Abstract

This contribution adds to our growing understanding of the side effects of the bilateral sagittal split osteotomy @SSO). Although a hypothesis is not specifically stated, the study goal is to increase understanding of lingual nerve (L.m injury after BSSO, because the incidence and duration of this complication are not well documented, and risk factors have not been identified. The authors acknowledge the retrospective, subjective nature of the study and offer it as such at this level in the evidenced-based heirarchy.’ The low patient response percentage is typical of such projects, but nevertheless provides some valuable information. As stated, the reported initial incidence of 19.4% lingual nerve (LN) injury is probably higher than the actual occurrence in the total patient population because patients with complaints may be more prone to answer. Six percent of the patients had LN changes lasting more than 1 year. One would hope that an incidence of 1 in 5 initially and 1 in 17 long-term for LN injury grossly overestimates the actual incidence. Given these limitations, there are several significant findings from this study; 1) the ratio of LN (19.4%) to inferior alveolar nerve (IAN) (95.5%) injuries, 2) the different rates of improvement over one year postoperatively (LN, 69.3%; resolved vs. 27.3% for IAN), 3) the greater alteration in daily activity caused by L.N injuries, 4) the lack of a relationship between LN or IAN changes and such risk factors as age, gender, surgeon, surgical movement, removal of third molars, or intraoperative complications, and 5) the relationship of the three types of fixation to LN injury. Of particular interest is the last finding, that a combination of rigid fixation (RF) with screws plus circumandibular wires resulted in twice the LN sensory change as did RF or skeletal wire fixation alone. Unfortunately, it is not clear whether circumandibular wires were used with the skeletal wire fixation group, but I assume that they were from the discussion. The discussion references literature indicating that subjective IAN neurosensory complaints are greater initially than objective test findings, but that these same patient observations are less than the objective test findings in the longterm.*s3 Therefore, in the current study, one would expect objective testing to find more than 19.4% LN deficits. However, because of the different nature of tongue function versus lip function, the differences between the findings on objective and subjective testing at early and late periods may not apply to LN injuries as it does to the IAN. Although it is probable that there is a greater tendency for those with sensory changes to respond to a questionnaire than those without complaints, the speculation about what the probable outcome would be if all 316 questionnaires were returned seems unnecessary. Also, the subjective LN sensory changes seen in the genioplasty group (GP) were of such short duration they may simply represent the patient’s sensory confusion after surgical trauma. The GP sensory changes seem to disappear about the same time that swelling and outward visual evidence of surgery normally resolve. No doubt, a short questionnaire brings a better response than a lengthy one, but the answers to several additional questions would have been interesting. Would the patients have surgery again? If not, is the paresthesia the reason? The number of patients with long-term (permanent?) altered daily activity is not clear. Because we are frequently asked by patients whether numbness will ever end, and if so, when, it would be valuable to know whether the paresthesia that lasted for more than a year ultimately resolved. What was the sensory level after 18 months, 2 years or more, especially in light of data from 5 and 16 years*? Most importantly, was the paresthesiapainful? Hypesthesia is annoying, but dysesthesia is quite another story. Perhaps if this information is available, the authors can update us on these data.

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