Botulinum Toxin A for Lower Facial Contouring: A Prospective Study

Abstract

This article, on the surface, appears similar to other articles describing the effects of botulinum toxin type A on masseter muscles to improve facial contour. Other articles, as the authors duly note, have been written about this technique previously. The technique has, in fact, become rather commonplace. I have injected the masseters of more than 100 patients since 1992, with slight variations in the technique. However, one thing had always bothered me about the technique: Why was it that the cosmetic result seemed to last almost twice as long in the masseter as in, say, the glabella, forehead, crow’s feet, or other lower facial musculature at the first injection (which rules out long-term atrophy as the cause)? I had always entertained a theory to explain why this was so, but certainly no objective proof. The fact that the effect of botulinum toxin type A on axillary hyperhidrosis lasted significantly longer than that of cosmetic denervation techniques had never bothered me. The end organs (muscle and eccrine glands) were completely different. But why should effects on the masseter differ so greatly from a temporal standpoint than, say, the effects on the glabella? If anything, longer-lasting results might be expected in the glabellar region because the clinician often completely paralyzes the area, leaving no apparent functioning muscle. To my knowledge, no one advocates completely paralyzing the masseters, yet the results are surprisingly long lived. Each of 10 patients had a masseter injected with 120 units of Dysport-brand botulinum toxin type A in a grid type pattern for even distribution throughout the muscle. The patients all had good cosmetic results lasting up to 9 months. This reflects prior papers and true life practice results. If this were all that the article noted, the discussion would end right here. But the beauty of this paper lies in its objective measurements to back up the aesthetic changes. Each patient underwent bite force measurements at each visit as well as preinjection and 3-month postinjection three-dimensional (3D) computed tomography (CT) scans. The correlation of these data yields significant insight into the actions of the toxin beyond the molecular level of a presynaptic neuromuscular blockade. The masticatory muscles (masseters, temporalis, and lateral and medial pterygoids) all were measured for volumetric changes at 3 months, which could be compared with bite force at the same time. As we know, the effect of the toxin begins at about 48 h. Therefore, as the authors note, it is not surprising that the bite force is decreased at 1 week. However, the bite force is not really decreased. If the error range is taken into account, there is no objective loss of strength at all. For argument’s sake, we will forget about statistical significance and measuring error. We will agree with the authors that there is a real (although small) decrease in bite force. But the bite force returns rather quickly, and yet the cosmetic result lags. Although they are both muscles, there is a fundamental difference between how the masseters and corrugators yield a cosmetic result when chemodenervated. The corrugators yield their result due to a loss of strength from origin to insertion of the muscle. The masseters yield their result from a loss of volume due to muscular atrophy. Although both are muscles, the mechanisms are entirely different. If, say, the cosmetic results were due to a loss in strength (as in the glabella) rather than a loss of volume (as in the masseters), the cosmetic effect in this study would be gone in 3 weeks! That is, if it existed at all (remember the error range). M. A. C. Kane (&) Manhattan Eye, Ear and Throat Hospital, Department of Plastic Surgery, 630 Park Avenue, New York, NY 10021, USA e-mail: michaelkanemd@earthlink.net