Inferior alveolar nerve injury resulting from different implant rotary instruments: An ex vivo comparative study in human cadaveric mandibles.

The present study aimed to evaluate the degree of nerve injury on inferior alveolar nerve (IAN) by different implant drills resulting from direct canal intrusion into inferior alveolar canal (IAC). A cadaveric study involving 7 human mandibles was performed to evaluate mechanical injury of canal enclosed IAN resulting from different drills. In group 1, osteotomies were created using different drills with 1 mm of intracanal intrusion, simulating accidental drill intrusion into canal. In group 2, drilling was stopped when the tip has breached into IAC, limited by tactile feedback of operator. The depth and width of nerve defects were assessed using optical coherence tomography. A significant difference in defect depth was found (p < 0.001) in group 1. A sinus lift reamer inflicted the least damage (0.068 ± 0.022 mm). It was also found that the mean defect depth was significantly different when a twist drill was used (p = 0.016). Sinus lift reamer can be used safely for osteotomy preparation in mandible when bone height is limited or when radiographic visualization of canal is poor. Bone corticalization around IAC does not provide adequate protection for IAN in the event of accidental intracanal intrusion.

Inferior alveolar nerve transection disturbs innate immune responses and bone healing after tooth extraction.

Coordination between the nervous and innate immune systems to maintain bone homeostasis is largely uncharacterized. The present study investigated the sensory-immune interaction in resting alveolar bone and healing socket by surgical sensory denervation. Bone histomorphometry and immunohistochemistry showed that sensory denervation resulted in moderate suppression of bone remodeling, with a proinflammatory milieu manifested by increased neutrophil recruitment and possible alternations in macrophage phenotypes along the resting bone surface. This denervation effect intensified when bone remodeling was triggered by tooth extraction, as revealed by disrupted temporospatial variations in macrophage subpopulations and neutrophil infiltration, which were closely associated with a dramatic decline in socket bone filling and residual ridge height. Antagonism of calcitonin gene-related peptide (CGRP) brought about similar antianabolic and proinflammatory effects as sensory denervation, suggesting that sensory nerves may monitor the bony milieu by CGRP. Depletion of macrophages, rather than neutrophils, ruled out CGRP effects, illustrating that macrophages were the primary immune mechanism that linked sensory innervation, innate immunity, and bone. The data support that sensory innervation is required for control of innate immune responses and maintenance of bone homeostasis. Sensory neuropeptides, such as CGRP, are a possible target for the development of proanabolic treatments in bone disease by modulating innate immune responses.