Injuries to the inferior alveolar nerve (IAN) and lingual nerves (LNs) have long been known complications of the mandibular sagittal split ramus osteotomy (SSRO). Most postoperative paresthesias resolve without treatment. However, microsurgical exploration of the nerve may be indicated in cases of significant persistent sensory dysfunction associated with observed or suspected localized IAN or LN injury. We report the demographics and outcome of microsurgical exploration and repair of peripheral branches of the trigeminal nerve injured because of the SSRO. A retrospective chart review was completed on all patients who had microsurgical repair of peripheral trigeminal nerve injuries caused by mandibular SSRO and were operated on by the senior author (R.A.M.) between March 1986 and December 2005. A physical examination, including standardized neurosensory testing (NST) as described by Zuniga et al, was completed on each patient preoperatively. All patients were followed periodically after surgery for at least 1 year with NST repeated at each visit. NST results obtained at the last patient visit were used to determine the final level of recovery of sensory function. Sensory recovery was evaluated using guidelines established by the Medical Research Council scale. The following data were collected and analyzed: age of patient, gender, nerve injured, chief sensory complaint (numbness, pain, or both), duration (months) from injury to surgical intervention, intraoperative findings, surgical procedure, and neurosensory status at final evaluation. Given the retrospective nature of this study, the research was exempt from our institutional review board ethics committee. There were 54 (n = 54) patients (8 males and 46 females) with an average age of 36.9 years (range, 16 to 55 years) and a follow-up of at least 12 months. The most commonly injured/repaired nerve was the IAN (n = 39), followed by the LN (n = 14), and the long buccal nerve (n = 1). In 31 patients (57.4%), the chief sensory complaint was numbness, while 20 patients (37%) complained of pain and numbness, and 3 patients (5.5%) complained of pain without mention of numbness. The average time from nerve injury to repair was 9.4 months (range, 3 to 50 months). The most common intraoperative finding was a discontinuity defect (n = 18, 33.3%), followed by partial nerve severance (n = 15, 27.8%), neuroma-in-continuity (n = 11, 20.3%), and compression injury (n = 10, 18.5%). The most frequent surgical procedure was autogenous nerve graft reconstruction of the IAN using the sural or great auricular nerve (n = 22, 40.7%), followed by excision of a neuroma with or without neurorrhaphy (n = 13, 24.1%). All the LN injuries (n = 14) were partial or complete severances, of which 2 were reconstructed with autogenous nerve grafts and the other 12 underwent neurorrhaphy. The long buccal nerve injury required excision of a proximal stump neuroma without neurorrhaphy. After a minimum of 1-year follow-up, NST showed that 8 nerves (14.8%) showed no sign of recovery; 19 nerves (35.2%) had regained "useful sensory function," and 27 nerves (50%) showed full recovery as described by the Medical Research Council scale. Microsurgical repair of the IAN or LN injured during the SSRO can be considered in patients with persistent, unacceptable sensory dysfunction in the distribution of the involved nerve. Modifications of surgical technique may be helpful in reducing the incidence of such injuries. Based on our experience, an algorithm for evaluation and treatment is presented.