Osteoporosis in Light of a New Mechanism Theory of Delayed Onset Muscle Soreness and Non-Contact Anterior Cruciate Ligament Injury

Osteoporosis is a disorder, with a largely unknown pathomechanism, that is often marked as a silent thief, because it usually only becomes undisguised when fractures occur. This implies that the pathological damage occurs earlier than the sensation of pain. The current authors put forward a non-contact injury model in which the chronic overloading of an earlier autologously microinjured Piezo2 ion channel of the spinal proprioceptor terminals could lead the way to re-injury and earlier aging in a dose-limiting and threshold-driven way. As a result, the aging process could eventually lead the way to the metabolic imbalance of primary osteoporosis in a quad-phasic non-contact injury pathway. Furthermore, it is emphasised that delayed onset muscle soreness, non-contact anterior cruciate injury and osteoporosis could have the same initiating proprioceptive non-contact Piezo2 channelopathy, at different locations, however, with different environmental risk factors and a different genetic predisposition, therefore producing different outcomes longitudinally. The current injury model does not intend to challenge any running pathogenic theories or findings, but rather to highlight a principal injury mechanism.

Automated summary

Osteoporosis is a disorder with an unknown pathomechanism, which may result from chronic overloading of the Piezo2 ion channel, leading to re-injury and early aging. The study suggests that delayed muscle soreness, non-contact anterior cruciate injury, and osteoporosis could share a common mechanism involving the Piezo2 channelopathy, but with different outcomes due to environmental factors and genetic predisposition.