MATERIAL and METHODS: A total of 40 albino Wistar rats have been randomly divided into four groups: group 1 (n=10): crushlike nerve damage was created by pinching the left mental nerve for 60 s with an aneurysm clip and intraperitoneally administered 1 ml of saline for 14 days; group 2 (n=10): the left mental nerve was pinched for 60 s with an aneurysm clip and intraperitoneally administered 2 mg/kg of methylprednisolone for 14 days; group 3, experimental group (n=10): the left mental nerve was pinched for 60 s with an aneurysm clip and intraperitoneally administered 2 mg/kg of vitamin B12 for 14 days; and group 4, experimental group (n=10): the left mental nerve was pinched for 60 s and intraperitoneally administered 2 mg/kg of methylprednisolone and 2 mg/kg of vitamin B12 for 14 days. All rats were sacrificed on the 28^th postoperative day, and histopathological evaluation was performed.

RESULTS: Nerve damage was higher in the control group than in other groups (p<0.05). When Neural Cell Adhesion Molecule (NCAM) expression levels were compared, no major differences were observed between the methylprednisolone and control groups (p>0.05). The B12 and B12+methylprednisolone groups reached significantly higher NCAM expression levels compared to the control and methylprednisolone groups. When the myelin basic protein (MBP) expression levels were compared (p<0.05), the MBP expression was significantly higher in all experimental groups than in the control group (p<0.05).

CONCLUSION: Systemic vitamin B12 and methylprednisolone administration effectively supported remyelination in the crushed mental nerve by increasing Schwann cell proliferation and differentiation. Keywords : Vitamin B12, Methylprednisolone, Mental nerve damage, Nerve regeneration, Nerve crush injury, Rat