CHONDROMALACIA PATELLAE

813 CHONDROMALACIA PATELLAE

SIR,-Your March over a

editorial, despite providing a rapid gallop rather uncertain field, does little to answer some of the

pressure.6 The cartilage lesion of chondromalacia probably results from a shearing force. Ultrastructurally, cartilage can be divided into zones7 containing collagen fibres arranged in different ways. This arrangement must create significant stresses at junctions between zones and at the interface between cartilage and subchondral bone. The continual gliding movement of patella on femur will result in shearing at any of these interfaces, particularly if trauma is superimposed upon normal patellofemoral movements. I am wary of doing bony procedures on adolescents who have not stopped growing. Success rates of over 6507o are very rare and

usually confined to small

series. Few orthopaedic surgeons would obtain results better than 5007o and would normally inform expect the patient of such odds before beginning any treatment at all. Attractive though a primary patellectomy may sound, one should not forget that there is much evidence to show that the loss of a patella will significantly decrease the mechanical efficiency of the knee.8-10 There is a place for patellectomy in chondromalacia, but as a last resort rather than the initial blow. The development of chondromalacia patellae is not always more so idiopathic. Trauma is a well-recognised cause-nowhere than in Pinal’s amusing paper, Genu Amoris. 11l to

Mayor Treloar Hospital,

Alton, Hants

R. N. VILLAR

RE The etiology of chondromalacia patellae. -7 Bone Jomt Surg 196 1; 43B: 752-57 2 Ftcat P, Hungerford DS Disorders of the patellofemoral joint. Baltimore: Williams and Wilkins, 1977. 3. Dehaven KE, Dolan WA, Mayer PJ. Chondromalacia patellae and the painful knee. Am Fam Phys 1980; 21: 117-24. 4. Kelly L Jr Chondromalacia patellae. J Med Soc NJ 1974; 71: 319-20. 5 Meachim G, Emery IH Quantitative aspects of patellofemoral cartilage fibrillation in Liverpool necropsies. Ann Rheum Dis 1974; 33: 39-47. 6 Waisbrod H, Treiman N Intraosseous venography in patellofemoral disorders: a J Bone Jomt Surg 1980; 62B: 454-56. preliminary report. 7 Weiss C, Rosenburg L, Helfet AJ. An ultrastructural study of normal young adult human articular cartilage. J Bone Jomt Surg 1968; 50A: 663-74 8 Hemeck AP. The modern operative treatment of fractures of the patella. Surg Gynecol Obsiet 1909; 9: 177-248. 9 SmUlie IS. Dtseases ofthe knee joint, 2nd ed. Edinburgh: Churchtll Livingstone, 1980. 10. DePalma AF, Sawyer B, Hoffman JD. Reconsideration of lesions affecting the patellofemoral joint. Clin Orthop 1960; 18: 63-85. II. Pinals RS Genu amons. Arthrztzs Rheum 1976, 19: 637-38.

Outerbndge

1

BONE SETTERS

9

dominant questions that surround the complex condition of chondromalacia patellae. "Chondromalacia patellae" is exactly what it says-ie, softening of patellar cartilage. Though in days past it was a diagnosis made on purely clinical grounds, now, in the era of the arthroscope, it should only be diagnosed after inspection of the retropatellar surface. Treatment can then be given according to the degree of patellar (and femoral) involvement. 1,2 The traditional concept of chondromalacia as a condition of overweight adolescent females with knock-knees is outdated. Any military surgeon will tell you that 10% or more of an average military orthopaedic outpatient session involves young men with patellofemoral pain who, if arthroscopy were done, would all have chondromalacia. Either the Services are dealing with a totally different disease entity or chondromalacia patellae is not as biased towards the fair sex as you would have us believe. 3,4 There is no relation between the degree of cartilage destruction and the pain. A patient with crippling patellofemoral pain may, on arthroscopy, show no retropatellar cartilage changes. Such findings have given rise to the opinion that the cartilage change of chondromalacia is a normal part of ageing5and that the pain must therefore arise for other reasons, such as increased intraosseous

Lord

GAS GANGRENE AFTER LIMB FRACTURES TREATED BY TRADITIONAL

TRADITIONAL BONE SETTERS AND GAS GANGRENE

SIR,-Your editorial (Nov 13, p 851) highlighted the severity of problem of gas gangrene, especially in developing countries.

the

Many types of injury and other predisposing factors to gas gangrene were discussed. While improvement in sanitation and in the care of

wounds has resulted in fewer cases of gas gangrene being seen in many hospitals, a major worrying predisposing factor in Nigeria (and, probably, other developing countries) is the mismanagement of limb fractures by traditional bone setters. Between November, 1983, and November 1984, we treated four cases of fast-spreading gas gangrene by limb amputation and antibiotics (table). All four patients had had simple fractures which had been splinted with "bamboo mats" by different traditional bone setters, a procedure that led to ischaemia of the limb and gas gangrene. Patient 3 died of uncontrollable toxaemia postoperatively. Facilities for conservative management of gas gangrene in developing countries are limited and we tend to operate early if gangrene seems to be spreading despite high-dose penicillin injections. Attempts are being made to embark on a health education

campaign. Nigerian Army Reference Hospital, Department of Surgery, Kaduna, Nigeria

J. BRUME E. O. IJAGHA

TRANSGLUTAMINASE: CO-FACTOR IN AETIOLOGY OF AIDS? groups at risk of acquired the number of haemophiliacs with clinical manifestations of AIDS is small. However, the incidence rate is high (3’ 6 cases per 1000 patients with haemophilia A in the United States and 0-66 per 1000 haemophilia B patients 1 ); and the case fatality rate for AIDS in haemophilia has been higher (58%) than that in all AIDS patients (48%).Furthermore many as yet symptom-free heterosexual haemophiliacs have evidence of immunological dysfunction comparable with that seen in clinical AIDS.3 However, despite evidence that human T-lymphotropic virus type III (HTLV-III) is the cause of AIDS, antibodies to HTLV-III may be found at very high frequencies in symptomless heterosexual haemophiliacs, especially in those who have received factor VIII concentrates and have altered immune function. These observations, together with the occurrence of immune dysfunction in haemophiliacs treated with factor VIII or IX prepared from donors from countries where AIDS is still rare and the absence of Kaposi’s sarcoma in haemophilia-associated AIDS, are consistent with the view that the pathogenesis of AIDS involves something other than infection with HTLV-III. Association is not proof of cause, and agents such as HTLV-III may turn out to be passengers on an already sinking ship. It would be reasonable to postulate some other transmissible agent, even a non-infectious one, which contributes to the immune dysfunction and possibly predisposes to opportunistic infections. ElsewhereIhave suggested that access of immunocompetent cells to the allogeneic enzyme transglutaminase that is abundant in seminal plasma and present in anti-haemophilic factor(s) is a possible common denominator responsible for immunosuppression in homosexuals and in haemophiliacs. The secretions of male accessory sexual glands’ and human seminal plasma6,7 are immunosuppressive. There is in-vitro and in-vivo evidence for an association between anti-haemophilic factors such as lyophilised factor VIII concentrate and the immunological aberrations found in symptomless heterosexual haemophiliacs. Furthermore, the lymphadenopathyfever syndrome, thought to represent the early clinical manifestations of AIDS, has been observed in recipients of factor VIII or IX concentrates.8,9

SIR,-Relative

to

other

immunodeficiency syndrome