OBJECTIVE: To investigate muscle tissue in patients with polymyalgia rheumatica (PMR). METHODS: Deltoid muscle biopsies obtained from 10 female patients with PMR before corticosteroid therapy and from 5 healthy female controls of similar age were studied using light microscopy. Serial cryosections were stained for the activity of myofibrillar ATPases at various pH and for oxidative and glycolytic enzymes. Sections were also incubated with antibodies against different myosin heavy chain (MyHC) isoforms, and the laminin alpha1 chain, identifying capillaries and cell borders, and against ligands for selected adhesion molecules. RESULTS: The muscle fibers in patients and controls were mainly of type I containing slow MyHC, or type II AB containing both fast A and fast B MyHC isoforms. The oxidative capacity of the muscle fibers was in general low. In the patients with PMR the numbers of capillaries per unit area of type I and type II fibers were higher than in controls (p = 0.05 and p < 0.5, respectively). No accumulation of inflammatory cells or increased expression of adhesion molecules in the muscle sections from patients with PMR was found. CONCLUSION: There is increased microvascularization of the deltoid muscle fibers in patients with PMR. Whether this is directly associated with the systemic inflammation and the musculoskeletal symptoms or is mainly due to muscle fiber atrophy could not be determined.
OBJECTIVE: To investigate muscle tissue in patients with polymyalgia rheumatica (PMR). METHODS: Deltoid muscle biopsies obtained from 10 female patients with PMR before corticosteroid therapy and from 5 healthy female controls of similar age were studied using light microscopy. Serial cryosections were stained for the activity of myofibrillar ATPases at various pH and for oxidative and glycolytic enzymes. Sections were also incubated with antibodies against different myosin heavy chain (MyHC) isoforms, and the laminin alpha1 chain, identifying capillaries and cell borders, and against ligands for selected adhesion molecules. RESULTS: The muscle fibers in patients and controls were mainly of type I containing slow MyHC, or type II AB containing both fast A and fast B MyHC isoforms. The oxidative capacity of the muscle fibers was in general low. In the patients with PMR the numbers of capillaries per unit area of type I and type II fibers were higher than in controls (p = 0.05 and p < 0.5, respectively). No accumulation of inflammatory cells or increased expression of adhesion molecules in the muscle sections from patients with PMR was found. CONCLUSION: There is increased microvascularization of the deltoid muscle fibers in patients with PMR. Whether this is directly associated with the systemic inflammation and the musculoskeletal symptoms or is mainly due to muscle fiber atrophy could not be determined.