Whiplash, a unique type of microtrauma mainly occurring in vehicle collisions, is caused by sudden dynamics of hyperextension-hyperflexion on the cervical spine. [32] Among the patients with whiplash injury, approximately 23% suffered chronic pain and disabilities. [33] Thus, it lowers the patient's quality of life and increases health costs. Neck pain and stiffness, and headache are the most prominent symptoms in whiplash injury [6]. Recently, a possible association between whiplash injury and TMD has been studied. Carroll et al. reported that TMD was more prevalent in individuals with whiplash injury (15.8%) than in those without (4.7%) [34]. Conversely, the prevalence of whiplash injury in populations with TMD (median 35%) is higher than that in control groups without TMD (1.7–13%).[5] Although there is limited information on the neuropathophysiologies of TMD development and aggravation after whiplash injury, research to explore this is ongoing. As hypothesized, many of the clinical symptoms and MRI findings of masticatory muscles of whiplash-related TMD can be distinguished from those of TMD resulting from an unknown cause.
One of our main findings was that patients with wTMD had higher pain intensity across wider jaw and neck areas compared to those with iTMD. This was consistent with previous results that patients with whiplash injury report higher pain scores and larger areas of local and referred pain than healthy controls [35]. The increased clinical pain observed in the wTMD group may be due to impaired diffuse noxious inhibitory controls (DNICs), a measure of central nervous system pain inhibition[36]. Moreover, sleep disturbance is related to decreased DNICs in patients with TMD [37]. Reduced reactivity of the hypothalamic–pituitary adrenal (HPA) axis has been associated with chronic widespread body pain [38]. Furthermore, thalamic activity also contributes significantly to the pain processing. Decreased thalamic activity can cause exaggerated pain following innocuous peripheral stimulation [39]. Collectively, changes to the process of central endogenous pain inhibition through interference with DNICs, HPA axis, or thalamic activity can occur in patients with whiplash-related TMD, and pain is more likely to be amplified and prolonged in such patients.
Widespread pain, which is not limited to the injured area and increased pain intensity, is derived from the dynamics of the nociceptive pathway at the CNS level. Hypersensitivity after whiplash injury occurs both locally, i.e., throughout the neck area, and at more distant sites beyond the boundary of the damaged peripheral nerve [40]. Thus, deep tissue is damaged in the cervical joint by direct application of shear force, compression, and excessive stretching through whiplash injury, but it can also affect the TMJ area. Pain wind-up refers to the phenomenon of increased excitability of CNS induced by frequency-dependent electrical stimulation of afferent C-fibers [41]. Pain wind-up can also be a mechanism of hypersensitivity and in whiplash-associated TMD. There were clear experimental results showing that patients with painful TMD have reduced pain thresholds and sensory impairment after innoxious stimuli [40]. Interestingly, central hypersensitivity is not only specific to whiplash injury, even though this phenomenon is seen in a variety of chronic pain syndromes [40, 42]. Similar neuropathology may underlie a variety of chronic pain, including TMD, and further investigation is required on how it serves in detail.
Regarding MRI findings on TMJ, more than 50% of patients with wTMD had ADDWoR and condylar degeneration, and were significantly more prevalent than those with iTMD. In general, the TMJ is the most affected structure from TMD [43]. To the best of our knowledge, only a few MRI studies have validated the signs and symptoms of whiplash injury-induced TMD. During sudden macrotrauma, abrupt changes in the position of the mandible and TMJ disc followed by TMJ-ligament elongation and TMJ disc displacement may occur.[44] In a previous MRI study, displacement (56%) and abnormal joint fluid or edema (65%) of the TMJ were observed in the patients who had TMD after sustaining whiplash injury [45]. In addition, proper disc positioning is a prerequisite for normal movement of the mandibular condyle. Disc displacement progresses from reducible to non-reducible, and ADDWoR and condylar degeneration can be associated with each other [46]. Abnormal positioning of the articular disc may cause closed lock jaw position, which evokes TMJ clicking and pain, as well as limits jaw function [47]. Interestingly, the VAS score was positively related with ADDWoR and disc deformity only in iTMD, and this correlation was not observed in wTMD.
Our main MRI finding was that patients with wTMD had remarkable structural changes in the LPM. Substantial structural change in the LPM may have been observed considerably more frequently in wTMD than in iTMD because LPM is more susceptible to whiplash injury than other masticatory muscles. Additionally, LPM is a direct major factor in the occurrence of whiplash injury-related TMD. The LPM controls the rotation and translation of the disc and condyle, protrudes the mandible, and stabilizes the articular disc [48]. LPM plays a somewhat secondary role in mastication, but it is directly related to changes in the mandibular condyle and disc. Pathologic changes in the LPM can be associated with TMJ disc displacement [49, 50]. Recent MRI results have shown structural muscle changes in the form of reduced muscle volume, fatty infiltration, and muscle atrophy in patients with whiplash-related disorders. [51, 52] In our previous LPM-related MRI study, significant positive correlations were reported between structural changes in the LPM, ADDWoR, disc deformity, and condylar degeneration in patients with TMD after whiplash injury[6]. Furthermore, rapid LPM stretching induces reflex contracture with disc displacement, resulting in pain [6, 53]. On the contrary, no muscle changes were observed in asymptomatic individuals or individuals with idiopathic or non-traumatic neck pain [51]. We found that the VAS score was correlated with the structural changes of LPM only in wTMD.
Among and/or within the human masticatory muscles, many anatomical differences exist, indicating that different muscles are specialized for their resistance against whiplash injury. In our results, more than 60% of patients with wTMD had muscle tenderness in the masseter and temporalis muscles. Architecturally, the masseter and temporalis muscles can deliver higher forces than the pterygoid muscles. Thus, masseter and temporalis muscles play a more crucial role in mastication, which can lead to fatigue build-up and become vulnerable to tenderness [54]. In addition, the average thickness values of the masseter muscle (13.65 ± 2.19 mm), temporalis muscle (6.66 ± 1.14 mm), MPM (14.73 ± 1.32 mm), and LPM (15.59 ± 1.40 mm) were different [55–57]. Specialization in fiber type composition and fiber cross-sectional area can be reflected in these intramuscular differences. Compared to the masseter and pterygoid muscles, the temporalis has significantly larger fibers and a notably different fiber type composition [58]. Furthermore, the myosin heavy chain (MyHC) content of muscle fibers mainly determines their force–velocity properties [59]. A regionally higher proportion of MyHC type I, expressed in slow muscle fibers, was found in the anterior temporalis, deep masseter, and anterior MPM. [60]. However, a previous study showed that MyHC type and isoform composition do not sufficiently explain the difference between the form and function of the muscles [61]. Further research is needed to reach a clearer conclusion about the impact of whiplash-related TMD on each masticatory muscle.
Finally, we observed that headache, sleep problems, and psychological distress were significantly more prevalent in the wTMD group than in the iTMD group. We must focus on the fact that CNS-related factors were more prevalent in the wTMD group. Headache and sleep problems possibly co-occur from the result of the dysregulation of shared brain regions, such as the trigeminal nucleus caudalis and thalamus [62]. Sleep problems deleteriously affect central pain modulatory systems [37]. Headache has been suggested as an aggravating and potential risk factor for TMD symptoms [63]. Psychological distress is often accompanied by CNS-level symptoms, and is associated with more pain and disability in whiplash injury [42]. In addition, psychological factors, along with physical factors, can play a role in the progress or recovery from whiplash injury [64]. This suggests that neuropathophysiologies of wTMD may differ from that of iTMD, and that TMD should be understood in a biopsychosocial model considering macrotrauma. The interconnectivity between biological factors and psychological factors can involve the development, processing, and chronicity of whiplash-related TMD symptoms. Furthermore, we need to have specific coping and treatment strategies for patients with wTMD.
This study has several limitations. In our study, we only checked for the presence of self-reported psychological distress, not through elaborate questionnaires or diagnostic tests. To understand whiplash injury-related TMD in the biopsychosocial model, further systematic investigation of the psychological aspects of patients will be required. Axis II of the DC/TMD or RDC/TMD diagnostic tool might be helpful in examining psychosocial factors.[65, 66] In addition, this study has the advantage that it had a randomized controlled design, but a large-scale population-based study is needed to avoid bias due to data composition and to reach a more general conclusion. Because the masticatory muscles function cooperatively and elaborately during jaw movement,[67] the pathological changes in one masticatory muscle will ultimately affect other muscle pathologies. Therefore, it is necessary to further study the differences before and after whiplash injury of each muscle over a long period of observation, and the relationships among the masticatory muscles.