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Cite as: Balanta-Melo J & Buvinic S. Man-dibular bone loss: a hidden side effect of botulinum toxin type A injection in masticatory muscles. J Oral Res 2018; 7(2):44-46. doi:10.17126/joralres.2018.014 Botulinum toxin type A (BoNTA) is the most potent serotype of a group of neurotoxins produced by obligate anaerobic bacteria Clostridium botulinum. This neurotoxin blocks the release of acetylcholine from the motor neuron, uncoupling the neuromuscular junction that results in a reversible paralysis of skeletal muscles that lasts for 4 – 6 months in humans.1 Commercially available forms of BoNTA (e.g. Botox®, Dysport®, Xeomin®) are increasingly used by dentists worldwide.1 In dentistry, conditions that affect masticatory muscles such as benign masseter hypertrophy and myofascial pain are treated with intramuscular injections of BoNTA,1,2 However, this neurotoxin is not approved for interventions in the masticatory apparatus, according to the US Food and Drug Administration (Allergan Full Prescribing Information for Botox®); as such, its clinical use is off-label. The effects of BoNTA in skeletal muscles include paralysis, weakness, and atrophy,1 but much less studied are the side effects that could affect bone homeostasis. The musculoskeletal system maintains a fine regulation between muscles and bones, in which both tissues sustain a cross-talk through biomechanical (generation of force, tension) and biochemical signals (molecules released by the muscle that contribute to bone homeostasis and vice versa).3 So, what happens to the structure and function of the adjacent bone when muscle paralysis is induced by BoNTA injection? The intramuscular (IM) intervention with BoNTA promotes bone loss in underlying structures. As demonstrated by Warner et al in adult female C57BL/6 mice, IM intervention in the quadriceps and calf muscles with Botox® (0.5U/19.2μl) significantly reduced the trabecular bone volume fraction by 43%, in the distal femoral epiphysis and by 54% in proximal tibial metaphysis after 21 days.4 In the same model, Aliprantis et al described that acute bone loss induced by this intervention occurs as a response to a significant increase of the receptor activator for nuclear factor Kappa Beta ligand (RANKL) in the proximal tibia metaphysis. RANKL is necessary to differentiate and increase the number of osteoclasts (bone resorption cells). Moreover, the treatment with human recombinant osteoprotegerin (the RANKL physiological antagonist), or conditional deletion of the osteoclastogenesis master regulator “nuclear factor of activated T-cells c1” (NFATc1), prevented the bone loss in this animal model.5 In addition, direct effects of BoNTA on bone cells were not detected, suggesting that bone loss may be produced by muscle load or signaling after this intervention.5 Considering that the temporomandibular joint requires the activity of Mandibular bone loss: a hidden side effect of botulinum toxin type A injection in masticatory muscles.