis. Murray believes that in these hips an unrecognized minor epiphyseal slip has occurred in adolescence, leading to osteoarthrosis in middle age. Whilst the concept may be valid, this exclusive aetiology of the tilt deformity is in dispute. Meachim et al. (1972) have shown clearly by slab radiographs that such a deformity may be produced by downgrowth of an osteophyte from the inferior margin of the femoral head. This results logically from the common upward migration of the femoral head with osteophyte growth in an area of low joint stress (Harrison et al., 1953). No evidence is forthcoming to indicate that an osteophyte itself causes displacement of the femoral head. A similar patho-radiological study has been performed by Resnick (1976). The author suggests that changes in the acetabulum may initiate the tilt deformity rather than epiphyseal slip in adolescence. Murray and Duncan (1971) did further work on the presence of tilt deformity in adolescents and related it to athletic activity. This careful study suggested that the deformity was more common in the more active child. The relation to osteoarthrosis will require a prospective survey with a delay of at least a generation before the results are known. Another pattern of osteoarthrosis is that associated with protrusio acetabuli. The relative frequency of this deformity in rheumatoid arthritis has led to the suggestion that unrecognized rheumatoid arthritis has preceded degenerative change (Murray and Jacobson, 1971), particularly if osteophyte formation is minimal. To date, there is little histological or serological support for rheumatoid arthritis being a
VOL.
50, No. 590 D. J. Stoker
cause of degenerative hip disease. Where character- more recent years, however, the study of genetic, istic rheumatoid changes are present elsewhere, endocrine, metabolic, vascular and biochemical e.g. in films of the hands and feet, the diagnosis of factors has led to the accumulation of much data on rheumatoid hip disease is reasonable. If not, caution the subject, particularly in respect of articular should be exercised in making this diagnosis, based cartilage. Many questions remain unanswered. If on protrusio acetabuli alone. Alexander (1965) has osteoarthrosis is an aging process, why has ageproposed that primary protrusio in adults, progress- correlated change not been demonstrated in noning as it may to osteoarthrosis, can result from stress articular hyaline cartilage ? Why is involvement of the during the adolescent growth spurt. A subsequent hip, knee and terminal interphalangeal joints of the failure in pelvic remodelling, leading to protrusio, fingers so common, yet involvement of the ankle correlates with the female sex predominance, coxa and wrist relatively rare ? vara and premature epiphyseal fusion. To the general radiologist, osteoarthrosis of the Severe destructive change in the hips, often with hip is a frequent finding during routine film reportradiological features of aseptic necrosis, may follow ing. Most patients with the condition show changes therapy with corticosteroids (Sweetnam et al., which are advanced on presentation. X-ray examina1960). It is rare for a patient with significant tion may reveal reduction of the joint (or cartilage) degenerative hip disease, to escape treatment with space, sclerosis of subarticular bone (eburnation) either phenylbutazone or indomethacin. In a on both sides of the joint, and subarticular cystic minority of those so treated, the accelerated progress change. Perhaps the outstanding feature which may of a destructive arthropathy suggests that the drug lead the radiologist to diagnose degenerative change regime may be implicated (Arora, 1968; Allen and is the marginal osteophyte. However, Danielsson (1964), in a study of 86 patients where the diagnosis Murray, 1971). These various starting points might suggest that of osteoarthrosis was made solely on the presence of osteoarthrosis is due to a mixture of inherited and osteophytes, showed over the next 11 years only one environmental factors (Kellgren, 1961). Alter- patient who produced joint space narrowing. The natively, a final common pathway may exist in what remaining 85 patients exhibited no progressive is most probably a multifactorial disease. However, radiological change. On this evidence and that of the so little is known about the detailed pathogenesis that pathologists, one is forced to agree that the earliest these alternatives must remain unresolved. Most definable stage of progressive osteoarthrosis is pathologists seem to be in no doubt that osteo- narrowing of the joint space. But early loss of arthrosis begins in the cartilage, although the nature articular cartilage is often patchy or focal, and this of the process is obscure. It is claimed that the usually precludes its radiographic demonstration. earliest finding is a characteristic splitting and The width of the normal joint space varies from one fragmentation (fibrillation) of the articular cartilage. subject to another, although in unilateral disease the Byers et al. (1970, 1976a, b) have produced evidence width can be compared with the other hip, if that is from a study of cadaveric hips, which indicates that, presumed to be normal. The unequivocal diagnosis in this joint, two classes of process affect the of narrowing requires a reduction by at least onecartilage: (a) commonly occurring changes of third in the width of the joint space (Gofton, 1971). limited progression not leading to deformity of the The hip, being a ball and socket joint, presents a joint, and (b) less common progressive changes con- further problem because focal loss of articular sistent with a disease process. In any event a cartilage nearly always occurs in the antero-superior destructive process leads to thinning of the cartilage quadrant, and in the earlier stages will only be layer, and eventually to focal exposure of sub- shown in tangential (preferably weight-bearing) chondral bone. Whether such tissue response is due views. It therefore seems unlikely that the radito fatigue failure of the collagen network (Freeman, ologist will be able to diagnose the early changes in 1975), when abnormal structural relationships could articular cartilage observed by the pathologist. be implicated, to primary failure of the chondrocyte Where does the radiologist now stand in the {British Medical Journal, 1976), or to some other diagnosis of osteoarthrosis? He is unable to recogmechanism is unknown. Hypotheses abound nize the early disease, often unable to predict the (Kempson et al., 1975), including that the disease symptomatic patient, but able to identify various originates in bone or as a failure in joint lubrication. patterns of joint disease (Gofton, 1971; Jeffrey, The proposition that osteoarthrosis is an arthropathy 1975), the significance of which is not always clear. associated with the aging process has tended, in the More recently, attempts have been made to prove past, to deter investigation into its aetiology. In that osteoarthrosis is always a secondary disorder 82
FEBRUARY 1977
Radiology now. Osteoarthrosis of the hip: one disease or many} (Stulberg et al, 1975; Solomon, 1976). Solomon claimed that a predisposing abnormality was apparent in all but 27 of 327 patients with degenerative disease of the hip. Such correlation in excess of 90% is not within the experience of most practising skeletal radiologists, and leaves little room for the inclusion of other possible causes, such as disparity in leg length (Gofton, 1971). We must continue to observe critically the films of our patients with degenerative hip disease. All osteoarthrosis may be secondary, but proof will not come from subjective radiological impressions, but by future correlation of accurately observed diagnostic signs from clinical, radiological and pathological sources.
GOFTON, J. P., 1971. Studies in osteoarthritis of the hip: Part I Classification. Canadian Medical Association Journal, 104, 679-683. GOODFELLOW, J. W., and O'CONNOR, J., 1975. The trans-
mission of loads through the hips and knee: a hypothesis on the aetiology of osteoarthritis. Journal of Bone and Joint Surgery, 57B, 400. HARRISON, M. H. M., SCHAJOWICZ, F., and TRUETA, J.,
1953. Osteoarthritis of the hip: a study of the nature and evolution of the disease. Journal of Bone and Joint Surgery, 35B, 598-626. JEFFREY, A. K., 1975. Osteophytes and the osteoarthritic femoral head. Journal of Bone and Joint Surgery, 57B, 314-324. KELLGREN, J. H., 1961. Osteoarthrosis in patients and populations. British Medical Journal, 2,1-6. KEMPSON, G. E., MAROUDAS, A., and WEIGHTMAN, B., 1975.
(Editors) Conference on Articular Cartilage 1974. Annals of the Rheumatic Diseases, 34, Supplement No. 2, pp. 120-133.
DENNIS J. STOKER
MEACHIM, G., HARDING, K., and WILLIAMS, D. R., 1972.
Methods for correlating pathological and radiological findings in osteoarthrosis of the hip. British Journal of pathies. In Proceedings of the European Association of Radiology, 45, 670-676. Radiology, Amsterdam 1971. Pp. 204-210 (Excerpta MURRAY, R. O., 1965. The aetiology of primary osteoarthritis of the hip. British Journal of Radiology, 38, 810Medica, Amsterdam). 824. ALEXANDER, C , 1965. The aetiology of primary protrusio MURRAY, R. O., and DUNCAN, C , 1971. Athletic activity in acetabuli. British Journal of Radiology, 38, 567-580. adolesence as an aetiological factor in degenerative hip ARORA, J. S., 1968. Indomethacin arthropathy of the hips. disease. Journal of Bone and Joint Surgery, 53B, 406-419. Proceedings of the Royal Society of Medicine, 61, 669. MURRAY, R. O., and JACOBSON, H. G., 1971. The Radiology 1976. Leading article, British Medical Journal, 2, 4—5. of Skeletal Disorders, p. 645 (Churchill Livingstone, BULLOUGH, P., GOODFELLOW, J., and O'CONNOR, J., 1973. Edinburgh & London). The relationship between degenerative changes and loadbearing in the human hip. Journal of Bone and Joint RESNICK, D., 1976. The "tilt deformity" of the femoral head in osteoarthritis of the hip: a poor indicator of previous Surgery, 55B, 746-758. epiphysiolysis. Clinical Radiology, 27, 355—363. BYERS, P. D., CONTEPOMI, C. A., and FARKAS, T. A., 1970. A post-mortem study of the hip joint. Annals of the SOLOMON, L., 1976. Patterns of osteoarthritis of the hip. Journal of Bone and Joint Surgery, 58B, 176-183. Rheumatic Diseases, 29, 15-31. 1976a. Post-mortem study of the hip joint II. Histo- STULBERG, S. D., CORDELL, L. D., HARRIS, W. H., RAMSEY, P. L., and MACEWEN, G. D., 1975. Unrecognised childlogical basis for limited and progressive cartilage alterahood hip disease; a major cause of idiopathic osteotions. Annals of the Rheumatic Diseases, 35, 114—121. arthritis of the hip. In The Hip, Proceedings of the 3rd 1976b. Post-mortem study of the hip joint III. Coropen scientific meeting of the Hip Society (C. V. Mosby relations between observations. Annals of the Rheumatic Co.), 212-228. Diseases, 35,122-126. DANIELSSON, L. G., 1964. Incidence and prognosis of SWEETNAM, D. R., MASON, R. M., and MURRAY, R. O., 1960. Steroid arthropathy of the hip. British Medical coxarthrosis. Ada Orthopaedica Scandinavica SuppleJournal, 7,1392-1394. ment, 66,1. FREEMAN, M. A. R., 1975. The fatigue of cartilage in the SZE, T. S., 1963. In The Epidemiology of Chronic Rheumapathogenesis of osteoarthrosis. Acta Orthopaedica tism, 1, pp. 1-11. Edited by J. H. Kellgren (Blackwell Scandinavica, 46, 323-328. Scientific Publications, Oxford). REFERENCES
ALLEN, E. H., and MURRAY, R. O., 1971. Iatrogenic arthro-
83
VOLUME 50 NUMBER 590
FEBRUARY 1977
The British Journal of Radiology Radiology now Osteoarthrosis of the hip: one disease or many?* Osteoarthrosis of the hip is a common disorder. In Kellgren's (1961) population study, approximately 20% of people over the age of 55 years showed evidence of osteoarthrosis of the hip. The morbidity in the middle-aged white subject is considerable (Sze, 1963), but surveys of prevalence and morbidity are bedevilled by the lack of internationally recognized clinical criteria, and imprecision in radiological interpretation. Though the disease is so common, aetiology and pathogenesis are ill understood. This is reflected in nomenclature. Osteoarthritis is a well-established name, but there is no suggestion that the disorder is primarily inflammatory in nature, and osteoarthrosis is preferred by many. Degenerative disease of the hip is an unwieldy term and covers such a broad spectrum that its precise meaning is uncertain. A disease is generally authenticated by the establishment of a specific natural history and characteristic pathological changes. Traditionally, osteoarthrosis has been separated into primary and secondary types; the term secondary osteoarthrosis is applied where change is superimposed on a preceding abnormality of the hip. Secondary osteoarthrosis therefore follows local trauma, dysplasia, aseptic necrosis, inflammatory arthritis, etc. If it is assumed that the normal hip is ideally suited for load-bearing, then even slight alteration in the convex-concave surfaces may result in inequable distribution of compression forces over the articular surface (Bullough et al., 1973; Goodfellow and O'Connor, 1975). Further studies are proceeding, but at present the relevance of altered local stress is not proven. Of great interest is the suggestion that minor joint dysplasia or deformity may predispose to degenerative change. It is possible, radiologically, to recognize the shallow sloping dysplastic acetabulum, and although it is not proven that such patients form *Reprints from Dr. D. J. Stoker, Institute of Orthopaedics, Royal National Orthopaedic Hospital, 234 Great Portland Street, London WIN 6AD. 81
part of the spectrum of congenital dislocation per se, alterations in joint mechanics may result in osteoarthrosis. Murray (1965), postulating that minor anatomical abnormalities may lead to so-called primary osteoarthrosis, has drawn particular attention to the "tilt deformity" in certain femoral heads affected by degenerative change. In this group of patients, the femoral head bears a resemblance to the slipped femoral capital epiphysis. Murray believes that in these hips an unrecognized minor epiphyseal slip has occurred in adolescence, leading to osteoarthrosis in middle age. Whilst the concept may be valid, this exclusive aetiology of the tilt deformity is in dispute. Meachim et al. (1972) have shown clearly by slab radiographs that such a deformity may be produced by downgrowth of an osteophyte from the inferior margin of the femoral head. This results logically from the common upward migration of the femoral head with osteophyte growth in an area of low joint stress (Harrison et al., 1953). No evidence is forthcoming to indicate that an osteophyte itself causes displacement of the femoral head. A similar patho-radiological study has been performed by Resnick (1976). The author suggests that changes in the acetabulum may initiate the tilt deformity rather than epiphyseal slip in adolescence. Murray and Duncan (1971) did further work on the presence of tilt deformity in adolescents and related it to athletic activity. This careful study suggested that the deformity was more common in the more active child. The relation to osteoarthrosis will require a prospective survey with a delay of at least a generation before the results are known. Another pattern of osteoarthrosis is that associated with protrusio acetabuli. The relative frequency of this deformity in rheumatoid arthritis has led to the suggestion that unrecognized rheumatoid arthritis has preceded degenerative change (Murray and Jacobson, 1971), particularly if osteophyte formation is minimal. To date, there is little histological or serological support for rheumatoid arthritis being a
VOL.
50, No. 590 D. J. Stoker
cause of degenerative hip disease. Where character- more recent years, however, the study of genetic, istic rheumatoid changes are present elsewhere, endocrine, metabolic, vascular and biochemical e.g. in films of the hands and feet, the diagnosis of factors has led to the accumulation of much data on rheumatoid hip disease is reasonable. If not, caution the subject, particularly in respect of articular should be exercised in making this diagnosis, based cartilage. Many questions remain unanswered. If on protrusio acetabuli alone. Alexander (1965) has osteoarthrosis is an aging process, why has ageproposed that primary protrusio in adults, progress- correlated change not been demonstrated in noning as it may to osteoarthrosis, can result from stress articular hyaline cartilage ? Why is involvement of the during the adolescent growth spurt. A subsequent hip, knee and terminal interphalangeal joints of the failure in pelvic remodelling, leading to protrusio, fingers so common, yet involvement of the ankle correlates with the female sex predominance, coxa and wrist relatively rare ? vara and premature epiphyseal fusion. To the general radiologist, osteoarthrosis of the Severe destructive change in the hips, often with hip is a frequent finding during routine film reportradiological features of aseptic necrosis, may follow ing. Most patients with the condition show changes therapy with corticosteroids (Sweetnam et al., which are advanced on presentation. X-ray examina1960). It is rare for a patient with significant tion may reveal reduction of the joint (or cartilage) degenerative hip disease, to escape treatment with space, sclerosis of subarticular bone (eburnation) either phenylbutazone or indomethacin. In a on both sides of the joint, and subarticular cystic minority of those so treated, the accelerated progress change. Perhaps the outstanding feature which may of a destructive arthropathy suggests that the drug lead the radiologist to diagnose degenerative change regime may be implicated (Arora, 1968; Allen and is the marginal osteophyte. However, Danielsson (1964), in a study of 86 patients where the diagnosis Murray, 1971). These various starting points might suggest that of osteoarthrosis was made solely on the presence of osteoarthrosis is due to a mixture of inherited and osteophytes, showed over the next 11 years only one environmental factors (Kellgren, 1961). Alter- patient who produced joint space narrowing. The natively, a final common pathway may exist in what remaining 85 patients exhibited no progressive is most probably a multifactorial disease. However, radiological change. On this evidence and that of the so little is known about the detailed pathogenesis that pathologists, one is forced to agree that the earliest these alternatives must remain unresolved. Most definable stage of progressive osteoarthrosis is pathologists seem to be in no doubt that osteo- narrowing of the joint space. But early loss of arthrosis begins in the cartilage, although the nature articular cartilage is often patchy or focal, and this of the process is obscure. It is claimed that the usually precludes its radiographic demonstration. earliest finding is a characteristic splitting and The width of the normal joint space varies from one fragmentation (fibrillation) of the articular cartilage. subject to another, although in unilateral disease the Byers et al. (1970, 1976a, b) have produced evidence width can be compared with the other hip, if that is from a study of cadaveric hips, which indicates that, presumed to be normal. The unequivocal diagnosis in this joint, two classes of process affect the of narrowing requires a reduction by at least onecartilage: (a) commonly occurring changes of third in the width of the joint space (Gofton, 1971). limited progression not leading to deformity of the The hip, being a ball and socket joint, presents a joint, and (b) less common progressive changes con- further problem because focal loss of articular sistent with a disease process. In any event a cartilage nearly always occurs in the antero-superior destructive process leads to thinning of the cartilage quadrant, and in the earlier stages will only be layer, and eventually to focal exposure of sub- shown in tangential (preferably weight-bearing) chondral bone. Whether such tissue response is due views. It therefore seems unlikely that the radito fatigue failure of the collagen network (Freeman, ologist will be able to diagnose the early changes in 1975), when abnormal structural relationships could articular cartilage observed by the pathologist. be implicated, to primary failure of the chondrocyte Where does the radiologist now stand in the {British Medical Journal, 1976), or to some other diagnosis of osteoarthrosis? He is unable to recogmechanism is unknown. Hypotheses abound nize the early disease, often unable to predict the (Kempson et al., 1975), including that the disease symptomatic patient, but able to identify various originates in bone or as a failure in joint lubrication. patterns of joint disease (Gofton, 1971; Jeffrey, The proposition that osteoarthrosis is an arthropathy 1975), the significance of which is not always clear. associated with the aging process has tended, in the More recently, attempts have been made to prove past, to deter investigation into its aetiology. In that osteoarthrosis is always a secondary disorder 82
FEBRUARY 1977
Radiology now. Osteoarthrosis of the hip: one disease or many} (Stulberg et al, 1975; Solomon, 1976). Solomon claimed that a predisposing abnormality was apparent in all but 27 of 327 patients with degenerative disease of the hip. Such correlation in excess of 90% is not within the experience of most practising skeletal radiologists, and leaves little room for the inclusion of other possible causes, such as disparity in leg length (Gofton, 1971). We must continue to observe critically the films of our patients with degenerative hip disease. All osteoarthrosis may be secondary, but proof will not come from subjective radiological impressions, but by future correlation of accurately observed diagnostic signs from clinical, radiological and pathological sources.
GOFTON, J. P., 1971. Studies in osteoarthritis of the hip: Part I Classification. Canadian Medical Association Journal, 104, 679-683. GOODFELLOW, J. W., and O'CONNOR, J., 1975. The trans-
mission of loads through the hips and knee: a hypothesis on the aetiology of osteoarthritis. Journal of Bone and Joint Surgery, 57B, 400. HARRISON, M. H. M., SCHAJOWICZ, F., and TRUETA, J.,
1953. Osteoarthritis of the hip: a study of the nature and evolution of the disease. Journal of Bone and Joint Surgery, 35B, 598-626. JEFFREY, A. K., 1975. Osteophytes and the osteoarthritic femoral head. Journal of Bone and Joint Surgery, 57B, 314-324. KELLGREN, J. H., 1961. Osteoarthrosis in patients and populations. British Medical Journal, 2,1-6. KEMPSON, G. E., MAROUDAS, A., and WEIGHTMAN, B., 1975.
(Editors) Conference on Articular Cartilage 1974. Annals of the Rheumatic Diseases, 34, Supplement No. 2, pp. 120-133.
DENNIS J. STOKER
MEACHIM, G., HARDING, K., and WILLIAMS, D. R., 1972.
Methods for correlating pathological and radiological findings in osteoarthrosis of the hip. British Journal of pathies. In Proceedings of the European Association of Radiology, 45, 670-676. Radiology, Amsterdam 1971. Pp. 204-210 (Excerpta MURRAY, R. O., 1965. The aetiology of primary osteoarthritis of the hip. British Journal of Radiology, 38, 810Medica, Amsterdam). 824. ALEXANDER, C , 1965. The aetiology of primary protrusio MURRAY, R. O., and DUNCAN, C , 1971. Athletic activity in acetabuli. British Journal of Radiology, 38, 567-580. adolesence as an aetiological factor in degenerative hip ARORA, J. S., 1968. Indomethacin arthropathy of the hips. disease. Journal of Bone and Joint Surgery, 53B, 406-419. Proceedings of the Royal Society of Medicine, 61, 669. MURRAY, R. O., and JACOBSON, H. G., 1971. The Radiology 1976. Leading article, British Medical Journal, 2, 4—5. of Skeletal Disorders, p. 645 (Churchill Livingstone, BULLOUGH, P., GOODFELLOW, J., and O'CONNOR, J., 1973. Edinburgh & London). The relationship between degenerative changes and loadbearing in the human hip. Journal of Bone and Joint RESNICK, D., 1976. The "tilt deformity" of the femoral head in osteoarthritis of the hip: a poor indicator of previous Surgery, 55B, 746-758. epiphysiolysis. Clinical Radiology, 27, 355—363. BYERS, P. D., CONTEPOMI, C. A., and FARKAS, T. A., 1970. A post-mortem study of the hip joint. Annals of the SOLOMON, L., 1976. Patterns of osteoarthritis of the hip. Journal of Bone and Joint Surgery, 58B, 176-183. Rheumatic Diseases, 29, 15-31. 1976a. Post-mortem study of the hip joint II. Histo- STULBERG, S. D., CORDELL, L. D., HARRIS, W. H., RAMSEY, P. L., and MACEWEN, G. D., 1975. Unrecognised childlogical basis for limited and progressive cartilage alterahood hip disease; a major cause of idiopathic osteotions. Annals of the Rheumatic Diseases, 35, 114—121. arthritis of the hip. In The Hip, Proceedings of the 3rd 1976b. Post-mortem study of the hip joint III. Coropen scientific meeting of the Hip Society (C. V. Mosby relations between observations. Annals of the Rheumatic Co.), 212-228. Diseases, 35,122-126. DANIELSSON, L. G., 1964. Incidence and prognosis of SWEETNAM, D. R., MASON, R. M., and MURRAY, R. O., 1960. Steroid arthropathy of the hip. British Medical coxarthrosis. Ada Orthopaedica Scandinavica SuppleJournal, 7,1392-1394. ment, 66,1. FREEMAN, M. A. R., 1975. The fatigue of cartilage in the SZE, T. S., 1963. In The Epidemiology of Chronic Rheumapathogenesis of osteoarthrosis. Acta Orthopaedica tism, 1, pp. 1-11. Edited by J. H. Kellgren (Blackwell Scandinavica, 46, 323-328. Scientific Publications, Oxford). REFERENCES
ALLEN, E. H., and MURRAY, R. O., 1971. Iatrogenic arthro-
83
