Abstract
Pyroptosis is a caspase-dependent process relevant to the understanding of beneficial host responses and medical conditions for which inflammation is central to the pathophysiology of the disease. Pyroptosis has been recently suggested as one of the pathways of exacerbated inflammation of periodontal tissues. Hence, this focused review aims to discuss pyroptosis as a pathological mechanism in the cause of periodontitis. The included articles presented similarities regarding methods, type of cells applied, and cell stimulation, as the outcomes also point to the same direction considering the cellular events. The collected data indicate that virulence factors present in the diseased periodontal tissues initiate the inflammasome route of tissue destruction with caspase activation, cleavage of gasdermin D, and secretion of interleukins IL-1β and IL-18. Consequently, removing periopathogens’ virulence factors that trigger pyroptosis is a potential strategy to combat periodontal disease and regain tissue homeostasis.
Highlights
In clinical practice, clinicians frequently face situations where the periodontal or peri-implant tissues overreact to a stimulus promoted by dental materials or even do not respond to therapies, leading to inflammation
Part 2 discusses the results found in Tables 1 and 2, highlights the clinical relevance of pyroptosis on periodontal diseases, and considers pyroptosis in periodontal therapy
When the innate immune system is acting against pathogens or other potential dangers, the inflammatory responses are initiated through pattern recognition receptors, phagocytes, dendritic cells, epithelial cells that recognise pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs) [31,32,33]
Summary
Clinicians frequently face situations where the periodontal or peri-implant tissues overreact to a stimulus promoted by dental materials or even do not respond to therapies, leading to inflammation. Caspase-1 cleaves gasdermin D (GSDMD), resulting in cell membrane perforation through the release of the GSDMD N-terminal fragment [5]. This is known as the canonical inflammasome activation of pyroptosis. The mechanisms of pyroptosis involve different major signalling pathways, all activating the downstream of GSDMD Cytoplasmic molecules, such as interleukins-1β (IL-1β) and -18 (IL-18), are released from the pores formed by GSDMD and trigger a robust inflammatory response (Figure 1) [2,9,10]. The occurrence of pyroptosis can be determined by a combination of markers, including the activation of
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