The emerging (COVID-19) pandemic is a global health disaster, caused by infection with severe acute respiratory syndrome coronavirus-2. The disease spreads at an alarming rate all over the world and presents a range of disease manifestations including asymptomatic, mild, moderate and severe symptoms irrespective of age groups. Most patients with severe symptoms exhibit underlying comorbidities such as diabetes, hypertension and obesity. Alternatively, there is an existing evidence for an association between oral health and nonoral systemic diseases. Since the oral cavity is a significant pool for many respiratory pathogens, patients with oral infections are more likely to develop pneumonia as a complication. Therefore, we emphasize that the oral hygiene status has a great impact on the recession and progression of oropharyngeal and respiratory diseases.

The primary etiologic factor for periodontal diseases is “Dental plaque.” Although pathogenic bacteria in dental plaque are required for the incidence of periodontal disease, a susceptible host is also very important. The susceptibility of the host can be modified by many systemic factors with hormones level being one. The periodontium shows an exaggerated inflammatory response to plaque modified by female sex hormones during puberty, pregnancy, in women taking oral contraceptives, and at the postmenopausal stage. This review provides an in detail analysis of how periodontium is influenced by the fluctuation in sex steroid hormones of females during different phases of their lifetime and to discuss how much the same hormone at different ages and stages shows an exaggerated gingival response to plaque.

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ContextCigarette smoking is a well-established risk factor for periodontitis and carries an increased risk for loss of periodontal attachment as well as bone loss.AimsThe purpose of the present study was to investigate whether disease severity differs between smokers and nonsmokers in a group of chronic periodontitis patients by assessing the periodontal probing depth (PPD) and bleeding on probing (BOP).Materials and methodsThe study included 150 individuals, 75 smokers and 75 nonsmokers, in the age group of 35-60 years. Subjects with chronic periodontitis were selected and included in the study. Periodontal evaluation, including periodontal probing pocket depths and bleeding on probing, was performed on all four quadrants and at six sites per tooth using the Williams periodontal probe. The data were pooled from the anterior sextant and the posterior sextant as well as from the facial and lingual surfaces.Statistical analysisComparisons were made between smokers and nonsmokers using the z-test (two-tailed test). Probing pocket depth categories 0-3 mm, 4-5 mm, 6-7 mm, and ≥8 mm and the proportion of sites having a pocket depth of ≥5 mm were used in the analysis.ResultsThe mean percentage of sites that bleed upon probing was higher for nonsmokers as compared with smokers. Smokers had less shallow pockets (0-3 mm) than nonsmokers and more pockets of 4-7 mm (categories 4-5 mm, 6-7 mm). No significant differences were detected in the prevalence of pockets ≥8 mm. In the anterior, premolar, and molar regions, pockets of 6-7 mm were significantly more prevalent in smokers. The buccal and lingual sides also showed that smokers had more sites with deep probing depths ≥5 mm than nonsmokers. The data also showed that in the upper jaw, in the anterior and premolar teeth, the largest differences were found between smokers and nonsmokers.ConclusionsFrom the results, it can be concluded that cigarette smoking results in periodontal tissue destruction in the different areas of the oral cavity, with the maximum periodontal destruction in the maxillary anterior and premolar region.

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