Subgingival Environment Research Articles

Efficacy of Locally Delivered Herbal Chip Containing (8% Mimusops elengi) as an Adjunct to Scaling and Root Planing in Chronic Periodontitis: A Randomised Split-mouth Clinical Study

Introduction: Conventional mechanical debridement does not remove all pathogenic bacteria from the subgingival environment. To overcome these limitations, local drug delivery systems enhance the curative effect by combining with drugs, which promote bone and tissue regeneration. Thus, this study aims to evaluate the efficacy of locally delivered herbal chips containing (8% Mimusops elengi) as an adjunct to scaling and root planing (SRP) and compared to SRP alone for the treatment of chronic periodontitis. Materials and Methods: A randomised split-mouth clinical study was conducted among chronic periodontitis patients undergoing periodontal therapy. Thirty subjects with 60 sites were divided into test and control groups. The control sites were treated with SRP alone, whereas the test sites were treated with SRP followed by placement of an 8% M. elengi herbal chip within the pockets. Patients were recalled on the 21st and 45th day, and clinical parameters were measured. Results: An inter-group comparison of all the clinical parameters between the control and test sides was statistically analysed. At all periods of the study, the mean difference was observed to be highly significant (P < 0.001). Conclusion: The 8% M. elengi chip is effective as an adjunct to non-surgical periodontal therapy in chronic periodontitis probing depth. Further clinical studies are needed to evaluate the long-term efficacy of M. elengi.

Characterization of c-di-AMP signaling in the periodontal pathobiont, Treponema denticola.

Pathobionts associated with periodontitis, such as Treponema denticola, must possess numerous sensory transduction systems to adapt to the highly dynamic subgingival environment. To date, the signaling pathways utilized by T. denticola to rapidly sense and respond to environmental stimuli are mainly unknown. Bis-(3'-5') cyclic diadenosine monophosphate (c-di-AMP) is a nucleotide secondary messenger that regulates osmolyte transport, central metabolism, biofilm development, and pathogenicity in many bacteria but is uncharacterized in T. denticola. Here, we studied c-di-AMP signaling in T. denticola to understand how it contributes to T. denticola physiology. We demonstrated that T. denticola produces c-di-AMP and identified enzymes that function in the synthesis (TDE1909) and hydrolysis (TDE0027) of c-di-AMP. To investigate how c-di-AMP may impact T. denticola cellular processes, a screening assay was performed to identify putative c-di-AMP receptor proteins. This approach identified TDE0087, annotated as a potassium uptake protein, as the first T. denticola c-di-AMP binding protein. As potassium homeostasis is critical for maintaining turgor pressure, we demonstrated that T. denticola c-di-AMP concentrations are impacted by osmolarity, suggesting that c-di-AMP negatively regulates potassium uptake in hypoosmotic solutions. Collectively, this study demonstrates T. denticola utilizes c-di-AMP signaling, identifies c-di-AMP metabolism proteins, identifies putative receptor proteins, and correlates c-di-AMP signaling to osmoregulation.

Subgingival Plaque as a Potential Reservoir for SARS-CoV-2 Virus in Patients Recovered from COVID-19 Infection: A Cross-sectional Study

Background Subgingival plaque biofilm is a potential harboring site for bacteria and viruses, serving as a source of entry into the bloodstream. The presence of Severe Acute Respiratory Syndrome Coronavirus 2 RNA (SARS-CoV-2 RNA) in subgingival plaque could be a possible source for cross infection due to aerosol contamination during dental procedures. Objectives The objective of this study was to investigate the presence of SARS-CoV-2 RNA in the subgingival plaque biofilm of patients who recovered from COVID-19 infection. Materials and Methods Ten subjects visiting the Outpatient clinic with a previous history of COVID-19 infection were recruited for this cross-sectional study. Subgingival plaque sample was collected from all four quadrants using a sterile curette. Nasopharyngeal and oropharyngeal swabs were taken from all the subjects. Reverse transcriptase real-time qualitative polymerase chain reaction (RT-PCR) was used to determine the presence of SARS-CoV-2 RNA using BAG SARS-CoV-2 RT-PCR kit targeting E gene, RdRp gene, and internal control. Results Ten participants (seven females and three males) with a previous history of COVID-19 infection were included in the study. Six participants previously presented with mild COVID-19 infection (uncomplicated upper respiratory tract infection, mild fever, cough, sore throat, nasal congestion, malaise, headache, without evidence of breathlessness or hypoxia), and four participants previously presented with moderate COVID-19 infection (dyspnea and or hypoxia, fever, cough, SpO2 90%–94% on room air, respiratory rate more or equal to 24 per minute) according to clinical management protocol for COVID-19, Government of India. The nasopharyngeal, oropharyngeal, and subgingival plaque samples tested negative for SARS-CoV-2 RNA. Conclusion The absence of the SARS-CoV-2 virus in the subgingival plaque sample of patients recovered from COVID-19 infection suggests that dental plaque could not be a potential reservoir of the virus. However, clinicians should take at most precautions while treating the patients recovered from COVID-19 infection and should anticipate a change in subgingival environment leading to alteration in periodontal disease progression.

Modulatory Mechanisms of Pathogenicity in Porphyromonas gingivalis and Other Periodontal Pathobionts.

The pathogenesis of periodontitis depends on a sustained feedback loop where bacterial virulence factors and immune responses both contribute to inflammation and tissue degradation. Periodontitis is a multifactorial disease that is associated with a pathogenic shift in the oral microbiome. Within this shift, low-abundance Gram-negative anaerobic pathobionts transition from harmless colonisers of the subgingival environment to a virulent state that drives evasion and subversion of innate and adaptive immune responses. This, in turn, drives the progression of inflammatory disease and the destruction of tooth-supporting structures. From an evolutionary perspective, bacteria have developed this phenotypic plasticity in order to respond and adapt to environmental stimuli or external stressors. This review summarises the available knowledge of genetic, transcriptional, and post-translational mechanisms which mediate the commensal-pathogen transition of periodontal bacteria. The review will focus primarily on Porphyromonas gingivalis.

Macrophages in periodontitis: A dynamic shift between tissue destruction and repair.

Periodontitis is a chronic inflammatory disease associated with a dysbiotic bacterial biofilm in the subgingival environment that may disturb the balance between the oral microbiome and its host. The inability of the immune system to eliminate inflammation may result in the progressive destruction of tooth-support tissues. Macrophages are crucial cellular components of the innate immune system and play important roles in diverse physiological and pathological processes. In response to periodontitis-associated bacterial communities, macrophages contribute to inflammation and restoration of tissue homeostasis through pattern recognition receptor-induced signaling cascades; therefore, targeting macrophages can be a feasible strategy to treat patients with periodontitis. Although recent studies indicate that macrophages have a spectrum of activation states, ranging from pro-inflammatory to anti-inflammatory, the regulatory mechanism of the macrophage response to dysbiosis in a tissue-specific manner remains largely unclear. Herein, we attempt to summarize the potential role of macrophage activation in the progression of periodontitis, as well as its relevance to future approaches in the treatment of periodontitis.

Lipopolysaccharide-Preconditioned Dental Follicle Stem Cells Derived Small Extracellular Vesicles Treating Periodontitis via Reactive Oxygen Species/Mitogen-Activated Protein Kinase Signaling-Mediated Antioxidant Effect.

PurposeLipopolysaccharide (LPS) pretreatment can enhance the therapeutic effect of dental follicle stem cells-derived small extracellular vesicles (DFC-sEV) for periodontitis, and this study aimed to investigate the underlying mechanisms and clinical application Of LPS-preconditioned DFC-sEV in periodontitis.MethodsThe protein spectrum of DFC-sEV before and after LPS pretreatment was determined by liquid chromatography-tandem mass spectrometry and bioinformatic analysis. Their effects on inflammatory periodontal ligament stem cells (PDLSCs) and macrophages were investigated for cell proliferation, migration, type 2 macrophage (M2) polarization, and intracellular reactive oxygen species (ROS) levels separately. In addition, the regulation of ROS/Jun amino-terminal kinases (JNK) and ROS/extracellular signal-related kinases (ERK) signaling by LPS-preconditioned DFC-sEV was also studied to reveal the antioxidant mechanism. In vivo, two kinds of DFC-sEV loaded with 0.2% hyaluronic acid (HA) gel were applied for canine periodontitis to evaluate the therapeutic potential.ResultsThe proteomic analysis showed that thirty-eight proteins were differentially expressed in LPS-preconditioned DFC-sEV, and interestingly, the highly expressed proteins were mainly involved in antioxidant and enzyme-regulating activities. In addition to promoting PDLSCs and macrophage proliferation, LPS-preconditioned DFC-sEV inhibited intracellular ROS as an antioxidant. It reduced the RANKL/OPG ratio of PDLSCs by inhibiting ROS/JNK signaling under inflammatory conditions and promoted macrophages to polarize toward the M2 phenotype via ROS/ERK signaling. Furthermore, LPS-preconditioned DFC-sEV loaded with the HA injectable system could sustainably release sEV and enhance the therapeutic efficacy for periodontitis in canines.ConclusionLPS-preconditioned DFC-sEV could be effectively used as an auxiliary method for periodontitis treatment via antioxidant effects in a subgingival environment, and loading it with HA is feasible and effective for clinical applications.

A Comprehensive Review on Role of Viruses in Gingival and Periodontal Diseases

It is an already established fact that periodontal disease is principally caused by specific group of bacterial pathogens. The red complex of bacterial species plays an important role in periodontal disease progression. However, the 20th century marked an important turning point in the etiopathogenesis of periodontal disease. It was found that viruses can modify the host response as well as the pathogenesis by which bacteria affects the periodontium. This alteration in the pathogenesis of periodontopathic bacteria and the altered host immune response by the virus leads to periodontal disease progression. Over the years, various viruses have been associated with periodontal disease. In particular, the Herpesvirus species, human immunodeficiency virus and human papillomavirus has been widely researched. Moreover, the Epstein–Barr virus and human Cytomegalovirus co-exist in the subgingival environment along with the periodontal pathogens. The synergism among the bacteria and virus is a prime factor for severe periodontal breakdown. The present review article provides comprehensive information on the pathogenesis by which the viruses cause periodontal disease progression.

C3 Targeted Complement Therapy for Chronic Periodontitis - A Scoping Review.

Chronic Periodontitis (CP) is a complex disease initiated by inflammation caused by dysbiotic bacterial communities in the subgingival environment. The Porphyromonas gingivalis, a keystone pathogen at low colonization, causes immune subversion of complement component C5aR, leading to complement C3-dependent destructive inflammation responsible for the inflammatory bone loss in CP. Animal studies have shown that targeting complement C3 with its inhibitor like AMY-101 may help reduce inflammatory bone loss in CP. This scoping review elaborates on the role of complement C3 targeted therapy for CP. About 66 original studies were obtained during an initial electronic search in Medline (Pubmed), Scopus, Web of Science, and Embase. About four articles were included in the review after screening the duplicates and reading the full text. Their aims and objectives, drug dosage, route of administration, results, and conclusions were recorded. Of the four-original research, 3 were animal studies and one randomized Phase IIa clinical trial. They showed that C3 targeted complement therapy reduced the inflammatory and clinical periodontal parameters in CP. C3 targeted complement therapy may be regarded as a valuable adjunct to non-surgical periodontal treatment for CP. However, the results are still under investigation and require further verification through clinical trials.

Comparative evaluation of subgingival microbiome in healthy periodontium and gingivitis using next-generation sequencing technology: A case-control study.

Background:Human dental plaque is a complex microbial community containing millions of species. Gingivitis is a dysregulated immune-inflammatory response induced by dysbiotic plaque biofilm that interrupts symbiosis. The emergence of next-generation sequencing with 16S rRNA gene has greatly contributed in understanding the complexity of microbiota. However, studies focusing on microbiome in gingivitis are limited. The whole bacterial community is important in causing periodontal disease than a small number of periodontal pathogens. In this study, we attempted to profile the subgingival microbiome from individuals with healthy gingiva and in patients with gingivitis using next-generation sequencing technology.Materials and Methods:Subgingival plaque samples from 15 healthy periodontium (Group I) and 15 gingivitis (Group II) were collected and 16s rRNA sequencing was done in Illumina Solexa Sequencer. Data analysis using 16s metagenomics tool from BaseSpace onsite operational taxonomic units was assigned to each sequence using HOMD database. Individual variation in the microbiome of the subgingival samples between the two groups was also evaluated.Results:The comparison of top 20 species between Group I and Group II revealed no significant species group between them. Synergistetes was absent in Group I samples but found in Group II. At the genus level, HACEK group species were found in both the groups, while Dialister and Aneroglobus were found abundantly in the Group II.Conclusion:The presence of unique genera and species seen in Group II samples could point toward a dysbiotic shift that could be taking place in the subgingival environment leading to gingivitis.

Self-perceived halitosis among young adults undergoing orthodontic treatment.

Halitosis is a common oral health problem that significantly impacts the quality of life of the affected individuals. In most cases, poor oral hygiene is responsible for the problem. Orthodontic therapy aims to correct malocclusion using different devices. It has been suggested that orthodontic treatment can promote gingival health by facilitating daily oral hygiene measures. However, the treatment may harm gingival health as these appliances may lead to a more significant accumulation of plaque, increasing the microbial load in the subgingival environment leading to halitosis. The primary goal of this survey is to assess the prevalence of self-perceived halitosis in patients undergoing orthodontic treatment. An online questionnaire was randomly distributed to patients undergoing orthodontic treatment. A total of 289subjects completed the questionnaire. It included questions about: demographic data, medical history, social habits, past dental treatment and oral hygiene habits. Descriptive statistics as frequency distributions and percentages were calculated for the study variables. The prevalence of self-perceived halitosis was 41.5%. The majority of the participants started to notice this problem during and after orthodontic treatment (62.5%). A statistically significant correlation was found between the regular dental visits and halitosis in patients with fixed orthodontic appliances (p-value=0.010). Also, those patients had a substantial increase in tongue coating formation (p- value=0.010). Self-perceived halitosis is a common problem in patients receiving orthodontic treatment.

Periodontal bacterial species and target serotypes in individuals harboring Aggregatibacter actinomycetemcomitans: a retrospective study in a large Brazilian population

OBJECTIVE: The first aim of this study was to evaluate the prevalence of A. actinomycetemcomitans in a large Brazilian population. The second aim was to analyse the frequency of A. actinomycetemcomitans serotypes, P. gingivalis, P. intermedia, T. forsythia and C. rectus in the positive individuals for A. actinomycetemcomitans. MATERIAL AND METHODS: The population was composed of 1,320 individuals. Subgingival biofilm samples were taken for molecular analysis. RESULTS: It was revealed that 263 (19.9%) individuals tested positive for A. actinomycetemcomitans. Then, the genomic DNA of A. actinomycetemcomitans serotypes (a to f ) as well as P. gingivalis, P. intermedia, T. forsythia, and C. rectus were analysed. A. actinomycetemcomitans serotype a was detected in 28.5%, serotype b in 15.97%, serotype c in 51.71%, and serotype e in 3.80% of individuals, respectively. Serotypes d and f were not detected. The frequency of A. actinomycetemcomitans serotype a was significantly higher in C. rectus-positive individuals than in P. gingivalis-, P. intermedia-, or T. forsythia-positive individuals. Additionally, the frequency of serotypes b and c were significantly higher in both C. rectus- and T. forsythia-positive individuals in comparison to P. gingivalis- and P. intermedia-positive individuals. Meanwhile, the frequency of serotype e was not associated with the presence of the other periodontal pathogens. CONCLUSION: The data of this large population confirmed A. actinomycetemcomitans prevalence values previously observed in smaller groups. Further, suggested potential coaggregation among selected A. actinomycetemcomitans serotypes and other target periodontal bacterial species in the subgingival environment.

The Loop-Mediated Isothermal Amplification Technique in Periodontal Diagnostics: A Systematic Review.

The course of periodontal disease is affected by many factors; however, the most significant are the dysbiotic microflora, showing different pathogenicity levels. Rapid colonization in the subgingival environment can radically change the clinical state of the periodontium. This systematic review aims to present an innovative technique of loop-mediated isothermal amplification for rapid panel identification of bacteria in periodontal diseases. The decisive advantage of the loop-mediated isothermal amplification (LAMP) technique in relation to molecular methods based on the identification of nucleic acids (such as polymerase chain reaction (PCR or qPCR) is the ability to determine more pathogens simultaneously, as well as with higher sensitivity. In comparison with classical microbiological seeding techniques, the use of the LAMP method shortens a few days waiting time to a few minutes, reducing the time necessary to identify the species and determine the number of microorganisms. The LAMP technology requires only a small hardware base; hence it is possible to use it in outpatient settings. The developed technique provides the possibility of almost immediate assessment of periodontal status and, above all, risk assessment of complications during the treatment (uncontrolled spread of inflammation), which can certainly be of key importance in clinical work.

The role of inflammation and genetics in periodontal disease.

Periodontitis is a complex disease: (a) various causative factors play a role simultaneously and interact with each other; and (b) the disease is episodic in nature, and bursts of disease activity can be recognized, ie, the disease develops and cycles in a nonlinear fashion. We recognize that various causative factors determine the immune blueprint and, consequently, the immune fitness of a subject. Normally, the host lives in a state of homeostasis or symbiosis with the oral microbiome; however, disturbances in homeostatic balance can occur, because of an aberrant host response (inherited and/or acquired during life). This imbalance results from hyper‐ or hyporesponsiveness and/or lack of sufficient resolution of inflammation, which in turn is responsible for much of the disease destruction seen in periodontitis. The control of this destruction by anti‐inflammatory processes and proresolution processes limits the destruction to the tissues surrounding the teeth. The local inflammatory processes can also become systemic, which in turn affect organs such as the heart. Gingival inflammation also elicits changes in the ecology of the subgingival environment providing optimal conditions for the outgrowth of gram‐negative, anaerobic species, which become pathobionts and can propagate periodontal inflammation and can further negatively impact immune fitness. The factors that determine immune fitness are often the same factors that determine the response to the resident biofilm, and are clustered as follows: (a) genetic and epigenetic factors; (b) lifestyle factors, such as smoking, diet, and psychosocial conditions; (c) comorbidities, such as diabetes; and (d) local and dental factors, as well as randomly determined factors (stochasticity). Of critical importance are the pathobionts in a dysbiotic biofilm that drive the viscious cycle. Focusing on genetic factors, currently variants in at least 65 genes have been suggested as being associated with periodontitis based on genome‐wide association studies and candidate gene case control studies. These studies have found pleiotropy between periodontitis and cardiovascular diseases. Most of these studies point to potential pathways in the pathogenesis of periodontal disease. Also, most contribute to a small portion of the total risk profile of periodontitis, often limited to specific racial and ethnic groups. To date, 4 genetic loci are shared between atherosclerotic cardiovascular diseases and periodontitis, ie, CDKN2B‐AS1(ANRIL), a conserved noncoding element within CAMTA1 upstream of VAMP3, PLG, and a haplotype block at the VAMP 8 locus. The shared genes suggest that periodontitis is not causally related to atherosclerotic diseases, but rather both conditions are sequelae of similar (the same?) aberrant inflammatory pathways. In addition to variations in genomic sequences, epigenetic modifications of DNA can affect the genetic blueprint of the host responses. This emerging field will yield new valuable information about susceptibility to periodontitis and subsequent persisting inflammatory reactions in periodontitis. Further studies are required to verify and expand our knowledge base before final cause and effect conclusions about the role of inflammation and genetic factors in periodontitis can be made.

Biofilm Formation on Dental Implant Surface Treated by Implantoplasty: An In Situ Study.

Peri-implantitis is a biofilm-related disease whose characteristics are peri-implant tissues inflammation and bone resorption. Some clinical trials report beneficial effects after implantoplasty, namely the surgical smoothening of the implant surface, but there is a lack of data about the development of the bacterial biofilm on those smoothened surfaces. The aim of this study is to evaluate how implantoplasty influences biofilm formation. Three implants with moderately rough surfaces (control) and three implants treated with implantoplasty (test) were set on a tray reproducing the supra- and sub-gingival environment. One volunteer wore this tray for five days. Every 24 h, plaque coverage was measured and, at the end of the period of observartion, the implant surfaces were analyzed using scanning electron microscopy and confocal laser scanning microscopy. The proportion of implant surface covered with plaque was 65% (SD = 7.07) of the control implants and 16% (SD = 0) of the test implants. Untreated surfaces showed mature, complex biofilm structures with wide morphological diversity, and treated surfaces did not show the formation of mature biofilm structures. This study supports the efficacy of implantoplasty in reducing plaque adhesion and influencing biofilm formation. These results can be considered a preliminary proof of concept, but they may encourage further studies about the effects of implantoplasty on biofilm formation.

Porphyromonas gingivalis: Immune subversion activities and role in periodontal dysbiosis.

This review summarizes mechanisms by which Porphyromonas gingivalis interacts with community members and the host so that it can persist in the periodontium under inflammatory conditions that drive periodontal disease. Recent advances indicate that, in great part, the pathogenicity of P. gingivalis is dependent upon its ability to establish residence in the subgingival environment and to subvert innate immunity in a manner that uncouples the nutritionally favorable (for the bacteria) inflammatory response from antimicrobial pathways. While the initial establishment of P. gingivalis is dependent upon interactions with early colonizing bacteria, the immune subversion strategies of P. gingivalis in turn benefit co-habiting species. Specific interspecies interactions and subversion of the host response contribute to the emergence and persistence of dysbiotic communities and are thus targets of therapeutic approaches for the treatment of periodontitis.

Awareness of Periodontal Medicine among Medical Students at a Tertiary Care Center

Introduction: Tissue destruction of supporting periodontal tissues is mediated by an overreactive immune inflammatory response to bacteria in the subgingival environment. Tissue destruction in periodontitis occurs by the stimulatory action of pro inflammatory cytokines and proteolytic enzymes released by neutrophils, macrophages, and the action of bone resorption mediators, all of which are being regulated by B and T cells. Periodontitis act as a focus of infection and bacteria metastases through blood stream to various vital organs like heart, lungs, joints and amniotic fluid.
 Objective: To assess the awareness of periodontal medicine among medical students at a tertiary care center in Kathmandu.
 Methods: A total of 115 subjects were taken for the present study. Data was collected using a questionnaire which included questions used to assess the knowledge about periodontal diseases and its possible effects on systemic conditions.
 Results: Out of the total participants, 58 (50.4%) said that periodontal disease was not related to coronary heart diseases. Only 14 (12.2%) had an idea about the association of pre-term birth and periodontitis. While 86 (74.8%) knew the impact of diabetes on periodontium, only 34 (29.6%) said that there was an association between periodontitis and hospital acquired pneumonia.
 Conclusion: Knowledge about the association of periodontal disease with various systemic conditions is not satisfactory among the various medical students of this hospital.

Enrichment of periodontal pathogens from the biofilms of healthy adults

Periodontitis is associated with shifts in the balance of the subgingival microbiome. Many species that predominate in disease have not been isolated from healthy sites, raising questions as to the origin of these putative pathogens. The study aim was to determine whether periodontal pathogens could be enriched from pooled saliva, plaque and tongue samples from dentally-healthy adult volunteers using growth media that simulate nutritional aspects of the inflamed subgingival environment. The microbiome was characterised before and after enrichment using established metagenomic approaches, and the data analysed bioinformatically to identify major functional changes. After three weeks, there was a shift from an inoculum in which Streptococcus, Haemophilus, Neisseria, Veillonella and Prevotella species predominated to biofilms comprising an increased abundance of taxa implicated in periodontitis, including Porphyromonas gingivalis, Fretibacterium fastidiosum, Filifactor alocis, Tannerella forsythia, and several Peptostreptococcus and Treponema spp., with concomitant decreases in health-associated species. Sixty-four species were present after enrichment that were undetectable in the inoculum, including Jonquetella anthropi, Desulfovibrio desulfuricans and Dialister invisus. These studies support the Ecological Plaque Hypothesis, providing evidence that putative periodontopathogens are present in health at low levels, but changes to the subgingival nutritional environment increase their competitiveness and drive deleterious changes to biofilm composition.

OmpA-Like Proteins of Porphyromonas gingivalis Mediate Resistance to the Antimicrobial Peptide LL-37.

Subgingival bacteria are continually exposed to gingival crevicular fluids that are derived from serum, which contain various bactericidal agents. The periodontopathic bacterium Porphyromonas gingivalis has been demonstrated to possess a variety of abilities to resist bactericidal agents, due to which it is able to propagate in the subgingival environment. We previously demonstrated that the major surface glycoproteins of P. gingivalis—Pgm6 and Pgm7, also called outer membrane protein A-like proteins (OmpALPs)—mediate resistance to the bactericidal activity of human serum, but their precise role remains unknown. In this study, we investigated the sensitivity of the wild-type and Pgm6/Pgm7-deficient P. gingivalis strains toward major antimicrobial peptides in the oral cavity, human β-defensins (hBDs) 1-3, and human cathelicidin LL-37. hBDs showed a considerably weak bactericidal activity against both bacterial strains. LL-37 also showed a weak activity against the wild-type strain; however, it showed a significant activity against the Pgm6/Pgm7-deficient strain. In the Pgm6/Pgm7-deficient strain, LL-37 remarkably accumulated on the bacterial cell surface, which may result in the destruction of the outer membrane. Additionally, the bactericidal activity of hBDs against the Pgm6/Pgm7-deficient strain was found to be synergistically promoted in the presence of LL-37. Our results suggest that OmpALPs specifically protect P. gingivalis from the bactericidal activity of LL-37; thus, P. gingivalis may adeptly survive in LL-37-producing subgingival environments.

Insights into the Evolution of Host Association through the Isolation and Characterization of a Novel Human Periodontal Pathobiont, Desulfobulbus oralis.

ABSTRACTThe human oral microbiota encompasses representatives of many bacterial lineages that have not yet been cultured. Here we describe the isolation and characterization of previously uncultured Desulfobulbus oralis, the first human-associated representative of its genus. As mammalian-associated microbes rarely have free-living close relatives, D. oralis provides opportunities to study how bacteria adapt and evolve within a host. This sulfate-reducing deltaproteobacterium has adapted to the human oral subgingival niche by curtailing its physiological repertoire, losing some biosynthetic abilities and metabolic independence, and by dramatically reducing environmental sensing and signaling capabilities. The genes that enable free-living Desulfobulbus to synthesize the potent neurotoxin methylmercury were also lost by D. oralis, a notably positive outcome of host association. However, horizontal gene acquisitions from other members of the microbiota provided novel mechanisms of interaction with the human host, including toxins like leukotoxin and hemolysins. Proteomic and transcriptomic analysis revealed that most of those factors are actively expressed, including in the subgingival environment, and some are secreted. Similar to other known oral pathobionts, D. oralis can trigger a proinflammatory response in oral epithelial cells, suggesting a direct role in the development of periodontal disease.

Evaluation of superoxide dismutase levels in local drug delivery system containing 0.2% curcumin strip as an adjunct to scaling and root planing in chronic periodontitis: A clinical and biochemical study.

Aim:Curcumin has proven properties such as anti-inflammatory, antioxidant, antimicrobial, and it also accelerates wound healing. The purpose of this study was to investigate the level of superoxide dismutase (SOD) enzyme, in gingival crevicular fluid (GCF), and the impact of nonsurgical treatment on the antioxidant profile using 0.2% curcumin strip as local drug delivery.Materials and Methods:A total of twenty subjects of age 35–55 years and 15 subjects with chronic periodontitis, each with bilateral 5–6 mm probing pocket depth, were selected for this study. Healthy group consists of 5 sites in which no bleeding on probing, no pocket depth. Group I – It consists of 15 sites with chronic periodontitis, in which scaling and root planing (SRP) was done (control group). Group II – It consists of 15 sites, in which SRP followed by the placement of curcumin strip inside the pocket (SRP + curcumin strip) (test group). GCF collection was done preoperatively and postoperatively after 21 days. The SOD activity was assessed using enzyme-linked immunosorbent assay.Results:In this study, all the clinical parameters were significantly reduced in test and control sites. Further, SOD levels were significantly improved in test sites when compared with control sites.Conclusion:Thus, the present study concluded that curcumin strip can be effectively used as an adjunct to SRP in treatment of chronic periodontitis and serves as antioxidant in subgingival environment.