Temporomandibular disorder (TMD) and fibromyalgia (FM) have some clinical characteristics in common, for instance the chronic evolution, the pathophysiology incompletely understood and a multifactorial genesis. The incidence and the relationship between TMD and FM patients are the aims of this review. A MEDLINE and Pubmed search was performed for the key words “temporomandibular disorder” AND “fibromyalgia” from 2000 to present. A total of 19 papers were included in our review, accounting for 5449 patients. Ten studies, reporting a total of 4945 patients with TMD, showed that only 16.5% of these patients had diagnosis of FM, whereas 12 studies, reporting a total of 504 patients with FM, demonstrated that 77.0% of these patients had diagnosis of TMD. A comorbid relationship exists between TMD and FM. The complexity of both diseases shows the importance of a multimodal and interdisciplinary.

Background: The molecular crosstalk between periodontitis and diabetes is well established. The role of the NLRP3 inflammasome, a multicomponent inflammatory machinery, is an emerging field of research on the relationship between these two uncommunicable diseases. Recent advances are revealing further molecular details regarding the biological function and the mechanism behind the NLRP3 inflammasome dysregulation and highlighting an unexpected role for the caspase-1 in immune homeostasis. We aimed to understand which metabolic checkpoints are involved in contributing to and instigating the relationship between periodontitis and diabetes. We tried to explore the involvement of the NLRP3 in regulating the cytokine-chemokines profile and discussed the potential synergism in these mechanisms when these two diseases coexist in the same patient. Methods: A literature search was carried out in the electronic databases (MEDLINE, EMBASE, and Cochrane Library) for relevant studies from inception until January 2022 for trials and cohort studies that investigated the activation and regulation mechanism of the NLRP3 inflammasome in patients with periodontitis and type two diabetes. Two investigators independently extracted data. The data quality assessment was rated by the Joanna Briggs Institute (JBI). Results: from twenty-six references identified, three studies (two case-control and one cross-sectional) met the inclusion criteria. Analysis of periodontal tissue samples in diabetic individuals exhibited significant overexpression of the NLRP3 inflammasome when compared with healthy controls. Conclusions: there is insufficient evidence to sustain the involvement of the upregulation of genes and proteins involved in the activation of NLRP3 inflammasome components in patients with periodontitis and diabetes.