Viral Contributions to Periodontal and Peri-implant Disease: A Narrative Review

Abstract

Periodontal diseases, particularly periodontitis, are chronic inflammation with complex microbial and immunological etiologies. While bacterial pathogens such as Porphyromonas gingivalis are well-known contributors, emerging evidence indicates the role of viruses, especially herpesviruses, in the onset and progression of periodontal tissue destruction. In this review, the interplay between viral infections and periodontal health was explored, with an emphasis on the immunopathological mechanisms in which different viruses such as human herpesvirus, Epstein–Barr virus, and human cytomegalovirus aggravate periodontal tissue destruction. These viruses impair host defenses, promote bacterial colonization, and alter cytokine responses, leading to periodontal tissue damage. The review also addresses the impact of systemic viral infections, such as HIV and COVID-19, on periodontal diseases. Elevation in inflammatory mediators, including interleukin-6, link periodontitis with adverse clinical outcomes in viral infections. Moreover, interactions between P. gingivalis and respiratory viruses suggest oral pathogens may also influence systemic disease severity. Advances in diagnosis using molecular technology have improved viral detection in periodontal tissues, and previous studies support the use of antiviral therapies and gene-targeted interventions as potential adjuncts to traditional periodontal care. The integration of preventive strategies, such as vaccination and enhanced oral hygiene, is crucial in reducing the systemic consequences of viral–periodontal interactions. This review highlights the need for interdisciplinary collaboration and continued research to fully comprehend the virological dimensions of periodontal disease and develop effective, targeted therapeutic approaches.

INTRODUCTION

Periodontal diseases are characterized by chronic inflammation resulting from complex microbial and immune interactions, affecting approximately 20%–50% of the global population and representing the leading cause of tooth loss in adults.[1,2,3,4] The disease begins with a dysbiotic microbial biofilm that triggers a host immune response influenced by environmental, genetic, and microbial virulence factors.[2,3] While over 400 bacterial species have been identified in periodontal pockets, only a few such as Porphyromonas gingivalis, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans are considered key pathogens.[5,6,7] Species such as Prevotella intermedia, Fusobacterium, and Candida also contribute to disease progression.[7]

Viral involvement has recently gained attention, particularly human herpesviruses (HHVs), human papillomavirus, and hepatitis B and C viruses, which have been detected in periodontal tissues.[2] Epstein–Barr virus (EBV) and human cytomegalovirus (HCMV) are especially associated with aggressive forms of periodontitis.[8,9] These findings suggest viruses may exacerbate inflammation and immune dysregulation in periodontal and peri-implant diseases, potentially contributing to implant failure and systemic complications.[1,10] As many oral viruses, especially herpesviruses, have immunosuppressive properties and are acquired early in life, understanding their role could lead to new therapeutic strategies aimed at reducing recurrence and improving periodontal treatment outcomes.[11,12]

Despite significant insights into bacterial roles, viral contributions to periodontal and peri-implant diseases remain underexplored, creating a crucial research gap.[1,12] Given the multifactorial nature of these diseases encompassing microbial biofilms, immune responses, and systemic health, viral involvement must be studied within a broader etiological framework.[13] This review aims to investigate the potential role of viruses in disease progression and their interaction with bacteria. Understanding these dynamics may support clinicians in integrating antiviral strategies into comprehensive treatment protocols for improved outcomes.

METHODOLOGY

This narrative review was based on a comprehensive literature search conducted in the following electronic databases: PubMed/MEDLINE, Scopus, and Web of Science. The search was last performed in April 2025 and included studies published from January 2000 to December 2024, to capture both foundational and recent findings related to viral contributions to periodontal disease.

The following keywords were used during the search

1. Virus-Periodontal Disease Interactions: (“periodontal disease” OR “periodontitis” OR “peri-implantitis” OR “peri-implant disease”) AND (“virus” OR “viral infection” OR “herpesvirus” OR “Epstein-Barr virus” OR “cytomegalovirus” OR “HIV” OR “SARS-CoV-2” OR “viral modulation” OR “immune response” OR “virus-bacterial interaction”)

2. Viral-Bacterial Synergy Mechanisms: (“virus-bacterial interaction” OR “viral-bacterial synergy”) AND (“periodontitis” OR “peri-implantitis”) AND (“pathogenesis” OR “biofilm” OR “dysbiosis”)

3. Viral Diagnostics and Periodontal Health: (“viral detection” OR “viral diagnostics”) AND (“periodontal health” OR “gingivitis”)

4. Saliva-Based Viral Detection: (“saliva diagnostics” OR “salivary biomarkers”) AND (“periodontitis” OR “oral virome”) AND (“point-of-care” OR “non-invasive”).

Inclusion criteria were human studies and relevant in vivo or in vitro research that were published in English. Articles discussing the association, mechanisms, or immune responses related to viral involvement in periodontal and peri-implant diseases were also included. Exclusion criteria included non-English publications, case reports, editorials, and conference abstracts, and studies unrelated to periodontal or peri-implant pathology or viral involvement. Additional articles were identified through manual screening of the reference lists of key publications. The selection of studies was based on relevance to the review topic and scientific merit.

The role of viruses in periodontal and peri-implant pathogenesis

Herpesviruses

Herpesviruses are double-stranded DNA viruses that can exist in latent and active states. They are the most abundant viruses found in the oral cavity and have been extensively studied for their role in the etiopathogenesis of periodontitis.[14] Herpesviruses can interfere with the antibacterial effects of macrophages and the complement system. Herpesviruses have been shown to promote periodontitis by decreasing local immunity, driving proinflammatory cytokine responses and tissue-destructive pathways, and cooperatively interacting with keystone periodontal bacteria to produce dysbiosis and severe periodontal breakdown.[15]

Herpesviruses in periodontal lesions alter innate and adaptive defenses, creating an environment permissive for bacterial overgrowth and chronic infection.[15] This local immune subversion is mediated both by direct viral effects on infected cells and by viral regulation of host immune signaling.[16] Herpesvirus infection of gingival tissues was commonly linked to reduced local antibacterial responses and to infection of inflammatory cells that diminishes bacterial clearance and promotes pathogen persistence.[17] HHV encodes multiple microRNAs that were observed to have a significant role in host-pathogen interaction by modulating both host biological pathways and controlling viral life cycle.[18] Moreover, herpesviruses have been documented to infect periodontal cells and inflammatory infiltrates, which can change cytokine output and cell-mediated immunity in situ, and thus blunt effective repair and microbial control.[16,17]

Herpes simplex virus

Herpes simplex virus-1 (HSV-1) causes oral infections, including herpetic gingivostomatitis, while HSV-2 primarily affects the genital area. A meta-analysis by Arduino et al.[19] revealed a significant association between the presence of HSV-1 and periodontitis. In addition, significant correlation has been found between the presence of HSV-1 in subgingival plaque and crevicular fluid and the incidence of periodontitis.

Varicella-zoster virus

Varicella-zoster virus, responsible for chickenpox, can reactivate in adults as herpes zoster (shingles), causing unilateral oral and gingival ulcers. Reactivation is more common in elderly or immunosuppressed individuals and may result in complications such as delayed tooth eruption or periodontium necrosis.[20]

Epstein-Barr virus

A study found that gingival epithelial cells in the periodontium were frequently infected with EBV and may act as a significant oral reservoir for latently EBV-infected cells. Additionally, the baseline level of EBV infection in the epithelium is markedly elevated in case of periodontitis and the extent of EBV infection was shown to correlate with the severity of the disease.[21] A meta-analysis[22] has reported that subgingival EBV identification was correlated with an odds ratio of 7.069 for the onset of periodontitis, indicating a significantly increased disease risk.

Human cytomegalovirus

HCMV has been linked to periodontitis, with higher prevalence in diseased sites compared to healthy ones.[23] Studies suggest that HCMV contributes to oral dysbiosis and intensifies inflammation triggered by plaque, promoting tissue destruction.[24,25] HCMV can establish latent and active infections in periodontal tissues, altering cytokine production and fibroblast function, thereby increasing the risk of periodontal attachment loss.[23,25]

A previous study[26] revealed a significant association between severe periodontitis progression and EBV, HCMV, and HSV-1 infection.

Human herpesvirus 6 and 7

HHV-6 and HHV-7 are commonly detected in gingival tissues of periodontal patients and may worsen outcomes by impairing CD4+ and CD8+ lymphocytes, especially in immuno-compromised individuals such as those with HIV.[27] Their role in periodontal disease remains unclear and warrants further investigation.[27]

Human herpesvirus 8

HHV-8, the causative agent of Kaposi’s sarcoma, has been found in biopsies of periodontitis lesions.[28] Immunosuppression appears to trigger its reactivation, with Kaposi’s sarcoma lesions often involving the gingiva and underlying alveolar bone.[28]

Herpesvirus-bacterial synergy, clinical implications, and disease progression

Herpesviruses act as partners of keystone periodontopathogens, producing bidirectional interactions that favor dysbiosis and destructive inflammation.[13] Mechanistic syntheses emphasize a two-way interaction wherein herpesviruses promote bacterial upgrowth and tissue susceptibility while bacterial components (lipopolysaccharide and proteases) can trigger viral reactivation, sustaining a pathogenic loop that amplifies inflammation and destruction.[16,17] This pathogenic model underpins calls for combined diagnostic approaches and exploration of antiviral adjuncts in trials, as only targeting bacteria may not fully reverse virus-driven disease processes.[17] Previous studies have detected herpesviruses, particularly HSV, CMV, and EBV, in periodontal pockets and were associated with increased clinical parameters of disease severity, such as probing depth and clinical attachment loss.[29,30] These viruses were reported to deteriorate the host’s immune response, allowing for the overgrowth of periodontopathic bacteria such as P. gingivalis and A. actinomycetemcomitans.[13] This suggests a synergistic relationship between herpesviruses and periodontopathic bacteria, which may play a significant role in the pathogenesis of periodontal diseases.[8,13]

Studies have shown that herpesvirus-infected periodontal sites exhibit more tissue breakdown compared to herpesvirus-free sites, indicating a higher risk of disease progression.[31,32] Herpesviruses were commonly associated with specific bacterial pathogens, in severe forms of periodontitis, suggesting that the clinical outcome of periodontal infections may depend on these viral–bacterial interactions.[8] However, the precise molecular and cellular mechanisms remain unexplained.

It has been demonstrated that the presence of viruses, particularly herpesviruses, can influence the broader composition of the oral microbiome beyond classical periodontal pathogens.[33] Herpesvirus-positive sites have shown increased prevalence of Fusobacterium nucleatum, P. intermedia, and T. forsythia, suggesting a potential shift toward a more proinflammatory and anaerobic community.[1,3] These microbial shifts may reflect a disruption in host immune regulation that allows opportunistic bacteria to flourish. Metagenomic analyses also indicate that viral load may correlate with overall microbial diversity and coinfection patterns, rather than a single pathogenic species dominance.[32,34] These findings highlight the importance of viewing periodontal pathogenesis through a polymicrobial and polymodal view, where viruses act as modulators of community structure rather than independent causative agents.

Human herpesviruses and peri-implantitis

Peri-implantitis is a pathological condition occurring in tissues around dental implants, characterized by inflammation in the peri-implant connective tissue and progressive loss of supporting bone.[35] Research indicates variable prevalence of peri-implantitis across populations. Previous meta-analysis found the overall prevalence to be 22%, though individual study results ranged widely from 1% to 47%.[36] EBV and HCMV were frequently detected in peri-implantitis lesions and were associated with increased prevalence of periodontopathogenic bacteria such as Treponema denticola and T. forsythia.[37]

HHVs were reported to impair immune cells such as polymorphonuclear leukocytes, macrophages, and lymphocytes, which are crucial for maintaining periodontal health.[8] Moreover, viral infections lead to increased release of pro-inflammatory cytokines, that promote further peri-implant tissue destruction.[38] The detection of HHVs in peri-implantitis lesions was reported in a previous systematic review,[36] and thus, the use of antiviral therapy should be further investigated in managing peri-implantitis lesion.

While the role of HHVs in peri-implantitis is supported by various studies,[36,38,39] it is important to consider the heterogeneity in findings and the need for further research. The variability in viral prevalence and the complex interactions between viruses, bacteria, and host immune responses highlight the multifactorial nature of peri-implantitis. Additionally, methodological differences in studies, such as sampling techniques and population demographics, can influence the detection and interpretation of viral involvement in peri-implantitis.[38]

Systemic viral infections and periodontal and peri-implant health

Human immunodeficiency virus

HIV has transitioned from a fatal disease to a chronic condition with advancements in antiretroviral therapy (ART), significantly extending the lifespan of those affected.[40] However, HIV remains linked to increased susceptibility to non-HIV-related chronic conditions, including periodontitis.[41] Periodontal disease progression in HIV patients is likely influenced by immunosuppression, although specific mechanisms require further exploration.[41]

Immunological aspects of periodontal disease in HIV patients

In HIV patients, periodontal disease involves dysregulated immune responses to bacterial infection. Inflammation and elevated prostaglandin E2 levels contribute to tissue destruction, especially in immunosuppressed individuals.[42] A shift from T-cell to B-cell dominance and reduced CD4+ T-cell levels correlate with disease severity.[43] Langerhans cells, key to antigen presentation,[44] are reduced in HIV-infected gingiva but may recover with HAART, while mast cell levels remain largely unaffected by HIV status.[45]

Necrotizing periodontal diseases in HIV

Severe forms of periodontal destruction, such as necrotizing ulcerative periodontitis and necrotizing gingivitis, are more common in HIV patients due to profound immunosuppression. These conditions are exacerbated by co-infections, antibiotic resistance, and the impact of ART on oral microbiota.[46] Since the introduction of ART in 1996, HIV/AIDS was transformed into a manageable chronic disease, improving life expectancy and reducing morbidity. Additionally, ART has significantly reduced the prevalence of oral manifestations in HIV patients, including angular cheilitis, oral warts, and necrotizing gingivitis.[47]

Mechanisms of HIV-bacterial interactions

HIV-bacterial interactions play a significant role in the development and progression of periodontal disease in immunocompromised individuals.[48] The weakened immune system in HIV patients facilitates colonization by periodontopathic bacteria such as P. gingivalis, A. actinomycetemcomitans, and T. denticola.[48] These bacteria not only exacerbate periodontal destruction but may also reactivate latent HIV, particularly through metabolites such as butyric acid produced by P. gingivalis, which influence chromatin modification.[49]

HIV infection impairs antibody responses to oral pathogens, with elevated antibody levels against Campylobacter rectus linked to higher gingivitis scores.[50] As a result, HIV-infected individuals have higher rates of conditions such as linear gingival erythema and necrotizing ulcerative periodontitis, often involving atypical pathogens.[41]

While ART has improved systemic health, its effects on periodontal health remain mixed. ART may partially restore oral microbiota balance but does not consistently prevent periodontal disease progression.[51,52] Chronic oral inflammation in HIV-infected patients may also contribute to broader systemic complications and could potentially serve as a viral reservoir, complicating HIV eradication strategies.[52] Additionally, co-infections with herpesviruses further impair host defenses and worsen periodontal outcomes, emphasizing the complex, multifactorial nature of periodontal disease in HIV patients and the need for integrated treatment approaches.[53]

HIV and peri-implantitis

HIV contributes to the development of peri-implantitis through immune dysregulation and microbial interactions. The reduction in CD4+ T cells in HIV-infected individuals compromises immune function, impairing the body’s ability to manage infection and inflammation, thereby facilitating peri-implant tissue breakdown.[41,54] Additionally, HIV promotes a shift toward pro-inflammatory M1 macrophage polarization, which exacerbates local inflammation and tissue destruction around implants.[55]

HIV is also associated with increased inflammatory cytokines, contributing to bone loss and implant failure.[56] Furthermore, the oral microbiome is altered in HIV patients, increasing the prevalence of pathogenic bacteria capable of forming biofilms on implant surfaces, one of the primary drivers of peri-implantitis.[57] Despite these risks, dental implants show generally favorable outcomes in HIV-positive individuals, especially due to the benefits of HAART.[54,57,58,59,60,61]

Research has revealed significant immunological correlations in implant outcomes for HIV patients. Elevated viral loads show a strong association with early implant failure, while abnormal CD4+/CD8+ ratios correlate with late failure due to peri-implantitis.[54] Previous studies reported that the immune dysregulation caused by HIV may impair the integration process, increasing the risk of peri-implantitis.[60] Interestingly, short-term implant survival (1-year follow-up) appears unaffected by CD4+ cell counts.[61] However, current evidence remains insufficient to fully characterize the relationship between immune status and implant success, highlighting the need for further investigation.[62]

A previous systematic review and meta-analysis[60] indicated that while short-term data suggests HIV infection does not seriously threaten implant survival and success rates can be comparable to those in healthy patients, the overall evidence is weak. In contrast, a 12-year follow-up study[59] demonstrated that dental implants in HIV-positive patients achieved long-term survival, with a success rate comparable to that observed in healthy patients.

SARS-CoV-2 and periodontal disease

Emerging evidence suggests a bidirectional relationship between COVID-19 (SARS-CoV-2) and periodontal disease as both conditions involve systemic inflammation.[63] Periodontitis may worsen COVID-19 outcomes by increasing inflammatory markers such as interleukin-6 (IL-6), a key player in the cytokine storm seen in severe cases. The compromised oral epithelial barrier in periodontitis may facilitate COVID-19 and SARS-CoV entry and persistence.[63,64,65]

It has been shown that oral tissues serve as reservoirs for SARS-CoV-2, with the virus detected in gingiva and gingival crevicular fluid.[66] Clinical evidence indicated that poor oral health is associated with more severe COVID-19 symptoms and ICU admissions.[63] Similarly, Marouf et al.[67] reported that patients with moderate-to-severe periodontitis had a significantly higher risk of serious COVID-19 complications. de Aguiar et al.[68] observed that oral lesions were common among COVID-19 patients, regardless of their symptom severity. It was also observed that most of the patients had poor oral hygiene, periodontal issues, and tooth loss.

These findings highlight the potential role for improved oral hygiene in reducing systemic disease burden and suggest that oral health should be integrated into broader public health strategies for COVID-19 management.

Mechanistic link between SARS-CoV-2 and periodontal disease

Periodontitis may exacerbate COVID-19 through multiple pathways: (1) A strong Th17 response in periodontitis could amplify the cytokine storm associated with severe COVID-19 outcomes.[67,69] (2) Periodontal pockets may act as SARS-CoV-2 reservoirs, prolonging viral persistence.[70] (3) Aspiration of periodontopathic bacteria may upregulate ACE2 and cytokine production in the respiratory tract, worsening symptoms.[71] (4) Bacterial proteases (e.g., from P. gingivalis) could enhance viral infectivity by cleaving the SARS-CoV-2 spike protein.[67] (5) Elevated Galectin-3 (Gal-3) in periodontitis may facilitate viral attachment and immune dysregulation.[67,71] Periodontitis-driven systemic inflammation may synergize with COVID-19’s cytokine storm, increasing risks of acute respiratory distress syndrome and multi-organ failure.[67,71] Therefore, managing periodontal disease may help reduce COVID-19 complications by lowering systemic inflammatory burden.[72]

Additionally, interactions between SARS-CoV-2 and periodontal bacteria may further drive the progression of periodontal disease. These interactions, involving both direct viral effects on periodontal tissues and indirect changes in the oral microbiome, create a favorable environment for viral persistence and oral inflammation, contributing to a vicious cycle of co-pathogenicity.[72]

Viral entry and persistence

SARS-CoV-2 can enter and persist in periodontal tissues due to the presence of ACE2 receptors and proteases like TMPRSS2 and furin, which are also mimicked by periodontal pathogens to enhance viral entry. The virus may persist in dental biofilms, acting as reservoirs for reinfection.[73,74]

Inflammatory response and cytokine storm

SARS-CoV-2 infection induces a cytokine storm, worsening periodontal inflammation and tissue destruction. Systemic inflammation from COVID-19 exacerbates gingival tissue damage due to elevated circulating cytokines.[75]

The virus also disrupts the oral microbiome, causing dysbiosis that promotes the virulence of periodontal pathogens.[76] While some bacteria, such as P. gingivalis, may inhibit SARS-CoV-2 through cytotoxicity, others exploit the inflammatory environment to worsen periodontal damage.[77] SARS-CoV-2 can also cause fibrotic changes in periodontal tissues via mitochondrial dysfunction, contributing to disease progression.[78] Gofur[75] found that superinfection risk increases due to the synergy between SARS-CoV-2 and periodontal pathogens.

Poor oral health disrupts the oral microbiome and weakens the local immune response, creating an inefficient defense against SARS-CoV-2. This impaired antiviral immunity may increase the risk of co-infections and contribute to the systemic inflammation seen in post-acute sequelae of COVID-19, potentially explaining the persistence of both oral and non-oral symptoms.[79]

COVID-19 and peri-implantitis

Peri-implantitis, an inflammatory disease affecting implants, shares similar immune and inflammatory mechanisms with periodontitis but progresses faster due to differences in anatomy, such as lack of periodontal ligament and lower vascularity.[80,81]

Both COVID-19 and peri-implantitis showed elevated levels of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α, and IFN-γ) that may exacerbate oral tissue damage and worsen clinical outcomes in susceptible individuals. A proposed mechanistic link between peri-implantitis and COVID-19 is the dysregulation of IL-6. This pro-inflammatory cytokine, which drives the destructive inflammation in peri-implantitis, is also significantly elevated in severe COVID-19, suggesting a common pathway that may exacerbate disease progression.[82,83,84] However, there is no clear and evident correlation between both diseases. According to Kadkhodazadeh et al., the global pandemic caused by COVID-19 may prevent patients from performing their regular peri-implant and periodontal health maintenance, and thus the reinforcement of oral hygiene is recommended to maintain proper oral health during COVID-19 infection.[85]

COVID-19 has been found in the saliva of positive patients.[86] Sorsa et al.[87] suggested that the active metalloproteinase-8 (aMMP-8) point-of-care test can serve as a non-invasive, rapid, real-time tool to identify active peri-implant disease. Elevated aMMP-8 levels (>20 ng/ml) may help recognize peri-implant pathology as a potential risk factor for COVID-19 severity. Given these similarities, further research is needed to explore links between peri-implantitis and COVID-19 severity and infection.

Viral diagnostic advances

Virus diagnosis

Diagnosing viral involvement in periodontal disease has improved with molecular tools such as PCR, RT-PCR, and sequencing, replacing older culture methods. Techniques such as DNA microarrays, multiplex PCR, DNA probes, and immunofluorescence allow detection of viruses like HHV, EBV, and CMV. Metagenomics remains essential to identify previously unknown oral viruses.[88,89]

Advantages of saliva-based diagnostics

Saliva-based diagnostics have emerged as a non-invasive, cost-effective, and scalable alternative to traditional sampling methods. They offer high reliability in detecting viruses such as SARS-CoV-2 using rRT-PCR and rapid antigen tests.[90,91] Saliva collection enhances patient compliance, reduces infection risk to healthcare workers, and supports early disease detection and monitoring of viral load.[90] It also provides insight into the host immune response and disease progression, aiding in the development of personalized care and prognostic tools.[90,91] Despite their advantages, widespread use of saliva-based diagnostics requires standardized collection protocols and further validation of salivary biomarkers.[91]

Saliva-based diagnostics and self-administered testing

During the COVID-19 pandemic, self-administered saliva-based testing proved to be an effective alternative to nasopharyngeal swabs. Studies have shown that saliva, either collected by coughing out or oral swabs, could be a valid specimen for COVID-19 detection.[92,93] While promising for mass screening, these tests may require confirmatory testing due to variability in sensitivity over time.[94] Continued research and technological refinement are crucial for their integration into routine clinical practice.

While saliva-based diagnostics hold promise for non-invasive detection of viral pathogens and have proven valuable in systemic and respiratory infections such as COVID-19, it is important to emphasize that they do not replace subgingival sampling for site-specific periodontal assessment. The subgingival environment has unique microbial and virological characteristics that cannot be fully captured through salivary analysis alone. Therefore, saliva-based diagnostics should be viewed as supportive tools, potentially useful for initial screening, patient monitoring, or adjunctive surveillance, rather than as primary diagnostic methods for periodontal disease.

CONCLUSION

Current evidence indicates that viruses such as HHV, EBV, and CMV may play a contributory role to periodontal disease progression and persist in oral tissues by modulating host immune responses and facilitating bacterial colonization. Saliva-based testing can be utilized for periodontal disease diagnosis and maintenance.

Periodontal treatment protocols may need to be modified when viral involvement is suspected. Clinicians should consider incorporating host-modulation strategies, such as improved plaque control, salivary diagnostics for viral detection, and careful monitoring during maintenance.

Emerging evidence from in vitro and limited clinical studies suggests that adjunctive antiviral therapy (e.g., acyclovir or ganciclovir) may reduce viral loads and improve clinical outcomes, particularly in patients with high-risk profiles or persistent disease. However, these findings are preliminary, and current guidelines do not yet support routine antiviral use in periodontal therapy. Antiviral agents may be considered on a case-by-case basis, especially in immunocompromised patients or when viral persistence is confirmed through diagnostic testing.

Peer review

This article was peer-reviewed by two independent and anonymous reviewers.

Data availability statement

Data sharing is not applicable for this article, as no new data were created or analyzed.

Conflicts of interest

There are no conflicts of interest.

Funding Statement

Nil.