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| ORIGINAL ARTICLE |
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| Year : 2023 | Volume
: 13
| Issue : 1 | Page : 9-16 |
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Herpes virus and periodontitis: A cross sectional questionnaire survey based on attitude, perception, knowledge, and awareness among dental practitioners in Tamil Nadu
Gunalan Kalaivani
Periodontist and Implant Dentistry, Consultant and Private Practitioner, Sivakasi, Tamil Nadu, India
| Date of Submission | 27-Mar-2022 |
| Date of Acceptance | 27-Feb-2023 |
| Date of Web Publication | 28-Apr-2023 |
Correspondence Address:
Dr. Gunalan Kalaivani
1/6/1129, Asari Colony, Satchiyapuram, Sivakasi - 626 124, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jid.jid_10_22
 Abstract | | |
Aim: To assess the relationship between herpes virus (HV) and periodontitis (PI) among dental practitioners (DP). Objective: This survey aims to assess attitude, perception, knowledge, and awareness about HV and its role in PI patients. Materials and Methods: The study was conducted on DP in the southern states of Tamil Nadu. A self-assessed questionnaire was prepared, and the survey was done through a web-based system (GOOGLE FORMS). Two experts did a pretest to assess its validity and reliability. Twenty questions (each 5) were designed to assess attitude, perception, knowledge, and awareness. They all had to be answered without exception before submission. Chi-square test and Student's t-test were used to compare the responses of attitude, perception, knowledge, and awareness. Results: About 30% of DP supported that HV can lead to PI. Among them, mostly MDS-qualified DP (P < 0.05) supported that HV's could worsen the clinical parameters (CP) of PI diseases with increased periodontal pocket depth, bleeding on probing and clinical attachment level. Only 45% accepted that periodontal therapy could improve CP by reducing subgingival bacterial and viral counts. Nearly 74% were unaware of HV examination to consider in refractory and recurrent PI patients. Significant results (P < 0.01) were observed for mean responses of attitude, perception, knowledge, and awareness-related question based on sex and qualification of DP. Conclusion: Still, many dental surgeons were unaware of the HV role and its management in PI patients. There is a requisite to incorporate more subject-related scientific programs to update the DP about the current evolving etiology and its treatment sequences in PI patients to achieve successful practice.
Keywords: Antiviral treatment, clinical attachment loss, gingival crevicular fluid, herpes virus, nonsurgical periodontal treatment, periodontitis, polymerase chain reaction
How to cite this article:
Kalaivani G. Herpes virus and periodontitis: A cross sectional questionnaire survey based on attitude, perception, knowledge, and awareness among dental practitioners in Tamil Nadu. J Interdiscip Dentistry 2023;13:9-16 |
How to cite this URL:
Kalaivani G. Herpes virus and periodontitis: A cross sectional questionnaire survey based on attitude, perception, knowledge, and awareness among dental practitioners in Tamil Nadu. J Interdiscip Dentistry [serial online] 2023 [cited 2023 Jun 2];13:9-16. Available from: https://www.jidonline.com/text.asp?2023/13/1/9/375281 |
| Clinical Relevance to Interdisciplinary Dentistry | |  |
Herpes virus (HV) is found to be one of the emerging etiological factors in aggravating periodontal disease activity. It was found to worsen the clinical parameters of the disease status. Proper diagnosis with effective periodontal management was found to resolve the disease activity into a healthy state and prevent further periodontal complications.
| Introduction | | |
Herpes virus (HV) is an icosahedral-shaped DNA virus, which belongs to the Herpesviridae family. It has special characteristic features with viral envelope, tissue tropism, and latent in the infected host cells. Among various types of HV, herpes simplex virus (HSV), cytomegalovirus (CMV), and Epstein–Barr virus (EBV) were found to relate to periodontitis (PI).
PI is an infectious disease caused by a specific group of bacteria and viruses like HV.[1] Compared to gingivitis and healthy periodontal sites, PI showed more genomic copies of HV.[2] It resided in a deeper periodontal pocket and showed more synergistic interaction with subgingival periodontopathic bacteria (SPB).[1],[2],[3]
The pathogenesis of this virus was found to have direct and indirect tissue damage by infecting or altering the periodontium, thereby decreasing the resistance to infectious agents. HV multiplies and damages the gingival tissue (GT) integrity. It impairs the local host defense by attacking polymorphonuclear neutrophils (PMN), lymphocytes, and macrophages.[4]
Indirectly, immune responses are altered by the selective regulation of cytokines. It includes tumor necrotic factor-alpha (TNF-α) and interleukin-I (IL-Iβ, IL-6, and IL-8), leading to reactivation and coinfection with SPB.[1] More periodontal tissue damage could be caused by an active release of destructive inflammatory mediators due to repeated mechanisms of pathogenic bacterial multiplicity. Clinical parameters (CP) are worsened by increased clinical attachment loss (CAL).[5] Specific studies showed that more tissue breakdown occurs in HV-infected sites than HV-free sites.[6]
HSV, CMV, and EBV were detected in gingival crevicular fluid (GCF), subgingival plaque, saliva, or GT.[2],[7],[8],[9] As mentioned in earlier studies, the real-time polymerase chain reaction (RT-PCR) was a better diagnostic tool in detecting such viruses.[10] The nonsurgical periodontal therapies (NSPTs) decreased the viral and bacterial load in diseased sites, improving the CP.[7],[11],[12] Even a combination of antiviral (AV) treatment was effective in the case of refractory PI.[13]
Upcoming scientific evidence supports the role of HV in causing PI other than pathogenic bacteria and resolves complications like mobility and tooth loss by arresting or preventing tissue destruction.[14] Still, many dental surgeons were unmindful about HV development and progression in PI patients. As a result, the primary objective of this study was to determine dental practitioners' (DP) attitudes, perceptions, knowledge, and understanding of HV's role in developing PI and managing it in patients in southern Tamil Nadu (TN).
| Materials and Methods | | |
A cross-sectional study, based on the attitude, perception, knowledge, and awareness about HV and its role in PI among DP, was done through a web-based system (GOOGLE FORMS). The sample size was predicted using OpenEpi software, and the survey contains 500 DP. The samples were selected randomly. A 95% confidence interval and 80% power were used to assess the sample size. Twenty questions (each 5) were designed, so that they all had to be answered without exception before submission [Chart 1].
Two subject experts in the periodontics branch evaluated the structured questionnaire's validity and reliability. The inclusion criteria included DP of any age, sex, qualification, place of work, and years of experience in dental practice. Those who were disinterested in answering the question were excluded from the study. Among 500 DP, only 253 showed their active participation.
The responses for attitude and knowledge-based questions included yes, no, and maybe with scores 1, 2, and 3. The Likert scale responses included strongly agree to strongly disagree with scores 0–5 for perception and awareness-based questions. The study was designed based on STROBE criteria.
The statistical analysis was performed using IBM Corp. Released 2013. IBM SPSS Statistics for Windows, Version 22.0. Armonk, NY: IBM Corp. The percentage frequency is used for assessing the attitude, perception, knowledge, and awareness-based answers. The responses of attitude, perception, knowledge, and awareness had been compared using the Chi-square test. The overall mean responses were analyzed using the Student's t-test. P <0.05 was considered statistically significant.
| Results | | |
Among 500 DP, 253 were responded. The overall response rate included 50.6%. The significant results were shown in the demographic details provided by the DP based on age, sex, qualification, place of work, and years of experience [Table 1]. The percentage frequency was used in [Figure 1] to depict the demographic details. The attitude, perception, knowledge, and awareness-based responses are tabulated in [Table 2], [Table 3], [Table 4], [Table 5]. The mean value for each questionnaire-based response is shown in [Figure 2] and [Figure 3], with significant results. | Figure 2: Mean comparison of attitude, perception, knowledge, and awareness based on sex
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 | Figure 3: Mean comparison of attitude, perception, knowledge, and awareness based on education
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 | Table 1: Demographic details of the dental practitioners who participated in the questionnaire study
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 | Table 2: Percentage of attitude based responses of the dental practitioners
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 | Table 3: Percentage of perception based responses of the dental practitioners
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 | Table 4: Percentage of knowledge based responses among the dental practitioners
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 | Table 5: Percentage of awareness based responses among the dental practitioners
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| Discussion | | |
PI is a noncommunicable infectious disease caused by a specific group of bacteria and some viruses like HV. HV is supposed to play a synergistic role but not act as a mere bystander in the etiology of the PI. PI showed more infected HV residing in a deeper periodontal pocket than gingivitis and healthy periodontal sites.[1],[6],[15] Kazi and Bharadwaj.[16] in their study stated that HV was detected predominately from severe PI patients compared to mild and moderate PI patients.
Slots.[1] mentioned that the diseased site usually contained an influx of various inflammatory cells with a presence of latent HV. Conditions including infection, immunosuppression, stress, and hormonal change can activate latent HV to multiply, infect, and overwhelm the growth of SPB in the GT. Thus, HV-infected PI sites harbored elevated levels of SPB, including Porphyromonas gingivalis  , Actinobacillus actinomycetemcomitans itans (Aa), Dialister pneumosintes s (Dp), Prevotella nigrescens Pn), Treponema denticola Td), and Prevotella intermedia Pi), as explained by Contreras and Slots.[2]
Studies proved that HSV-1, HSV-2, CMV, and EBV are the types of HV related to PI.[6] Among them, Bilichodmath et al.,[17] in their study, reported that the prevalence of HSV-1 was found to be 100% in PI sites. In contrast, Kazi et al.[15] and Imbronito et al.[18] reported that the prevalence of HSV-1 in PI sites was 81.2% and 40%. Even few studies did not report the presence of HSV-1 from PI patients.[19],[20] Uncommonly, patients with PI harbors HSV-2 in the range of 12%–20%, as mentioned by Singh et al. and Das et al.[21],[22] Studies reported that the prevalence of EBV in PI sites was found to be 32%–79%.[2],[17],[22] Moreover, CMV was found to be 26.3% in the PI site as reported by Bilichodmath et al.,[17] 12% by Das et al.,[22] and 59% by Chalabi et al.[19] From the above studies, it was clear that HSV-1, CMV, and EBV were found to exhibit stronger association with PI, whereas HSV-2 found to have little association or no association among them.[14],[23]
HV-infected PI sites exhibited complex pathogenesis involving direct and indirect mechanisms, as stated by Slots.,[1] by damaging or infecting the tissue integrity. Chen et al.[24] detailed the mechanism of HV, stating initially, it multiplies in the GT, causing direct damage to native cells such as keratinocyte, fibroblast, endothelial cells, and alveolar bone cells. Later, it permits overgrowth of SPB due to impaired periodontal defense cells by attacking PMN, lymphocytes, and macrophages. Conversely, in their study, Brockman and Knipe.[25] enlightened the role of HV as a tool in redefining the immune pattern of the host cell due to peripheral infection. PI, considered a peripheral infection, is worsened by HV targeting the most potent immune cells and altered cytokine regulation such as TNF-α and IL-Iβ to induce further damage. It also alters the regulation of T helper cells (Th1) and the complement pathway.[1],[25] Therefore, active tissue destruction occurred with the massive release of destructive inflammatory mediators and repeated a multiplicity of SPB in PI sites as stated by Contreras and Slots.[2]
Saygun et al.,[5] in their study, explained that a strong relationship status was evident between HV and PI by worsening of the CP including plaque index (PI), gingival index (GI), pocket depth (PD), CAL, and bleeding on probing. Kazi and Bharadwaj.[15] proved that the HV-infected PI site showed more CP worsening, especially PD and CAL, than the HV-free PI site. Shah and Mehta.[12] found that EBV was positively associated with increased PI, GI, PD, and CAL in HV-infected PI sites than gingivitis. Contreras et al.[26] stated that severe PI sites showed more infected HV with worsened PD and CAL than mild and moderate PI sites. Moreover, Kazi and Bharadwaj.[15] in their study showed that HSV-1+ HSV-2 and HSV-1+ HSV-2+ EBV are the most common combination present in the severe PI patient. Grenier et al.[7] stressed that CMV was found to be higher in deep PD, and Ding et al.[11] reported that EBV+ CMV was found to reside in the deep PD. Hence, the interplay between HV and SPB showed more destruction in PI sites.
The samples for HV examination from PI sites can be collected from GCF, subgingival plaque, saliva, or GT.[2],[7],[8],[9] Maheaswari et al.[27] suggested PCR is one of the standard diagnostic tools for detecting viruses in PI sites. The advantage of using PCR is that it is a more sensitive and faster diagnostic tool than traditional viral culture methods. Kubar et al.[10] in the study have reported that RT-PCR is one of the promising tools to monitor and quantify the genome copies of HV in PI sites. Saygun et al.,[5] using RT-PCR, confirmed that more than 80% of CMV and EBV are associated with SPB in PI sites, causing more periodontal tissue destruction than healthy periodontal sites. The disadvantage of this laboratory procedure includes technique sensitivity and expenses.[1]
Grenier et al.[7] and Ding et al.[11] confirmed that NSPT could manage HV-infected PI effectively by decreasing the viral and bacterial load in the infected site with an improved CP. Shah and Mehta.[12] reported that NSPT showed a significant improvement in gingivitis patients by reducing the count of HSV-1 and EBV and PI patients with reduced HSV-1, CMV, and EBV. Few studies stressed that the prevalence of HV can change after NSPT, where CMV was found to elevate after 2 weeks of treatment. Hence, periodic recall visits and revaluation are mandatory in recurrent PI patients to compare HV counts after NSPT.[10] Sunde et al.[13] explained NSPT with AV treatment for 10 days (valacyclovir hydrochloride) decreased the viral load subgingivally. It maintained the stable periodontal condition with a 1-year follow-up in refractory PI patients. Future studies are required to evaluate the effects of AV therapy as adjunct in HV-infected PI.
According to the author's perception, many DP were unaware of the relationship between HV and PI. Hence, the study was done to assess the attitude, perception, knowledge, and awareness among DP about the relationship between HV and PI. For attitude-related questions, our study showed that only 34% of the DP responded to know the PI patient's etiology that was treated. Among them, 53% of the DP with <5 years of clinical practice were supposed to answer with significant results to improve their periodontal diagnostic aids for knowing the etiology in PI patients. Still, 18% of female DP answered that treating PI patient is more important than knowing the etiology of the disease. Mostly, 30% of the BDS-qualified DP supported that HV can lead to PI. Positively, many DP accepted that the HV would affect the periodontium other than the human immunodeficiency virus, as mentioned in an earlier study done by Slots.[1]
Based on perception-related responses, only 36.7% of the female DP agreed that bacteria are the main etiological factor causing PI. About 32% of DP with <5 years of clinical experience accepted multifactorial causes (virus, genetic, and environmental) will play an essential role in PI. An average of 6.3% of MDS-qualified DP are willing to accept that the herpes group of viruses like HSV, CMV, and EBV will lead to PI. Furthermore, MDS-qualified DP supported that HV-infected PI sites have more worsened CP than HV-free PI sites, with significant results shown in the study confirmed by Saygun et al.[5]
Expectantly, 7.1% of the private DP supported that HV cannot cause direct tissue damage to the periodontium, and they strongly agreed that HV would remain latent in the GT. Despite this, many DP accepted that GCF and saliva might contain HV to cause PI. Positively, DP, with all years of experience, accepted that neutrophils can be impaired by HV and can alter immune function to lead to PI. From knowledge-based questions, it was clear that only a few DP knew that HV could damage the periodontal defense mechanism, leading to more periodontal tissue destruction, as Saygun et al.[14] observed in another study.
Twenty percentage of the DP were aware that the etiology and pathogenesis of PI changed recently. Even 26% of the DP were aware of HV examination in refractory PI patients. Among 253 participants, 18% of the DP were aware of viral testing for PI, and they accepted it would be expensive. 45% of the DP responded with awareness about these viral count reductions in the subgingival area after periodontal therapy, supporting the study results stated by Grenier et al.[7] and Ding et al.[11] NSPT involving antibacterial debridement and AV agents could prove to be a valuable treatment strategy in patients with refractory and recurrent PI.[12],[13] Still, there is a lack of ample evidence to associate the role of HV in refractory or recurrent PI.[1]
In addition, periodontal therapy aims to decrease HV concentrations in saliva that may facilitate the reduction of virus transmission between close associates.[1],[28] Interestingly, 33% of the responders reported that awareness about the association between HV and PI was gained through the electronic database. More subject-related scientific programs or questionnaire surveys are mandatory for DP to know the changing concepts in upcoming periodontal disease.
Based on gender, mean responses showed no significant differences regarding attitude-based responses. However, the mean perception score was higher in male DP, and the mean knowledge and awareness score was higher in female DP with significant results. A significant difference was noted in the mean responses based on the qualification. Thus, knowing the patients' etiology and the nature of the progressing disease may pave a better diagnosis and management to the DP.
| Conclusion | | |
HV is involved in the etiopathogenesis of PI by several complex mechanisms. More evidence is needed to support the association between HV and its management in PI. Our study aims to educate and update current facts about the role of HV in etiology, diagnosis, and treatment planning among DP of southern TN. We must make some efforts for DP practicing in various states of our country, helping them understand a recent and trending periodontal concept regarding the etiology and treatment strategy of PI.
Acknowledgment
Special thanks to my professors Dr V.R. Balaji M.D.S (HOD in CSI College of dental science and Research) and Dr. S. Kalaivani M.D.S, and to my colleagues who participated in this study.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]
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