Bone mass and metabolism in patients with myastenia gravis: a possible anabolic role for pyridostigmine on bone tissue

Myasthenia gravis (MG) is a neuromuscular junction disease which has been previously associated to an increased risk of falls and glucocorticoid-induced osteoporosis. Recently, oral glucocorticoids, drugs often prescribed in MG subjects, have been reported not to increase the risk of fractures as in general population; and as an explanation it has been suggested that pyridostigmine, a cornerstone in the treatment of MG, may have an anabolic effect on bone. MG is caused by circulating antibodies that block the postsynaptic cholinergic receptor (AChR) or proteins MuSK (muscle-specific tyrosine kinases). MuSK related MG patients do not receive pyridostigmine. Aim of our research was to investigate the bone involvement in AChR and MuSK related MG. We measured bone mineral density by DXA scan, bone remodeling markers (i.e. serum CTX, osteocalcin, alkaline phosphatase) and markers of bone and mineral metabolism (i.e. calcium, phosphorus, vitamin D, PTH) in 24 AChR related MG patients, exposed to a prolonged steroids and pyridostigmine treatment, and in 16 MuSK related MG patients exposed only to steroids treatment. We have found that a reduction of bone mineral density was more evident in patients affected by MuSK related MG, compared to those affected by AChR related MG patients, the former exhibiting an unbalanced bone turn-over with a reduction in bone formation coexisting with an increase in bone resorption markers. These preliminary data could account for a different fracture risk in relation to the type of MG and may suggest a screening program for bone fragility especially in anti Musk related MG.