University of Washington, Box 357446, Department of Orthodontics, Seattle, WA 98195-7446, USA.
Bone. 2012 Mar;50(3):651-62. doi: 10.1016/j.bone.2011.11.015. Epub 2011 Dec 2.
Paralysis of the masticatory muscles using botulinum toxin (BTX) is a common treatment for cosmetic reduction of the masseters as well as for conditions involving muscle spasm and pain. The effects of this treatment on mastication have not been evaluated, and claims that the treatment unloads the jaw joint and mandible have not been validated. If BTX treatment does decrease mandibular loading, osteopenia might ensue as an adverse result. Rabbits received a single dose of BTX or saline into one randomly chosen masseter muscle and were followed for 4 or 12 weeks. Masticatory muscle activity was assessed weekly, and incisor bite force elicited by stimulation of each masseter was measured periodically. At the endpoint, strain gages were installed on the neck of the mandibular condyle and on the molar area of the mandible for in vivo bone strain recording during mastication and muscle stimulation. After termination, muscles were weighed and mandibular segments were scanned with micro CT. BTX paralysis of one masseter did not alter chewing side or rate, in part because of compensation by the medial pterygoid muscle. Masseter-induced bite force was dramatically decreased. Analysis of bone strain data suggested that at 4 weeks, the mandibular condyle of the BTX-injected side was underloaded, as were both sides of the molar area. Bone quantity and quality were severely decreased specifically at these underloaded locations, especially the injection-side condylar head. At 12 weeks, most functional parameters were near their pre-injection levels, but the injected masseter still exhibited atrophy and percent bone area was still low in the condylar head. In conclusion, although the performance of mastication was only minimally harmed by BTX paralysis of the masseter, the resulting underloading was sufficient to cause notable and persistent bone loss, particularly at the temporomandibular joint.
使用肉毒毒素 (BTX) 使咀嚼肌瘫痪是一种常见的治疗方法,用于美容减少咬肌的大小,以及涉及肌肉痉挛和疼痛的情况。这种治疗方法对咀嚼的影响尚未得到评估,声称治疗可减轻下颌关节和下颌的负荷也未得到验证。如果 BTX 治疗确实减少了下颌的负荷,则可能会导致骨质疏松症等不良后果。兔子的一侧咬肌随机接受单次 BTX 或生理盐水注射,并随访 4 或 12 周。每周评估咀嚼肌活动,定期测量刺激每块咬肌时切牙的咬合力。在终点,在颈状突和下颌骨磨牙区安装应变片,用于在咀嚼和肌肉刺激期间进行体内骨应变记录。终止后,称重肌肉并对下颌骨段进行微 CT 扫描。一侧咬肌的 BTX 瘫痪并没有改变咀嚼的侧别或速度,部分原因是由于翼内肌的代偿。咬肌诱导的咬合力显著降低。骨应变数据分析表明,在 4 周时,BTX 注射侧的下颌骨髁突受力不足,磨牙区的两侧也是如此。特别是在这些受力不足的部位,特别是注射侧的髁突头部,骨量和质量严重下降。12 周时,大多数功能参数接近注射前的水平,但注射的咬肌仍有萎缩,髁突头部的骨面积百分比仍然较低。总之,尽管 BTX 使咬肌瘫痪对咀嚼的影响很小,但由此导致的负荷不足足以引起明显且持续的骨丢失,特别是在颞下颌关节。