MPS appears to be mainly regulated by psychological and pathophysiological factors, hence, morphological factors [6,7]. Psychosocial factors such as stressful life events, emotional disturbances, psychological distress, and psychiatric disorders (hypervigilance, depression, anxiety, post-traumatic stress disorder, and neurosis) [8,9,10,11,12] contribute to arousal of the central nervous system (CNS). This in turn leads to excessive masticatory muscle activity (MMA) [13]. The masticatory muscles should only be active while chewing and swallowing [14]. However, MMA can result from increased activity in the central nervous system (CNS) triggered by excessive stimuli delivered to the body [15,16,17]. MMA can appear during sleep, which is called sleep bruxism, and/or during wakefulness, which is called awake bruxism [18]. International Consensus from 2018 defined sleep bruxism as a “rhythmic or non-rhythmic muscle activity” and awake bruxism as a “repeated or sustained tooth contact and bracing or thrusting of the mandible” [19]. A new definition points out that both behaviours are neither sleep nor movement disorders in healthy individuals [19]. Functional muscle activity (swallowing and chewing) lasts less than 20 min/day [14], the average bite force is 30.16 kg for a swallow and 26.63 kg for a chew, which totals 7801.8 kg/s per day. In contrast, the average bruxer’s bite force is 54.43 kg (some patients produce up to 113 kg) resulting in 26126.92 kg/s per day [20]. Nevertheless, they can lead to various consequences: flattened/chipped tooth surfaces, microfractures of the tooth enamel, gum recession, loss of teeth, hypersensitivity of teeth to hot/cold/sweet, tongue impaction, ear buzzing/ringing, headache, neck pain, clicking/stiffness/pain in the temporomandibular joints (TMJ), diminished opening, difficulty chewing, sore jaw muscles, changes in facial appearance, and myofascial pain syndrome (MPS, masticatory myalgia) [21,22,23,24,25].

Thus, prolonged exposure to physical and emotional stress can contribute to chronic pain stemming from the TP formation [26]. As much as 75% of patients report that stress is the main reason for a doctor visit [25].

Psychosocial findings are mirrored by Axis II of the DC/TMD protocol which is based on dual-axis diagnosis [2,27]. Axis I assesses a diagnosis with respect to signs and symptoms, and Axis II is used to evaluate psychosocial factors [28]. In Axis II, special attention is given to graded chronic pain, depression, anxiety, somatic symptoms, jaw functional limitations, and oral behaviours [29]. Clinical examination with respect to DC/TMD reveals an important role of the biopsychosocial components in TMD MPS development.

Pathophysiological factors are certain medications (SSRI—selective serotonin reuptake inhibitors, antipsychotics, and psychotropic drugs), CNS disorders, and genetic or familial predisposition [30,31,32]. Other risk factors (potential causes) may be micro- and macro-traumas, overloads, postural disorders, incorrect ergonomics, nutritional deficiencies, infections (e.g., parasitic diseases, babesiosis, Lyme disease, or fungal infections), and sleep deprivation. Furthermore, research has shown that sleep disorders lead to a vicious cycle by increasing pain, which in turn causes further sleep disturbances [33]. Hypothyroidism, low levels of vitamins D, B12, or iron can also play a significant role [34]. Moreover, low-level (sustained or repetitive), eccentric, and concentric (maximal or submaximal) muscle contractions are thought to evoke muscle overload which can lead to the development of TPs [35]. It is worth mentioning that substances connected with increased MMA are nicotine, caffeine, alcohol, and psychoactive substances [36].

The aetiology of TMD also includes biological factors (e.g., sex, hormones), endogenous opioid function, and variations in anatomical genotypes and parafunction [37]. The role of dental occlusion still remains controversial [38]. In turn, adolescents in Class II and III demonstrate a higher prevalence of myofascial pain (1.73 times and 2.53 times) than adolescents Class I [39]. Special attention is attributed to the whiplash injury which is considered as an initiating and aggravating factor of TMD [40]. Currently, the pathophysiology of TMD shifted from mechanical-based theory to a chronic pain biopsychosocial model [40].