Myofascial pain, the most prevalent subtype of temporomandibular disorders (TMD), often persists despite conventional therapies such as oral appliances, physiotherapy, behavioral interventions, and pharmacological agents. In refractory cases, botulinum toxin type A (BTX-A) has emerged as a promising adjunctive treatment, targeting both neuromuscular hyperactivity and nociceptive signaling. This editorial review the biological rationale, clinical evidence, and future directions for BTX-A in managing myofascial TMD pain. Mechanistically, BTX-A inhibits acetylcholine release and reduces sensitization by blocking the exocytosis of calcitonin gene-related peptide, substance P, and glutamate within trigeminal pathways—mechanisms shared with migraine, where BTX-A is already an established therapy. Clinical studies, including randomized trials and case series, report consistent improvements in pain and jaw function, particularly in localized myalgia following failed conservative care. Benefits are most pronounced in well-profiled patients, sometimes with coexisting headache features, though methodological heterogeneity limits certainty. Reported adverse effects are generally mild and transient. Conversely, some trials show neutral results, underscoring the need for standardized protocols, precise case definitions, and robust comparators. BTX-A should not be considered first-line therapy but occupies a defined role as an evidence-informed option for refractory myofascial TMD, with future multicenter studies required to validate its long-term efficacy and safety.