Dr. Mehdi Jafari
The delayed onset of dysfunction in the area of anesthesia gives rise to several etiologic questions: the flap design and extent of dissection, the loop of the mandibular nerve as it approaches the mental foramen, the compressibility of cancellous mandibular bone and its ability to transfer force or pressure to a nearby nerve from an implant (remote nerve compression), surgical trauma of treatment, postoperative inflammation, Herpes zoster and other viral or bacterial infections, mental nerve block, neoplastic compression, compartment syndrome, and hematoma.
Postoperative nerve dysfunction is a condition that is almost totally dependent on the patient’s perception and reporting of the deficit. We must rely on this perception to assess an occurrence, improvement, recovery, or non-recovery of a sensory nerve dysfunction. During surgery, nerves can be stretched, compressed, or partially or totally transected. The factors that affect nerve response to injury include the size, number, and pattern of nerve bundles in the nerve trunk; the amount of epineural tissue surrounding the nerve; the position of the nerve fibers in the nerve trunk (the most distal fibers are at the center of the trunk); the type of injury (compressed nerves regenerate faster than severed nerves); and physiologic susceptibility. Peripheral nerves show a greater capacity for regeneration than central nervous system nerves.
A nerve can be compressed by various materials that can cause an altered sensation. Compression of the pudendal nerve while bicycle riding has been shown to cause neuropathy. Cancellous bone that is compressed by a dental implant might press against the nerve, causing a dysfunction. Implants are slightly larger that the receiving osteotomy, usually about 0.5 mm. When the implant is placed, a compression of bone may occur. Human trabecular bone has variable Young’s modulus related to its density and a compressive strength range between 18,000 and 24,000 pounds per square inch. A trabeculation of cancellous bone would have enough induration to transfer compression force and subsequent stretching of the nerve.
If an implant is seated and the apex presses on a segment of trabecular bone that happens to be positioned in the same axis as the implant, it is conceivable that the piece of trabecular bone could be displaced 0.5 mm toward the mental nerve, distal to the bifurcation, inducing a neural inflammatory degenerative process .The bifurcation of the mandibular nerve into the mental and incisive nerves occurs in the molar area well before reaching the mental foramen.
The possibility also exists of an interposition of the mental artery that may act to compress the nerve, as has been found in some cases of blood-vessel compression trigeminal neuralgia; decompression of the nerve in this situation can produce rapid relief, probably from release of demyelinated axonal distortion from the compression and remyelination. An arterial compression of the nerve may induce a delayed neural inflammatory process. The implant in this case does not radiographically show to touch the nerve. The term “remote nerve compression†might be used in these situations to better characterize the condition, if it indeed exists.
Some clinicians recommend reversing fully seated implants a quarter of a turn to alleviate bone compression.