Superolateral Hoffa's Fat Pad Edema and Trochlear Sulcal Angle Are Associated With Isolated Medial Patellofemoral Compartment Osteoarthritis.

PURPOSE: To evaluate whether mediopatellar plica and knee morphometric measurements obtained from magnetic resonance imaging (MRI) studies are associated with isolated medial patellofemoral osteoarthritis in young adults. METHODS: MRI studies from 60 patients with isolated medial patellofemoral osteoarthritis and 90 control patients with normal knee MRI studies were reviewed. The presence of mediopatellar plica, the presence of edema in the superolateral aspect of Hoffa's fat pad and suprapatellar fat pad, quadriceps and patellar tendinosis, and axial and sagittal alignment of the patellar and trochlear morphology were assessed using MRI. The relationship between mediopatellar plica, alignment, or morphology and the presence of isolated medial patellofemoral osteoarthritis was evaluated using logistic regression. RESULTS: Superolateral Hoffa's fat pad edema (odds ratio [OR] = 3.4, P = .009) and decreased trochlear sulcal angle (OR = 0.95, P = .045) were associated with increased odds of isolated medial patellofemoral osteoarthritis. Decreased lateral patellar tilt (OR = 0.93, P = .087) and patellar tendinosis (OR = 4.13, P = .103) trended toward being associated with increased odds of isolated medial patellofemoral osteoarthritis but were not statistically significant. No significant association was seen between the presence of mediopatellar plica and medial patellofemoral osteoarthritis (OR = 0.95, P = .353). CONCLUSIONS: Medial patellofemoral osteoarthritis is associated with trochlear morphology and patellar alignment but not with mediopatellar plica.

Quickly progressive amyotrophy of the thigh: An unusual cause of rapid chondrolysis of the knee.

While rapidly destructive OA is more recognized in hip, we report the case of a 50-year-old woman who presented a rapid chondrolysis in the patellofemoral joint in a context of rapid loss of muscular strength. She had arthralgia, myalgia and proximal muscular deficit of the limbs. Creatine phospho kinase level was elevated and electromyogram exam showed a myogenic syndrome. Neither immune nor visceral disease was highlighted. As we suspected a polymyositis, we started corticosteroids and physiotherapy, then methotrexate and intravenous immunoglobulin. Concomitantly to the worsening of the muscular deficit and atrophy of hamstrings, she developed a persistent and disabling knee pain. Initial radiographs and magnetic resonance imaging (MRI) showed only a patellofemoral dysplasia and tiny cartilage damages. Because of aggravation of myalgia, we treated by mycophenolate mofetyl then rituximab. One year later, the knee remained painful and swollen. MRI showed signs of advanced osteoarthritis including an important loss of cartilage with an atrophy of hamstrings. Several articular corticosteroids injections were done. In the same time, the evolution of the muscular disease was unusual. Another histological analysis of muscle has highlighted a genetic myopathy due to mutation of calpain. Immunosuppressive treatments were stopped and a total joint replacement was performed. We show for the first time a case of rapid chondrolysis of patellofemoral joint related to a severe genetic myopathy.