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

Abstract

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.

Delayed Onset Muscle Soreness and Critical Neural Microdamage-Derived Neuroinflammation

“…As a result of the primary noncontact microdamage, a secondary injury phase could succeed in the form of harsher tissue damage [ 8 , 53 ]. This more pervasive tissue damage in DOMS is due to the primary impairment of proprioceptive protection, as we could experience in other noncontact injuries [ 8 , 31 , 53 , 57 , 85 ]. The pivotal involvement of other sensory neurons, such as nociceptive neurons [ 24 ], and other ion channels, e.g., TRPV1 and TRPV4 [ 25 ], could occur in this stage of the noncontact pathophysiology of DOMS [ 8 ].…”

Psoriasis, Is It a Microdamage of Our “Sixth Sense”? A Neurocentric View

“…Fernández-Trillo et al also proposed that Piezo2-containing neurons are key and may have different genetic signatures [ 48 ]. Indeed, recent papers addressing Piezo2 microinjury suggest that it could be a principal gateway to pathology [ 14 , 15 , 18 , 30 , 33 , 49 ]. The tertiary injury phase in DOMS is called the repeated bout effect, and is basically the re-injury of the initiating primary sensory terminal microdamage by the same repetitive forced lengthening contractions under an acute stress response [ 15 ].…”

“…The tertiary injury phase in DOMS is called the repeated bout effect, and is basically the re-injury of the initiating primary sensory terminal microdamage by the same repetitive forced lengthening contractions under an acute stress response [ 15 ]. Repetitive re-injury of these non-contact injuries could evolve into chronic conditions or to ganglionopathy associated with genetic predisposition or environmental risk factors, as suggested in osteoarthritis (OA), post-orgasmic illness syndrome (POIS), dry eye disease (DED), and osteoporosis [ 15 , 30 , 33 , 49 ]. This concept has already been hypothesized, in the association of repetitive microdamage and mechanical stress with the triggering of lesions in psoriatic arthritis [ 50 , 51 , 52 , 53 ].…”

“…This concept has already been hypothesized, in the association of repetitive microdamage and mechanical stress with the triggering of lesions in psoriatic arthritis [ 50 , 51 , 52 , 53 ]. Finally, the quadric phase of the injury mechanism is suggested to be the aging process and the associated inflammaging (see Table 1 ) [ 33 , 49 , 54 ].…”

“…An important clinical observation is that psoriasis frequently manifests in locations where the skin is rubbed and undergoes strong repetitive mechanical, such as the elbows, knees, and the scalp [ 55 ]; indeed, shear stress could be relevant in the proposed somatosensory microdamage [ 14 , 30 , 33 , 49 ]. In addition, it has been suggested that mechanical stretch might be a factor in the pathogenesis of psoriasis [ 55 , 56 ].…”