SARS-CoV-2, periodontal pathogens, and host factors: The trinity of oral post-acute sequelae of COVID-19.

COVID-19 as a pan-epidemic is waning but there it is imperative to understand virus interaction with oral tissues and oral inflammatory diseases. We review periodontal disease (PD), a common inflammatory oral disease, as a driver of COVID-19 and oral post-acute-sequelae conditions (PASC). Oral PASC identifies with PD, loss of teeth, dysgeusia, xerostomia, sialolitis-sialolith, and mucositis. We contend that PD-associated oral microbial dysbiosis involving higher burden of periodontopathic bacteria provide an optimal microenvironment for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. These pathogens interact with oral epithelial cells activate molecular or biochemical pathways that promote viral adherence, entry, and persistence in the oral cavity. A repertoire of diverse molecules identifies this relationship including lipids, carbohydrates and enzymes. The S protein of SARS-CoV-2 binds to the ACE2 receptor and is activated by protease activity of host furin or TRMPSS2 that cleave S protein subunits to promote viral entry. However, PD pathogens provide additional enzymatic assistance mimicking furin and augment SARS-CoV-2 adherence by inducing viral entry receptors ACE2/TRMPSS, which are poorly expressed on oral epithelial cells. We discuss the mechanisms involving periodontopathogens and host factors that facilitate SARS-CoV-2 infection and immune resistance resulting in incomplete clearance and risk for 'long-haul' oral health issues characterising PASC. Finally, we suggest potential diagnostic markers and treatment avenues to mitigate oral PASC.

Covid-19 and oral diseases: Crosstalk, synergy or association?

The coronavirus disease 2019 (Covid-19) is a viral infection caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that clinically affects multiple organs of the human body. Cells in the oral cavity express viral entry receptor angiotensin-converting enzyme 2 that allows viral replication and may cause tissue inflammation and destruction. Recent studies have reported that Covid-19 patients present oral manifestations with multiple clinical aspects. In this review, we aim to summarise main signs and symptoms of Covid-19 in the oral cavity, its possible association with oral diseases, and the plausible underlying mechanisms of hyperinflammation reflecting crosstalk between Covid-19 and oral diseases. Ulcers, blisters, necrotising gingivitis, opportunistic coinfections, salivary gland alterations, white and erythematous plaques and gustatory dysfunction were the most reported clinical oral manifestations in patients with Covid-19. In general, the lesions appear concomitant with the loss of smell and taste. Multiple reports show evidences of necrotic/ulcerative gingiva, oral blisters and hypergrowth of opportunistic oral pathogens. SARS-CoV-2 exhibits tropism for endothelial cells and Covid-19-mediated endotheliitis can not only promote inflammation in oral tissues but can also facilitate virus spread. In addition, elevated levels of proinflammatory mediators in patients with Covid-19 and oral infectious disease can impair tissue homeostasis and cause delayed disease resolution. This suggests potential crosstalk of immune-mediated pathways underlying pathogenesis. Interestingly, few reports suggest recurrent herpetic lesions and higher bacterial growth in Covid-19 subjects, indicating SARS-CoV-2 and oral virus/bacteria interaction. Larger cohort studies comparing SARS-CoV-2 negative and positive subjects will reveal oral manifestation of the virus on oral health and its role in exacerbating oral infection.

Detection rates of periodontal bacteria and herpesviruses in different forms of periodontal disease.

The aim was to investigate the detection rates of periodontal bacteria (Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, and Aggregatibacter actinomycetemcomitans) and herpesviruses (herpes simplex virus-1 [HSV-1], cytomegalovirus [CMV], and Epstein-Barr virus [EBV]) in different forms and severity of periodontal disease, and to compare them with those in periodontally healthy subjects. One hundred and twenty-nine patients participated in the study: 39 diagnosed with periodontal abscess (PA), 33 with necrotizing ulcerative periodontitis (NUP), 27 with chronic periodontitis (CP), and 30 participants with healthy periodontal tissue represented a healthy control group. All patients with periodontal disease (PA, NUP, and CP) were also divided into two groups according to the severity of their disease: moderate and severe periodontitis. The subgingival samples were collected from the periodontitis active sites and the detection of microorganisms was performed by end-point polymerase chain reaction analyses. The results revealed significantly higher detection rates of P. gingivalis, T. forsythia, and P. intermedia in all three groups of patients with periodontitis than in healthy participants. The highest detection rate of A. actinomycetemcomitans was noticed in CP, which was significantly higher than that in PA, NUP, and healthy control. The occurrence of EBV was significantly higher in NUP than in CP and healthy participants. CMV was detected significantly more frequently in PA and NUP than in CP and healthy participants. Comparisons among healthy participants and patients with moderate and severe periodontitis showed significantly higher detection rates of EBV and CMV in patients with severe forms of periodontitis than in healthy participants and those with moderate periodontitis.

Is periodontal disease a risk factor for developing severe Covid-19 infection? The potential role of Galectin-3.

IMPACT STATEMENT: There could be a close relationship between periodontal diseases (PDs) severity and Covid-19 infections. This relationship could be caused by Galectin-3-mediated increased immune response and increased viral attachment. Keeping PDs under control and maintaining rigorous oral hygiene during this troubled Covid-19 pandemic period is very important.Patients with older age and pre-existing conditions like cardiovascular disease, hypertension, diabetes, and obesity are in the higher risk group for developing severe Covid-19 infections. The inflammatory pathways that are involved in these conditions are the same pathways that we see in periodontal diseases (PDs). This raises a significant question: Is PD a pre-existing condition that can increase the risk of developing severe Covid-19 infection? Several studies have shown that Galectins play a key role in the homeostasis of immune cells, and recently, a relationship was found between Covid-19 and Galectin-3 (Gal-3).It has been determined that an important area in the spike protein of Coronavirus-19 is almost exactly the same as the morphology of Gal-3, and these spike proteins are critical for the entry of the virus into host cells. We suspect that there is enough evidence to support a close relationship between PDs severity and Covid-19 infections. There is accumulating evidence to suggest a relationship between the severity of PD and the risk of infection with Covid-19, which requires further investigation. This relationship could be caused by Gal-3-mediated increased immune response and increased viral attachment. In this context, we want to emphasize the importance of keeping PD under control by maintaining rigorous oral hygiene during this troubled Covid-19 pandemic period. We would also like to point out the possibility that having PD may be a pre-disposition toward developing a severe Covid-19 infection.

Polymicrobial periodontal disease triggers a wide radius of effect and unique virome.

Periodontal disease is a microbially-mediated inflammatory disease of tooth-supporting tissues that leads to bone and tissue loss around teeth. Although bacterially-mediated mechanisms of alveolar bone destruction have been widely studied, the effects of a polymicrobial infection on the periodontal ligament and microbiome/virome have not been well explored. Therefore, the current investigation introduced a new mouse model of periodontal disease to examine the effects of a polymicrobial infection on periodontal ligament (PDL) properties, changes in bone loss, the host immune response, and the microbiome/virome using shotgun sequencing. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum were used as the polymicrobial oral inoculum in BALB/cByJ mice. The polymicrobial infection triggered significant alveolar bone loss, a heightened antibody response, an elevated cytokine immune response, a significant shift in viral diversity and virome composition, and a widening of the PDL space; the latter two findings have not been previously reported in periodontal disease models. Changes in the PDL space were present at sites far away from the site of insult, indicating that the polymicrobial radius of effect extends beyond the bone loss areas and site of initial infection and wider than previously appreciated. Associations were found between bone loss, specific viral and bacterial species, immune genes, and PDL space changes. These findings may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium. This new polymicrobial mouse model of periodontal disease in a common mouse strain is useful for evaluating the features of periodontal disease.

Herpesvirus-encoded microRNAs detected in human gingiva alter host cell transcriptome and regulate viral infection.

MicroRNAs (miRNAs) are small, non-coding RNAs of ~18-25 nucleotides that have gained extensive attention as critical regulators in complex gene networks including immune cell lineage commitment, differentiation, maturation, and maintenance of immune homeostasis and function. Many viruses encode miRNAs that directly downregulate the expression of factors of the innate immune system, which includes proteins involved in promoting apoptosis and recruitment. In this study, we examined the expression profiles of three previously identified viral miRNAs (v-miRs) from the human herpesvirus (HHV) family, HSV-1 (miR-H1), KSHV (miR-K12-3-3p), and HCMV (miR-US4) in healthy and diseased periodontal tissues and observed increased levels of v-miRs in diseased tissues. To understand the significance of this increase, we overexpressed v-miRs in human oral keratinocytes (HOK), a common target for various HHV, and analyzed the impact of miR-H1 and miR-K12-3-3p on the host transcriptome. More than 1300 genes were altered in HOK overexpressing miR-H1 and miR-K12-3-3p. Global pathway analysis of deregulated genes identified several key cellular pathways that may favor viral persistence. Using bioinformatic analysis, we predicted hundreds of potential v-miR binding sites on genes downregulated by miR-H1 and miR-K12-3-3p and validated three novel target v-miR sites suggesting widespread direct and indirect modulation of numerous host genes/pathways by a single v-miR. Finally, in vitro HSV-1 infection assays showed that miR-H1 can regulate viral entry and infection in human oral keratinocytes (HOK). Overall, our results demonstrate clinical and functional relevance of pathogenic viral molecules viz., v-miRs that regulate both host and viral functions and may contribute to the pathogenesis of inflammatory oral diseases.

Characterization and serotype distribution of Aggregatibacter actinomycetemcomitans: Relationship of serotypes to herpesvirus and periodontal status in Indian subjects.

BACKGROUND: The virulence of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) in any individual depends on the type of strain of this bacterium. To our knowledge, there have been no studies reported in Indian subjects about A. actinomycetemcomitans serotype occurrence, co-existence with herpes virus and the possible influence of such co-existence on periodontal pathology. METHODS: Subjects for this study were a subset of a larger study to identify the prevalence of A. actinomycetemcomitans in chronic periodontitis. A total of 63 subjects (12 periodontally healthy and 51 with chronic periodontitis) who were positive for A. actinomycetemcomitans were serotyped for strain-level identification. The presence of Human Cytomegalovirus (CMV) and Epstein-Barr virus (EBV) was tested in subgingival plaque samples by polymerase chain reaction. RESULTS: All five serotypes a to e were detected. Of the samples analyzed 38.09% harbored a single serotype, 36.5% had two serotypes, 6.3% demonstrated three and 4.7% demonstrated four serotypes. None of the samples showed presence of JP2 strain. Serotypes b, c, and e were most frequently identified in these individuals (46.03%, 36.5% and 38.09% respectively). Presence of serotypes b and c and absence of serotype d was associated with increased PD and CAL. Among 63 samples analyzed, 11 samples had CMV, four samples had EBV and nine samples had both these viruses. The PD and CAL were significantly higher (p = 0.04) when a combination of CMV and one of the serotypes was present indicating a pathological role of the coexistence. CONCLUSION: Multiple serotypes are associated with chronic periodontitis in Indians, however, JP2 strains are not detectable in this cohort. Presence of multiple serotypes and a combination of any serotype with herpesvirus is associated with greater severity of the disease.

Increased expression of CD38 and HLADR in HIV-infected patients with oral lesion.

Persistent immune actiation is associated with innadequate immune recovery in HIV-patients. This study assessed the relationship between frequency of expression of cell activation markers (CD38 and HLADR) and presence of oral lesions in HIV-1 infected patients. Fifty-seven HIV-infected persons, undergoing antiretroviral treatment, were divided into three groups, according to the number of CD4+ T cells and CD4+ /CD8+ ratio: adequate, partial, and inadequate immune restauration. All patients underwent full mouth assessments for saliva flow measurement, oral mucosal lesion, periodontal disease, and severity of periodontitis. Immune activation markers levels were compared according to three groups of periodontal disease ("No periodontal disease," "gingivitis," and "periodontitis"). Oral mucosal lesions (P = 0.03) and peridodontal disease (P = 0.03) were associated with lower CD4+ /CD8+ ratio. Patients with oral mucosal lesions had significantly higher median levels of HLADR and CD38 markers in all T-lymphocytes populations than patients without oral lesions. Patients with gingivitis and with periodontitis presented significantly higher median levels of CD3+ HLADR+ , CD4+ HLADR+ , CD8+ HLADR+ , and CD3+ CD38+ and significantly lower CD4+ /CD8+ ratio than patients with no periodontal disease. Increased levels of HLADR and CD38 expressions in peripheral blood were associated with oral lesions in HIV-positive patients. Periodontal disease was associated with HLADR expression.

The role of bacteriophages in periodontal health and disease.

The human periodontium health is commonly compromised by chronic inflammatory conditions and has become a major public health concern. Dental plaque, the precursor of periodontal disease, is a complex biofilm consisting mainly of bacteria, but also archaea, protozoa, fungi and viruses. Viruses that specifically infect bacteria - bacteriophages - are most common in the oral cavity. Despite this, their role in the progression of periodontal disease remains poorly explored. This review aims to summarize how bacteriophages interact with the oral microbiota, their ability to increase bacterial virulence and mediate the transfer of resistance genes and suggests how bacteriophages can be used as an alternative to the current periodontal disease therapies.

The Burden of Oral Disease among Perinatally HIV-Infected and HIV-Exposed Uninfected Youth.

OBJECTIVE: To compare oral health parameters in perinatally HIV-infected (PHIV) and perinatally HIV-exposed but uninfected youth (PHEU). METHODS: In a cross-sectional substudy within the Pediatric HIV/AIDS Cohort Study, participants were examined for number of decayed teeth (DT), Decayed, Missing, and Filled Teeth (DMFT), oral mucosal disease, and periodontal disease (PD). Covariates for oral health parameters were examined using zero-inflated negative binomial regression and ordinal logistic regression models. RESULTS: Eleven sites enrolled 209 PHIV and 126 PHEU. Higher DT scores were observed in participants who were PHIV [Adjusted Mean Ratio (aMR) = 1.7 (95% CI 1.2-2.5)], female [aMR = 1.4 (1.0-1.9)], had no source of regular dental care [aMR = 2.3 (1.5-3.4)], and had a high frequency of meals/snacks [≥5 /day vs 0-3, aMR = 1.9 (1.1-3.1)] and juice/soda [≥5 /day vs 0-3, aMR = 1.6 (1.1-2.4)]. Higher DMFT scores were observed in participants who were older [≥19, aMR = 1.9 (1.2-2.9)], had biological parent as caregiver [aMR = 1.2 (1.0-1.3)], had a high frequency of juice/soda [≥5 /day vs 0-3, aMR = 1.4 (1.1-1.7)] and a low saliva flow rate [mL/min, aMR = 0.8 per unit higher (0.6-1.0)]. Eighty percent had PD; no differences were seen by HIV status using the patient-based classifications of health, gingivitis or mild, moderate, or severe periodontitis. No associations were observed of CD4 count and viral load with oral health outcomes after adjustment. CONCLUSIONS: Oral health was poor in PHIV and PHEU youth. This was dismaying since most HIV infected children in the U.S. are carefully followed at medical health care clinics. This data underscore the need for regular dental care. As PHIV youth were at higher risk for cavities, it will be important to better understand this relationship in order to develop targeted interventions.

Transcriptome analysis of bacteriophage communities in periodontal health and disease.

BACKGROUND: The role of viruses as members of the human microbiome has gained broader attention with the discovery that human body surfaces are inhabited by sizeable viral communities. The majority of the viruses identified in these communities have been bacteriophages that predate upon cellular microbiota rather than the human host. Phages have the capacity to lyse their hosts or provide them with selective advantages through lysogenic conversion, which could help determine the structure of co-existing bacterial communities. Because conditions such as periodontitis are associated with altered bacterial biota, phage mediated perturbations of bacterial communities have been hypothesized to play a role in promoting periodontal disease. Oral phage communities also differ significantly between periodontal health and disease, but the gene expression of oral phage communities has not been previously examined. RESULTS: Here, we provide the first report of gene expression profiles from the oral bacteriophage community using RNA sequencing, and find that oral phages are more highly expressed in subjects with relative periodontal health. While lysins were highly expressed, the high proportion of integrases expressed suggests that prophages may account for a considerable proportion of oral phage gene expression. Many of the transcriptome reads matched phages found in the oral cavities of the subjects studied, indicating that phages may account for a substantial proportion of oral gene expression. Reads homologous to siphoviruses that infect Firmicutes were amongst the most prevalent transcriptome reads identified in both periodontal health and disease. Some genes from the phage lytic module were significantly more highly expressed in subjects with periodontal disease, suggesting that periodontitis may favor the expression of some lytic phages. CONCLUSIONS: As we explore the contributions of viruses to the human microbiome, the data presented here suggest varying expression of bacteriophage communities in oral health and disease.

Altered oral viral ecology in association with periodontal disease.

UNLABELLED: The human oral cavity is home to a large and diverse community of viruses that have yet to be characterized in patients with periodontal disease. We recruited and sampled saliva and oral biofilm from a cohort of humans either periodontally healthy or with mild or significant periodontal disease to discern whether there are differences in viral communities that reflect their oral health status. We found communities of viruses inhabiting saliva and the subgingival and supragingival biofilms of each subject that were composed largely of bacteriophage. While there were homologous viruses common to different subjects and biogeographic sites, for most of the subjects, virome compositions were significantly associated with the oral sites from which they were derived. The largest distinctions between virome compositions were found when comparing the subgingival and supragingival biofilms to those of planktonic saliva. Differences in virome composition were significantly associated with oral health status for both subgingival and supragingival biofilm viruses but not for salivary viruses. Among the differences identified in virome compositions was a significant expansion of myoviruses in subgingival biofilm, suggesting that periodontal disease favors lytic phage. We also characterized the bacterial communities in each subject at each biogeographic site by using the V3 hypervariable segment of the 16S rRNA and did not identify distinctions between oral health and disease similar to those found in viral communities. The significantly altered ecology of viruses of oral biofilm in subjects with periodontal disease compared to that of relatively periodontally healthy ones suggests that viruses may serve as useful indicators of oral health status. IMPORTANCE: Little is known about the role or the constituents of viruses as members of the human microbiome. We investigated the composition of human oral viral communities in a group of relatively periodontally healthy subjects or significant periodontitis to determine whether health status may be associated with differences in viruses. We found that most of the viruses present were predators of bacteria. The viruses inhabiting dental plaque were significantly different on the basis of oral health status, while those present in saliva were not. Dental plaque viruses in periodontitis were predicted to be significantly more likely to kill their bacterial hosts than those found in healthy mouths. Because oral diseases such as periodontitis have been shown to have altered bacterial communities, we believe that viruses and their role as drivers of ecosystem diversity are important contributors to the human oral microbiome in health and disease states.

Viruses: are they really culprits for periodontal disease? A critical review.

Periodontal diseases are multifactorial, and many etiological agents are suggested to play a role in their etiopathogenesis. Various risk factors are also suggested to influence the progression of periodontal disease. Until recently, specific bacteria were considered the major pathogens for the disease. However, the occurrence of periodontal disease in some patient groups is still poorly understood, and the role of other initiating agents is being investigated. Evidence strongly suggests the presence of many strains of viruses in the periodontal environment, and possible mechanisms have also been suggested. Periodontal disease as a risk factor for other systemic diseases can also be better explained based on this viral etiology. In this review, we critically analyze the role of viruses in different periodontal diseases, and provide a categorical description of the underlying mechanisms. Clinical implications and future directions are also discussed. Evidence of a causal role of herpes viruses in periodontitis might revolutionize existing strategies to diagnose, prevent, and treat the disease.

Lessons learned and unlearned in periodontal microbiology.

Periodontal diseases are initiated by bacterial species living in polymicrobial biofilms at or below the gingival margin and progress largely as a result of the inflammation elicited by specific subgingival species. In the past few decades, efforts to understand the periodontal microbiota have led to an exponential increase in information about biofilms associated with periodontal health and disease. In fact, the oral microbiota is one of the best-characterized microbiomes that colonize the human body. Despite this increased knowledge, one has to ask if our fundamental concepts of the etiology and pathogenesis of periodontal diseases have really changed. In this article we will review how our comprehension of the structure and function of the subgingival microbiota has evolved over the years in search of lessons learned and unlearned in periodontal microbiology. More specifically, this review focuses on: (i) how the data obtained through molecular techniques have impacted our knowledge of the etiology of periodontal infections; (ii) the potential role of viruses in the etiopathogenesis of periodontal diseases; (iii) how concepts of microbial ecology have expanded our understanding of host-microbe interactions that might lead to periodontal diseases; (iv) the role of inflammation in the pathogenesis of periodontal diseases; and (v) the impact of these evolving concepts on therapeutic and preventive strategies to periodontal infections. We will conclude by reviewing how novel systems-biology approaches promise to unravel new details of the pathogenesis of periodontal diseases and hopefully lead to a better understanding of their mechanisms.

Oral conditions and their social impact among HIV dental patients, 18 years on.

BACKGROUND: A study undertaken in 1992-1993 identified that HIV-infected dental patients were substantially disadvantaged with regard to the social impact of their oral disease. The oral pain experienced by HIV-positive patients prior to the introduction of combination antiretroviral therapy (cART) was attributable to specific features of HIV-related periodontal disease and other oral manifestations of HIV such as candida infections and xerostomia. A repeat of this study in 2009-2010 provided additional information in the post-cART era. METHODS: Data were collected from three sources: the 2009-2010 HIV-positive sample, the National Survey of Adult Oral Health (NSAOH) and the original 1992-1993 study. Collation of data was by clinical and radiographic oral examination. Information about the social impact of oral conditions was obtained from the Oral Health Impact Profile. RESULTS: The caries experience of the 2009-2010 HIV-positive sample was improved with statistical significance for both mean DMFT and mean DT, while the presence of HIV-related periodontal disease still occurs. Statistically significant improvements were achieved for prevalence and severity of oral health related quality of life. CONCLUSIONS: The need for timely access to oral health care with a focus on prevention is essential for HIV-positive individuals whose health is impacted by chronic disease, smoking and salivary hypofunction.

Oral health profile in patients infected with HTLV-1: clinical findings, proviral load, and molecular analysis from HTLV-1 in saliva.

Human T-lymphotropic virus type 1 (HTLV-1) is associated with adult T-cell leukemia (ATL) and HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) and has also been implicated in several disorders, including periodontal disease. The proviral load is an important biological marker for understanding HTLV-1 pathogenesis and elucidating whether or not the virus is related to the clinical manifestation of the disease. This study describes the oral health profile of HTLV-1 carriers and HAM/TSP patients in order to investigate the association between the proviral load in saliva and the severity of the periodontal disease and to examine virus intra-host variations from peripheral blood mononuclear cells and saliva cells. It is a cross-sectional analytical study of 90 individuals carried out from November 2006 to May 2008. Of the patients, 60 were HTLV-1 positive and 30 were negative. Individuals from the HTLV-1 positive and negative groups had similar mean age and social-economic status. Data were analyzed using two available statistical software packages, STATA 8.0 and SPSS 11.0 to conduct frequency analysis. Differences of P < 0.05 were considered statistically significant. HTLV-1 patients had poorer oral health status when compared to seronegative individuals. A weak positive correlation between blood and saliva proviral loads was observed. The mean values of proviral load in blood and saliva in patients with HAM/TSP was greater than those in HTLV-1 carriers. The HTLV-1 molecular analysis from PBMC and saliva specimens suggests that HTLV-1 in saliva is due to lymphocyte infiltration from peripheral blood. A direct relationship between the proviral load in saliva and oral manifestations was observed.

HIV shedding in the oral cavity: an assessment of HIV type, immunovirologic, demographic and oral factors.

OBJECTIVE: To quantify the prevalence and burden of HIV type 2 (HIV-2) and HIV-1 RNA in the oral cavity of antiretroviral therapy-naive HIV-infected Senegalese individuals and to identify correlates of oral HIV viral loads. DESIGN: A cross-sectional study of 163 HIV-1 and 27 HIV-2-infected antiretroviral therapy-naive Senegalese adults. METHODS: Participants received clinical and oral exams and provided blood and oral wash samples for viral load and plasma CD4 count ascertainment. Logistic and interval regression models were used to identify univariate and multivariable associations between presence and level of oral HIV RNA and various immunovirologic, local and demographic factors. RESULTS: Presence of detectable oral HIV RNA was less common in HIV-2-infected compared with HIV-1-infected study participants (33% vs 67%, OR 0.25, 95% CI 0.11 to 0.59). HIV type was no longer associated with oral shedding of HIV when plasma viral load was considered. Detection of oral HIV RNA was associated with increased plasma viral load in both HIV-1-infected and HIV-2-infected individuals (HIV-1, OR 1.89, 95% CI 1.24 to 2.61; HIV-2, OR 1.93, 95% CI 1.1 to 3.39). Oral HIV-1 detection was also associated with periodontal disease (OR 3.02, 95% CI 1.16 to 7.87). CONCLUSIONS: Oral shedding of HIV-2 RNA is less common than HIV-1 RNA, a likely consequence of lower overall viral burden. Both systemic and local factors may contribute to shedding of HIV in the oral cavity.

The role of cytomegalovirus infection in the pathogenesis of periodontal diseases.

The main characteristic ofperiodontal disease is chronic inflammation that leads to progressive destruction of the connective tissues and bone with subsequent tooth mobility and finally tooth loss. Traditionally, the pathogenesis of periodontitis was based on the infection caused by bacteria that colonize tooth surface and gingival sulcus. Accumulated evidence show that host response factors such as inflammatory reaction and activation of the innate immune system are critical to the pathogenesis of periodontal disease. Periodontal disease has been widely recognized as a chronic disease but the nature of chronicity remains unclear. The question is whether periodontal disease is a continuous process or consists of episodes of exacerbations and remissions. Maybe cytomegalovirus infection of the periodontium, depending on the latent or active phase of infection, can partly explain the episodic progressive nature of periodontal disease. Cytomegalovirus infection impairs periodontal defense and permits overgrowth of periodontopathogenic bacteria. Owing to advances in new technologies, experimental evidence show the influence and interrelatedness of genomic, epigenetic, proteomic and metabolic factors in the pathogenesis of periodontal disease. Data on the pathogenesis of periodontal disease are reviewed.

Impact of Chikungunya virus infection on oral health status: an observational study.

BACKGROUND AND OBJECTIVE: Chikungunya fever outbreak started in December 2005 in India when the country experienced more than 13 lakhs of Chikungunya infected cases. We undertook this study to describe the impact of Chikungunya virus infection on oral health. MATERIALS AND METHODS: The confirmed seropositive patients were included for the study (N = 97). Oral hygiene index simplified, gingival index, plaque index were recorded. RESULTS: Of the 181 tested, 97 were confirmed seropositive for chikungunya infection. Pain and bleeding gums were seen in 55% of the subjects. Of them, 29.1% had poor oral hygiene, 42.27% had severe gingivitis, and 27.84% had severe plaque deposits. Severe gingivitis was observed in patients with chronic disease, this association was statistically significant (χ2 = 6.417, P = 0.040). CONCLUSION: Our findings showed that about more than half of the tested patients suffered severe pain and bleeding in the oral cavity thereby causing discomfort in chewing. About 1/3 patients had severe gingivitis and foul breath which caused discomfort in carrying out their day-to-day activities.