INTRODUCTIONOver the past decade, there has been an emerging interest in the interrelationship between systemic conditions and oral health. Diabetes is perhaps one of the best documented conditions that have been closely linked with periodontal disease. This paper reviews the role of diabetes as a risk factor in periodontal disease. The treatment implications in the management of periodontal disease as an integral component of diabetes care is also discussed in light of the current understanding of the pathogenesis of these 2 chronic conditions.

MATERIALS AND METHODSEpidemiological, clinical and laboratory studies examining the relationship between diabetes and periodontal diseases were selected from both medical and dental journals.

RESULTSThe severity of periodontal destruction has been shown to be related to the direct and indirect effects of glycaemic control, with other factors also being implicated. Although some studies have pointed towards a bi-directional relationship between glycaemic control and periodontal health, it is still not clear if improvement in periodontal health could lead to improved metabolic control.

CONCLUSIONDiabetes and periodontal disease are closely related in many ways, though the effect of periodontal disease on diabetes control remain to be determined, with larger intervention studies. In light of the increasing evidence of the relationship between diabetes and periodontal disease, management of oral health should form an integral part of diabetes management.

Anti-Infective Agents ; pharmacology ; Blood Glucose ; drug effects ; Diabetes Complications ; Diabetes Mellitus ; blood ; physiopathology ; Humans ; Periodontal Diseases ; drug therapy ; etiology ; immunology ; prevention & control ; Risk Factors

Positive-sense RNA viruses modify intracellular calcium stores, endoplasmic reticulum and Golgi apparatus (Golgi) to generate membranous replication organelles known as viral factories. Viral factories provide a conducive and substantial enclave for essential virus replication via concentrating necessary cellular factors and viral proteins in proximity. Here, we identified the vital role of a broad-spectrum antiviral, peruvoside in limiting the formation of viral factories. Mechanistically, we revealed the pleiotropic cellular effect of Src and PLC kinase signaling via cyclin-dependent kinase 1 signaling leads to Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1 (GBF1) phosphorylation and Golgi vesiculation by peruvoside treatment. The ramification of GBF1 phosphorylation fosters GBF1 deprivation consequentially activating downstream antiviral signaling by dampening viral factories formation. Further investigation showed signaling of ERK1/2 pathway via cyclin-dependent kinase 1 activation leading to GBF1 phosphorylation at Threonine 1337 (T1337). We also showed 100% of protection in peruvoside-treated mouse model with a significant reduction in viral titre and without measurable cytotoxicity in serum. These findings highlight the importance of dissecting the broad-spectrum antiviral therapeutics mechanism and pave the way for consideration of peruvoside, host-directed antivirals for positive-sense RNA virus-mediated disease, in the interim where no vaccine is available.