Posterior tibial tendon dysfunction: its association with seronegative inflammatory disease.
Idiopathic inflammation and rupture of the posterior tibial tendon (PTT) has received much attention in the recent literature. In this report of the presentation of PTT dysfunction as a manifestation of seronegative inflammatory disease, we describe the clinical and laboratory features of 76 patients with inflammation and/or rupture of the PTT. Analysis of all patients identified two discrete groups. Group A patients were younger (mean age 39 years) and had multiple manifestations of inflammation at other sites of ligament and tendon attachments (enthesopathy). Other features of a systemic inflammatory disorder such as oral ulcers, conjunctivitis, colitis, and especially psoriasis were common in the latter patients and their families. Group B consisted predominantly of elderly patients (mean age 64 years) with isolated dysfunction of the PTT. These two groups differed widely in the manner of clinical presentation, demographic data, family history, HLA data, and surgical pathology. These distinctions suggest different pathogeneses for posterior tibial tendinitis. Group A demonstrated local manifestations of a systemic inflammatory disease, whereas group B exhibited the effects of mechanical trauma and degeneration.
Myerson
M
M
Union Memorial Hospital, Department of Orthopaedics, Baltimore, MD 21218.
Solomon
G
G
Shereff
M
M
D000293:Adolescent; D000328:Adult; D000368:Aged; D001168:Arthritis / Q000150:complications / Q000276:immunology; D005260:Female; D006680:HLA Antigens / Q000032:analysis; D006801:Humans; D007249:Inflammation; D007866:Leg; D008297:Male; D008875:Middle Aged; D012421:Rupture; D012422:Rupture, Spontaneous; D013708:Tendon Injuries / Q000209:etiology*; D013710:Tendons / Q000503:physiopathology*; D013717:Tenosynovitis / Q000209:etiology* / Q000276:immunology
D006680:HLA Antigens