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Host modulation therapy (HMT), as a treatment concept for periodontitis, aims to modulate the host immune responses during the pathogenesis of periodontitis. Various drugs have been evaluated as HMT, including subdose doxycycline (SDD), nonsteroidal anti-inflammatory drugs (NSAIDs), bisphosphonates, and cytokine receptors, to modify or modulate inflammatory mediators and associated signaling pathways in the immune-inflammatory response, as well as connective tissue breakdown and bone resorption. SDD, a member of the tetracycline drug family, has been reported to improve periodontal treatment outcomes by inhibiting periodontal breakdown through inhibiting MMPs. NSAIDs may suppress periodontal inflammation by reducing cyclooxygenase-2(COX-2) activity. Combined application of SSD and NSAIDs may achieve a better clinical outcome. Recent studies of HMT treatment have focused on the prevention of excessive inflammation by regulating mediators using endogenous lipid mediators. Local administration of bisphosphonates and histone deacetylase inhibitors can inhibit osteoclast activity and regulate bone tissue remodeling. Currently, SSD is approved by the FDA for periodontal treatment. Other drugs, such as COX-2 selective inhibitor, nonsteroidal anti-inflammatory drugs, bisphosphonates, triclosan and iNOS inhibitors, have good application prospects in the prevention and treatment of periodontal disease, and the mechanism and side effects of these drugs remain to be further investigated.

Objectives: To investigate the effects of environmental tobacco smoke (ETS) on the inflammatory process of periodontitis by evaluating bone loss and the expression of cyclooxygenase‐2 (COX‐2) and Src homology phosphotyrosine phosphatase 2 (SHP‐2). Materials and Methods: Eighty 6‐month‐old male SD rats were randomized into four groups (10 rats/group/per time point): (a) normal group, (b) ETS group, (c) ligature‐induced periodontitis group, and (d) ligature‐induced periodontitis + ETS group. After treatment with ligature and/or ETS for 8 and 12 weeks, the levels of alveolar bone resorption and the expressions of COX‐2 and SHP‐2 in periodontal tissue were analyzed using histology and immunohistochemistry. Results: The ligature‐induced periodontitis group displayed increased bone resorption and elevated expression of COX‐2 and SHP‐2 in periodontal tissues compared to the normal and ETS groups at 8 and 12 weeks. Furthermore, bone resorption and COX‐2 and SHP‐2 levels in the ligature‐induced periodontitis + ETS group were significantly increased compared to those in the normal and ligature‐induced periodontitis groups at both 8 and 12 weeks. Conclusion: Environmental tobacco smoke increased alveolar bone loss in periodontitis with enhanced expression of COX‐2 and SHP‐2 in periodontal tissues. Further investigation is needed to explore the role of COX‐2 and SHP‐2 in ETS‐associated periodontitis. [ABSTRACT FROM AUTHOR]

Cannabis, also known as marijuana, is one of the most commonly used substances for medical and recreational purposes globally. With the trend of global legalization of medical use of cannabis and even the recreational use, the prevalence of recreational use of cannabis has increased markedly over the past few years. Correspondingly, the potential health concerns related to cannabis consumption have also increased. Therefore, it is necessary for oral healthcare providers to understand the effects of cannabis use on oral health. This review briefly summarizes the components of cannabis, biologic activities on tissues, and mechanisms of action in human cells and tissues. Oral tissue expression of cannabinoid receptors and the potential association of cannabis to oral diseases are also examined. The goals of this review are to (1) elaborate the basic biology and physiology of cannabis in human oral tissues, and (2) provide a better understanding the effects of its use and abuse on oral health. Due to insufficient information, more well‐designed studies should be conducted. It is urgent to include cannabis usage into dental patient health records. [ABSTRACT FROM AUTHOR]