ABSTRACT
The prevalence of dental caries in individuals who practice good oral hygiene increasingly indicates that other etiological factors, such as genetic factors, may be responsible for occurrence of caries, and its prevalence in younger individuals, such as adolescents, is an early manifestation of their genetic makeup. Therefore, there is a need to investigate the correlation of various genetic factors with the occurrence of dental caries in populations. Thus, this study assessed the relationship between single nucleotide polymorphism (rs2228570) in the vitamin D receptor gene and dental caries susceptibility. After obtaining ethical approval (NU/CEC/2020/0339), 377 adults, aged 18-40 years, were included in this study. Among the participants consenting to participate, salivary samples were collected, and an oral examination was conducted using the World Health Care Oral Health Survey Format 2013. The DMFT and PUFA index scores were recorded along with basic demographic details. The subjects were categorized as caries-free (controls, DMFT = 0) and caries-active (cases). The case group was further divided into the high-risk group (DMFT ≤ 10), moderate-risk group (DMFT = 4-9), and low-risk group (DMFT = 1-3). Saliva samples were used for vitamin D level analysis and DNA isolation. Polymerase chain reaction-based restriction fragment length polymorphism analysis using Fok1 digestion was performed on the isolated DNA. Salivary vitamin D levels were markedly higher in the caries-free group than in the caries-active group (p < 0.001). The T allele of rs2228570 was significantly associated with having active caries, while the C allele was associated with being caries-free. Individuals with the rs2228570 TC genotype had 2.814-fold increased likelihood, and individuals with the TT genotype had 3.116- fold increased likelihood of being caries-active. This finding is important in terms of patient counselling, as well as possibly in terms of prevention and treatment of caries.
ABSTRACT
Limiting the spread of virus during the recent pandemic outbreak was a major challenge. Viral loads in saliva, nasopharyngeal and oropharyngeal swabs were the major cause for droplet transmission and aerosols. Saliva being the major contributor for the presence of viral load is the major key factor; various mouthwashes and their combination were analyzed and utilized in health care centers to hamper the spread of virus and decrease viral load. The compositions of these mouthwashes to an extent affected the viral load and thereby transmission, but there is always a scope for other protocols which may provide better results. Here we evaluated the potential of antimicrobial peptide LL-37 in decreasing the viral load of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) through an in silico work and evidence from other studies. This narrative review highlighted a brief nonsystematic methodology to include the selected articles for discussion. Accessible electronic databases (Medline, Scopus, Web of Science, SciELO, and PubMed) were used to find studies that reported the salivary viral load of SARS-CoV-2 published between December 2019 and June 2021. The following keywords were utilized for brief searching of the databases: "saliva," "viral load," and "SARS-CoV-2." Articles in English language, in vitro cell-line studies, ex vivo studies, and clinical trials explaining the viral load of SARS-CoV-2 in saliva and strategies to decrease viral load were included in this review. The search was complemented by manual searching of the reference lists of included articles and performing a citation search for any additional reviews. The antiviral potential of cationic host defense peptide LL-37 was evaluated using computational approaches providing in silico evidence. The analysis of docking studies and the display of positive interfacial hydrophobicity of LL-37 resulting in disruption of COVID-19 viral membrane elucidate the fact that LL-37 could be effective against all variants of SARS-CoV-2. Further experimental studies would be needed to confirm the binding of the receptor-binding domain with LL-37. The possibility of using it in many forms further to decrease the viral load by disrupting the viral membrane is seen.
