Periodontitis is a chronic inflammatory disease that damages the tooth-supporting apparatus – that is, its soft tissue and bone – which, if untreated, will lead to tooth loss. Hajishengallis and Chavakisis note that periodontitis is epidemiologically linked to a number of chronic diseases, including type 2 diabetes mellitus, inflammatory bowel disease, rheumatoid arthritis, Alzheimer’s disease, non-alcoholic liver fattening, and some cancers (426). The unbalanced interaction of the periodontal microbiota with the host’s inflammatory response is how tissue destruction in periodontitis is usually explained. However, Hajishengallis and Chavakisis state that it has remained largely unclear whether this interaction can be a causal link between periodontitis and non-oral comorbidities (426). From a medical point of view, it is essential to understand whether the relationship between periodontitis and its comorbidities is simply correlative or arranged by causal mechanical interactions.
Many researchers have devoted their efforts to investigating the peculiarities of this issue. As per Hajishengallis and Chavakisis, epidemiological and clinical research combined with experimental studies provides enough evidence to conclude that periodontitis has adverse effects on systemic health via biologically plausible operations (437). Clinical interventional studies show that local treatment of periodontitis reduces the serum levels of inflammatory forces and enhances metabolism, lipid profile, and other systemic disease surrogate markers. However, there is no clear indication that successful periodontal treatment reduces the risks or incidences of epidemiologically related diseases (Hajishengallis and Chavakisis, 437). To establish it, multi-center randomized controlled trials are required; these could determine that peridontitis is a mutable risk factor for hazardous comorbidities. In this respect, further advancement of local therapy for periodontitis through adjunctive host-modulation techniques (for instance, by targeting programmable pathways) can help reduce systemic inflammation and encourage systemic health.
Work Cited
Hajishengallis, George, and Triantafyllos Chavakis. “Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities.” Nature Reviews Immunology, vol. 21, no. 7, 2021, pp. 426-440.