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.
