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Periodontitis and diabetes mellitus co-morbidity: A molecular dialogue.

AbstractBACKGROUND:
Type 2 diabetes mellitus (T2DM) and periodontitis are two biologically linked diseases that often coexist in complex interaction. While periodontitis may lead to insulin receptor desensitization, diabetes may increase the expression of inflammatory cytokines, such as Tumor Necrosis Factor-α (TNF-α) and Interleukin 6 (IL-6), in the gingival crevicular fluid and activate osteoclasts via Receptor activator of nuclear factor kappa-Β ligand (RANK-L) production, leading to bone resorption. However, the association between the two diseases processes, where one may exacerbate the progression of the other, is unclear. In addition, both diseases have similar mechanistic themes, such as chronic inflammation and oxidative stress. This review aimed to investigate the pathophysiological and molecular mechanisms underlying T2DM and periodontitis.
HIGHLIGHT:
Uncontrolled diabetes is often associated with severe periodontitis, measured by clinical attachment loss. Alteration in the oral microbiome composition, which may activate the host inflammatory response and lead to irreversible oxidative stress, is a common finding in both diseases. An understanding of the molecular crosstalk between the two disease processes is crucial for developing therapeutic targets that inhibit bone resorption and halt the progression of periodontitis in patients with diabetes.
CONCLUSION:
The Oral microbiome composition in T2DM and periodontitis shifts toward dysbiosis, favoring bacterial pathogens, such as Fusobacteria and Porphyromonas species. Both conditions are marked by pro-inflammatory immune activity via the activation of Interleukin 17 (IL-17), Interleukin 1 (IL-1), TNF-α, and Nuclear Factor Kappa Beta (NF-κB). Common molecular crosstalk signaling appears to involve advanced glycation end products (AGEs) and oxidative stress. Thus, future drug targets are multifactorial, ranging from modulatory of host inflammatory response to preventing the accumulation of AGEs and oxidative free radicals.
AuthorsAnthony Luong, Andy Nassif Tawfik, Hicret Islamoglu, Hanaa Selim Gobriel, Nada Ali, Pouya Ansari, Ruchita Shah, Tiffany Hung, Tanusha Patel, Bradley Henson, Finosh Thankam, Jill Lewis, Mark Mintline, Tobias Boehm, Zohra Tumur, Dalia Seleem
JournalJournal of oral biosciences (J Oral Biosci) Vol. 63 Issue 4 Pg. 360-369 (Dec 2021) ISSN: 1880-3865 [Electronic] Netherlands
PMID34728373 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2021 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved.
Topics
  • Diabetes Mellitus, Type 2 (complications)
  • Dysbiosis (complications)
  • Gingival Crevicular Fluid (metabolism)
  • Humans
  • Morbidity
  • Periodontitis (epidemiology)

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