Does Compression Sensory Axonopathy in the Proximal Tibia Contribute to Noncontact Anterior Cruciate Ligament Injury in a Causative Way?—A New Theory for the Injury Mechanism

Abstract

Anterior cruciate ligament injury occurs when the ligament fibers are stretched, partially torn, or completely torn. The authors propose a new injury mechanism for non-contact anterior cruciate ligament injury of the knee. Accordingly, non-contact anterior cruciate ligament injury could not happen without the acute compression microinjury of the entrapped peripheral proprioceptive sensory axons of the proximal tibia. This would occur under an acute stress response when concomitant microcracks-fractures in the proximal tibia evolve due to the same excessive and repetitive compression forces. The primary damage may occur during eccentric contractions of the acceleration and deceleration moments of strenuous or unaccustomed fatiguing exercise bouts. This primary damage is suggested to be an acute compression/crush axonopathy of the proprioceptive sensory neurons in the proximal tibia. As a result, impaired proprioception could lead to injury of the anterior cruciate ligament as a secondary damage, which is suggested to occur during the deceleration phase. Elevated prostaglandin E2, nitric oxide and glutamate may have a critical neuro-modulatory role in the damage signaling in this dichotomous neuronal injury hypothesis that could lead to mechano-energetic failure, lesion and a cascade of inflammatory events. The presynaptic modulation of the primary sensory axons by the fatigued and microdamaged proprioceptive sensory fibers in the proximal tibia induces the activation of N-methyl-D-aspartate receptors in the dorsal horn of the spinal cord, through a process that could have long term relevance due to its contribution to synaptic plasticity. Luteinizing hormone, through interleukin-1β, stimulates the nerve growth factor-tropomyosin receptor kinase A axis in the ovarian cells and promotes tropomyosin receptor kinase A and nerve growth factor gene expression and prostaglandin E2 release. This luteinizing hormone induced mechanism could further elevate prostaglandin E2 in excess of the levels generated by osteocytes, due to mechanical stress during strenuous athletic moments in the pre-ovulatory phase. This may explain why non-contact anterior cruciate ligament injury is at least three-times more prevalent among female athletes.

Post Orgasmic Illness Syndrome (POIS) and Delayed Onset Muscle Soreness (DOMS): Do They Have Anything in Common?

“…Activated N-methyl-D-aspartate receptors (NMDAR) on the spinal dorsal horn are suggested to be the gate controllers of this second-messenger pathway on the central terminals of these pseudounipolar proprioceptive sensory neurons [23]. The compensatory effect could be exaggerated contractions due to dendritic persistent inward sodium current (NaPIC) inducement on motoneurons [23,25].…”

“…There are proprioception receptors in the penis and deeper layers of the skin [32][33][34]. Skin and bone nerves are involved in, or theorized to contribute to, the stretch reflex in accordance with Hilton's law [12,25,35]. Therefore, superposition of compression forces of eccentric contractions could also cause potential microdamage to these dermal somatosensory nerves with the same consequences, as is hypothesized in the muscle spindle of the bulbospongiosus and ischiocavernosus muscles.…”

Finishing stationary cycling too early after anterior cruciate ligament reconstruction is likely to lead to higher failure

“…Non-contact ACL injury, involving around 80% of ACL injuries [ 1 , 6 – 11 ], is theorized to be a result of an acute proprioceptive axon terminal mechano-energetic microdamage in the proximal tibia in unaccustomed or strenuous eccentric exercise moments [ 5 ]. This peripheral proprioceptive neuronal microlesion could evolve into a bi-phasic injury mechanism, where the primary proprioceptive impairment could result in a secondary harsher tissue injury and that is when the ACL injury could also prevail [ 5 ]. The primary injury is theorized to be caused by the acute compression microlesion of the proprioceptive sensory terminals at the proximal tibia [ 5 ].…”

“…This peripheral proprioceptive neuronal microlesion could evolve into a bi-phasic injury mechanism, where the primary proprioceptive impairment could result in a secondary harsher tissue injury and that is when the ACL injury could also prevail [ 5 ]. The primary injury is theorized to be caused by the acute compression microlesion of the proprioceptive sensory terminals at the proximal tibia [ 5 ]. Part of the hypothesis that these sensory nerves contribute to the stretch reflex at the spinal dorsal horn [ 5 ].…”

“…Noteworthy, there has been even an estimate that an ACL rupture is accelerating the aging of the knee by 30 years [ 3 ]. New theories [ 4 , 5 ] could provide novel perspective how to fill in a supplemental puzzle piece in rehabilitation practices after ACLR.…”