LETTERS 815

1. Levy RN, Hermann G . Haimov M, Sherry HS, Train JS, Davi- son S: Rheumatoid synovial cyst of the hip. Arthritis Rheum 25:1382-1384, 1982

2. Steinbrocker 0, Traeger CH. Batterman RC: Therapeutic criteria in rheumatoid arthritis. JAMA 140:659-662, 1949

3. Penkeva RR: Iliopsoas bursitis demonstrated by computed to- mography. Am J Radio1 135: 175-176, 1980

Rehabilitation of severe hip damage in juvenile arthritis

To the Editor: We read with interest Dr. Jacobs’ letter ( I ) . He was

concerned about our treatment of hip damage in children with juvenile arthritis (JA) (2). Unfortunately, Dr. Jacobs seems to have misunderstood our paper. In none of our patients did severe hip damage follow our program of bed rest, skin traction, and active exercises. On the contrary, those treatment modalities were prescribed after severe changes had already occurred and patients were almost unable to walk. As soon as pain and flexion contractures improved, the patients were encouraged to restart aided ambulation. This approach to the management of hip damage is a recognized treatment program in well-known centers with vast experience in the care of children with chronic arthritis (3,4).

There is no doubt that prolonged bed rest is not an acceptable treatment and that maintenance of weight bearing is the primary goal, no matter how severe the disease. However, weight bearing should be restricted when flexion and adduction deformities are present. In cases such as those reported by us, these contractures should be corrected before restarting ambulation. The knowledge of these basic principles of rehabilitation, well understood by rheumatolo- gists, should be extended to all physicians engaged in the treatment of juvenile chronic arthritis.

Remodeling of the hip joint in JA is indeed an interesting phenomenon; we wish we could say more than that.

Osvaldo Garcia-Morteo, MD Jose A. Maldonado-Cocco, MD Instituto Nacionnl de Rehnhilitncibn Buenos Aires, Argentina

Jacobs JC: Treatment of hip damage in children with juvenile rheumatoid arthritis (letter). Arthritis Rheum 25: 1269, 1982 Garcia-Morteo 0, Babini JC, Maldonado-Cocco JA, Gagliardi S, Yabkowski J: Remodeling of the hip joint in juvenile rheumatoid arthritis. Arthritis Rheum 24: 1570-1574, 1981 Swann M: Managemedt of lower limb deformities, Surgical Management of Juvenile Chronic Polyarthritis. Edited by GP Arden, BM Ansell. London, Academic Press, 1978, pp 96-1 11 Ansell BM: Rehabilitation in juvenile chronic arthritis, Clinics in Rheumatic Diseases. Edited by D Woolf. London, W.B. Saunders Co., 1981, pp 476-478

Control of susceptibility of F344 rats to adjuvant arthritis: an alternative interpretation

To the Editor: Battisto and colleagues recently reported that sus-

ceptibility to adjuvant arthritis in DA and Fisher 344 (F344) rats is controlled by an autosomal dominant gene linked to the major histocompatibility complex (MHC) (1). Their claim is based in part on the observation that 14 convention- ally reared 3- to 4-month-old F344 rats uniformly failed to develop arthritis after a standard dose of Mycobncterium- containing adjuvant. However, other investigators have pre- viously found F344 rats to be susceptible to adjuvant arthri- tis (2). We propose an interpretation of Battisto’s data that is consistent with previous work by others.

Kohashi et al have demonstrated that the microbial environment has a drastic effect on the susceptibility of F344 rats to adjuvant arthritis (3). In their study, germ-free F344 rats had a 100% incidence of severe adjuvant arthritis after a standard dose of adjuvant; in contrast, conventionally housed F344 rats had a very low incidence of mild arthritis.

A suppressive effect of microbial infection on the development of adjuvant arthritis is not restricted to strains, such as F344, thought to have low susceptibility to adjuvant arthritis. We have recently found that intranasal inoculation of 4-week-old Lewis rats with viable Mycoplnsma pirimonis completely prevented the subsequent development of arthri- tis, following adjuvant injection at age 7 weeks, in all I I rats studied. Lewis rats are ordinarily highly susceptible to induction of adjuvant arthritis. M pitlrnonis is enzootic in conventional rat colonies, and is commonly transmitted via the respiratory tract (4). Other pathogens may have similar suppressive effects.

We propose that the results reported by Battisto and colleagues indicate an MHC-linked recessive immune sup- pression gene controlling the response to one or more as yet unidentified microbial antigens, rather than a true adjuvant arthritis susceptibility gene. The reason one-third of their RTI‘ homozygous F2 animals developed arthritis is much more likely t o have been variation in environmental factors such as infections, and/or contributions of other genes, than recombination events between the MHC and a postulated Ar gene.

Joel D. Taurog, MD Steven L. Leary, DVM University of Minnesota Minneapolis, MN

I . Battisto JR, Smith RN, Beckman K. Sternlicht M, Welles WL: Susceptibility to adjuvant arthritis in DA and F344 rats: a dominant trait controlled by an autosomal gene locus linked to the major histocompatibility complex. Arthritis Rheum 25: 1194- 1200, 1982

2. Kourounakis L, Kapusta M, Young-Rodenchuk M: Restoration of diminished splenic responses to phytohemagglutinin and con-