## 4 Discussion  
TMDs are examined in two groups: temporomandibular joint disorders and muscle originated disorders. TMDs include internal structure irregularities or involve mismatch disorders. Muscle hyperactivity is occasionally thought to be the root of intra-articular dysfunction and other times it is seen to be a contributing factor. In this context, bruxism is a parafunctional activity that is typically observed when sleeping and is characterized by  
Figure 2: RoB 2 assessment of RCTs. The randomization process reported 100% of the studies with a low risk of bias. Of the studies, 80% excluded a performance bias [23; 24; 25; 26; 27; 28; 30; 31; 33] but 75% reported all outcome data [23; 24; 25; 27; 30; 31; 32; 33] and 100% of included trials adequately left out bias in the selection of the reported results. [23; 24; 25; 26; 27; 28; 33] The overall ranking showed no studies with low risk of bias. Only 4 out of 11 RCT studies were shown to have a low risk of incurring bias. [23; 24; 27; 31]. involuntary spasmodic or rhythmic nonfunctional teeth grinding. Neck pain, headaches, a restriction in the mandibula's functional mobility, and pain and spasm in the masticatory muscles can all occur in bruxism sufferers. The most recent theory concerning the origins of bruxism affirms the contribution of the autonomic and central nervous systems to the development of oromandibular activity when we sleep. Particularly, sleep-related mechanisms influenced by brain chemical activity, airway patency maintenance during sleep, and rhythmic masticatory muscle action may heighten the motor activity that underlies the development of sleep bruxism. TMDs impair quality of life and create chronic discomfort. About two-thirds of TMD patients reported no or very minor functional limitations, which is a measure of functional impairment that takes into account pain-related disability. This may come as a surprise, given that the patients' levels of somatization and depression were relatively high; both of which have been associated with varying degrees of functional impairment. Although TMDs begin as a functional muscular disorder, it ultimately can cause degenerative changes and internal derangement in the temporomandibular joint. Various therapeutic procedures are available for the management of chronic orofacial pain and muscular diseases related to TMDs, such as pharmacological treatment, physiotherapy, behavioral approaches, and occlusal splints or surgical treatment, although no specific treatment has proven to be consistently effective. The most effective course of treatment is currently a matter of debate. Presynaptic neurotoxic BoNT-A impairs the release of acetylcholine from motor nerve ends via Ca + 2, leading to dose-dependent weakening or paralysis in skeletal muscle. By doing this, the afflicted muscle regions are functionally denervated. The neuroparalytic impact of the toxin may impair the delicate control between bones and muscles in the musculoskeletal system. Both tissues retain a cross-talk mechanism in this system. In vivo investigations [18; 19] showed bone alterations after a single BoNT-A injection in the masticatory muscles for 1 to 3 months. Similar to this, changes in mandibular structures following repeated injections of BoNT-A were observed in other clinical investigations [16; 17]. In fact, according to [PERSON] et al. [23], this negative effect persisted even after a single high-dose injection of BoNT-A. Therefore, it is possible to speculate that effects of BoNT-A on bone tissues may result in decreased bone loading, raising the mRNA expression of RANKL and block neurotransmitters. BoNT-A has been employed extensively in treatment of oromandibular dystonia, myofasical pain, and temporomandibular dislocation. Similarly, BoNT-A has been widely employed in the management of TMDs due to its analgesic and relaxing abilities; however, few scientific studies support its use on account of the heterogeneity of the populations studied so far.