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Purpose: To investigate the effect of full-mouth disinfection on the sizes of the periodontal wound and periodontal inflammatory burden and whether it leads to a decrease in C-reactive protein (CRP) levels. Materials and Methods: The study included 20 systemically healthy subjects (11 women and 9 men) 30 to 68 years old with localised or generalised periodontitis (stage III, grade C). The sizes of the periodontal wound and periodontal inflammatory burden were measured with the web application “Periodontalwound”, which is based on measurements of average tooth cervices, as well as probing depths and bleeding on probing assessed at six sites around each tooth present in the oral cavity. The levels of hsCRP (high-sensitivity CRP) were measured with an immunochemical method. All three parameters were measured before initial treatment and 3 months after therapy. Full-mouth disinfection included removal of plaque and calculus with ultrasonic and hand instruments in one session. Results: The results showed a statistically significant decrease in the size of the periodontal wound (p < 0.001), a statistically significant decrease in the size of periodontal inflammatory burden (p < 0.001), and a decrease in hsCRP levels 3 months after therapy. Conclusion: Full-mouth disinfection leads to a decrease in the periodontal wound and periodontal inflammatory burden size, as well as a decrease in the levels of hsCRP in patients with localised or generalised periodontitis (stage III, grade C) [ABSTRACT FROM AUTHOR]

Objective: The correlation between crestal bone loss at teeth and probing pocket depth (PPD) has been established. Whether these findings can also be applied to implants is not known. The objective of this study was to determine the correlation between crestal bone loss and PPD at teeth and implants. Method and materials: Thirty-one periodontitis-susceptible patients were rehabilitated with fixed implant-supported single crowns and fixed partial dentures. Each patient was examined over a 5- to 20-year period in a 3- to 6-month strict recall program. At each session, periodontal clinical parameters were recorded at teeth and implants. In addition, standardized periapical radiographs were taken after superstructure insertion (baseline) and then at 1,3,5,10,15, and 20 years. Results: The survival rate of implants (94.0%) and teeth (97.3%) did not significantly differ in all patients after 20 years (P = .68). Almost all patients had a PPD >5 mm at implants and teeth throughout the observation period. The crestal bone loss at implants and teeth increased continuously, especially in patients with advanced periodontitis, without a correlation with PPD. A few patients (n = 5) had a PPD>5 mm and annual bone loss >0.2 mm at one implant, with a correlation between bone loss and PPD. Conclusion: In healthy implants and teeth, moderate crestal bone loss is present without correlation with PPD. A few patients showed progressive crestal bone loss at only one implant, with a correlation with PPD. [ABSTRACT FROM AUTHOR]

Porphyromonas gingivalis is a major pathogenic oral bacterium that is responsible for periodontal disease. It is linked to chronic periodontitis, gingivitis and aggressive periodontitis. P. gingivalis exerts its pathogenic effects through mechanisms such as immune evasion and tissue destruction, primarily by secreting various factors, including cysteine proteases such as gingipain K (Kgp), gingipain R (RgpA and RgpB) and PrtH (UniProtKB ID P46071). Virulence proteins comprise multiple domains, including the pro‐peptide region, catalytic domain, K domain, R domain and DUF2436 domain. While there is a growing database of knowledge on virulence proteins and domains, there was no prior evidence or information regarding the structure and biological function of the well conserved DUF2436 domain. In this study, the DUF2436 domain of PrtH from P. gingivalis (PgDUF2436) was determined at 2.21 Å resolution, revealing a noncanonical β‐jelly‐roll sandwich topology with two antiparallel β‐sheets and one short α‐helix. Although the structure of PgDUF2436 was determined by the molecular‐replacement method using an AlphaFold model structure as a template, there were significant differences in the positions of β1 between the AlphaFold model and the experimentally determined PgDUF2436 structure. The Basic Local Alignment Search Tool sequence‐similarity search program showed no sequentially similar proteins in the Protein Data Bank. However, DaliLite search results using structure‐based alignment revealed that the PgDUF2436 structure has structural similarity Z‐scores of 5.9–5.4 with the C‐terminal domain of AlgF, the D4 domain of cytolysin, IglE and the extracellular domain structure of PepT2. This study has elucidated the structure of the DUF2436 domain for the first time and a comparative analysis with similar structures has been performed. [ABSTRACT FROM AUTHOR]

This review addresses the recent World Workshop Consensus Conference (WWCC) decision to eliminate Localized Aggressive Periodontitis (LAgP) in young adults as a distinct form of periodontitis. A "Consensus" implies widespread, if not unanimous, agreement among participants. However, a significant number of attendees were opposed to the elimination of the LAgP classification. The substantial evidence supporting a unique diagnosis for LAgP includes the (1) incisor/molar pattern of disease, (2) young age of onset, (3) rapid progression of attachment and bone loss, (4) familial aggregation across multiple generations, and (5) defined consortium of microbiological risk factors including Aggregatibacter actinomycetemcomitans. Distinctive clinical signs and symptoms of LAgP are presented, and the microbial subgingival consortia that precede the onset of signs and symptoms are described. Using Bradford–Hill guidelines to assess causation, well-defined longitudinal studies support the unique microbial consortia, including A. actinomycetemcomitans as causative for LAgP. To determine the effects of the WWCC elimination of LAgP on research, we searched three publication databases and discovered a clear decrease in the number of new publications addressing LAgP since the new WWCC classification. The negative effects of the WWCC guidelines on both diagnosis and treatment success are presented. For example, due to the localized nature of LAgP, the practice of averaging mean pocket depth reduction or attachment gain across all teeth masks major changes in disease recovery at high-risk tooth sites. Reinstating LAgP as a distinct disease entity is proposed, and an alternative or additional way of measuring treatment success is recommended based on an assessment of the extension of the time to relapse of subgingival re-infection. The consequences of the translocation of oral microbes to distant anatomical sites due to ignoring relapse frequency are also discussed. Additional questions and future directions are also presented. [ABSTRACT FROM AUTHOR]

The periodontal disease pathobiont Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) may exert a range of detrimental effects on periodontal diseases in general and, more specifically, with the initiation and progression of Localized Stage III Grade C periodontitis (molar–incisor pattern). In this review of the biogeography of this pathobiont, the full range of geographical scales for A. actinomycetemcomitans, from global origins and transmission to local geographical regions, to more locally exposed probands and families, to the individual host, down to the oral cavity, and finally, to spatial interactions with other commensals and pathobionts within the plaque biofilms at the micron/nanoscale, are reviewed. Using the newest technologies in genetics, imaging, in vitro cultures, and other research disciplines, investigators may be able to gain new insights to the role of this pathobiont in the unique initial destructive patterns of Localized Stage III Grade C periodontitis. These findings may incorporate the unique features of the microbiome that are influenced by variations in the geographic environment within the entire mouth. Additional insights into the geographic distribution of molar–incisor periodontal breakdown for Localized Stage III Grade C periodontitis may derive from the spatial interactions between A. actinomycetemcomitans and other pathobionts such as Porphyromonas gingivalis, Filifactor aclocis, and commensals such as Streptococcus gordonii. In addition, while the association of A. actinomycetemcomitans in systemic diseases is limited at the present time, future studies into possible periodontal disease–systemic disease links may also find A. actinomycetemcomitans and its geographical interactions with other microbiome members to provide important clues as to implications of pathobiological communications. [ABSTRACT FROM AUTHOR]

Objective: The present study aimed to evaluate the local effect of antimicrobial photodynamic therapy (aPDT) as adjunctive treatment for Grade C periodontitis in molars teeth. Method and materials: Thirty-eight molar teeth from 11 patients were included in this split-mouth randomized clinical trial. The teeth were randomly divided into two groups (n = 19 each) that were submitted to conventional scaling and root planing in addition to aPDT (test group) and to scaling and root planing in addition to aPDT simulation (control group). The following periodontal parameters were obtained prior to treatment (baseline) and at 3 months after the intervention: bleeding on probing, probing depth, gingival recession, clinical attachment level, and furcation level. A 5% significance level was adopted in the statistical analysis. Results: Both groups exhibited improvement in the clinical parameters (P < .001). However, the reductions in bleeding on probing and probing depth were greater in the test group (P < .001). There were no significant differences in the other clinical parameters between groups (P ≥ .130). Conclusions: Molar teeth treated with aPDT and scaling and root planing showed superior clinical improvement compared to those submitted only to scaling and root planing. aPDT may be used as adjunctive treatment for Grade C periodontitis affecting molar teeth since it seems to improve the clinical response to conventional debridement. [ABSTRACT FROM AUTHOR]

Introduction: The disruptions in the ectodermal layer during intrauterine growth in the process of the formation of epidermal ridges can be linked to the association between dermatoglyphics and abnormalities of the tooth and periodontium. Given the genetic linkage of periodontal disease this study was hypothesized at observing the association of chronic periodontitis, aggressive periodontitis, and individuals with healthy periodontium as per the 1999 AAP classification of periodontitis with their fingerprint patterns and ridge count. Materials and Methods: Patients belonging to an age cohort of 18–50 who visited the department of periodontics and implantology were included in the study. Patients’ periodontal status was determined and was enrolled in the study. A total of 114 subjects were compared, where 38 subjects belonged to the individual group of periodontal condition that are designated as Group A (healthy), Group B (chronic periodontitis), and Group C (aggressive periodontitis). A total of 1140 fingerprints were collected. They were analyzed and classified according to their patterns and also the ridges were counted. Results: The comparison between three groups showed a statistically significant difference between increased percentage frequency of radial loops (28%) in chronic periodontitis and plain whorls (26.3%) in aggressive periodontitis. There was a significant difference between ridge count among all the three groups, the highest being in healthy and the least between aggressive periodontal conditions. Conclusion: Observations of the study show that there was a difference in fingerprint pattern between patients of all the three periodontal conditions indicating a link between epidermal ridges and condition of periodontium.

Stage IV grade C localized periodontitis (pre-puberal localized aggressive periodontitis/LPP), an extremely rare form of periodontal disease, occurs in otherwise healthy individuals (no signs of dental plaque/calculus) due a hyper-aggressive auto-immune response to high periodontopathic bacteria levels. Methods: A 4-year-old Caucasian girl with unusually high mobility of the deciduous lower left canine and localized gingival inflammation was misrecognized by multiple clinicians (initially diagnosed with hypophosphatasia, genetic and metabolic disorders, all turning negative), over a period of 4–6 months, despite initial radiographs showing clear pathognomonic signs. The LPP diagnostic was made by the last clinician, but by then the tooth was lost. Similar inflammation signs appeared around the lower deciduous right canine. X-ray examination showed similar bone and periodontal loss as previously seen, while periodontopathic bacteria tested highly positive. The patient received both mechanical cleaning and ten days of systemic antibiotic treatment (Augmentin and Metronidazole). Results: Two months later, inflammation signs disappeared, with periodontal regeneration radiologically present, and only small periodontopathic bacteria precursor concentrations. Conclusions: Despite initial periodontal loss, an adequate treatment can keep under control an LPP disease. Moreover, bone and periodontal regeneration appears if periodontopathic bacteria scores are kept lower, showing the importance of fast adequate diagnostic and treatment. [ABSTRACT FROM AUTHOR]

This article discusses a recent study that examined the oral microbiome and its connection to periodontitis, a common dental condition that can have various health implications. The researchers analyzed data from multiple cohorts in different countries and continents to identify biomarkers for periodontitis. They found that certain species of bacteria and metabolic biomarkers consistently differed between healthy individuals and those with periodontitis. Machine learning models based on taxonomic profiles were able to accurately distinguish periodontitis patients from controls. The study suggests that metagenome-based diagnosis for periodontitis is possible and could lead to improved diagnostic and treatment approaches. However, further research and larger cohorts are needed to validate these findings. [Extracted from the article]

Background: Risk of disease progression and tooth loss is higher in cases where deep probing pocket depths (PPDs) and bleeding on probing (BOP) persist after active periodontal treatment. This study aimed to investigate the efficacy of non‐surgical periodontal therapy on pocket closure (PC), defined as PPD ≤4 mm without BOP (PC1) or PPD ≤4 mm solely (PC2) 3 months after non‐surgical periodontal treatment and to compare PC between smokers and non‐smokers. Methods: This cohort study is a secondary analysis from a controlled clinical trial consisting of systemically healthy patients with stage III or IV grade C periodontitis. All the sites with baseline PPD ≥5 mm are included as diseased sites and PC at 3 months after completion of non‐surgical periodontal treatment was calculated. PC was compared between smokers and non‐smokers at site and patient levels. Multilevel analysis is used to investigate factors at patient, tooth and site levels affecting PPD changes and the probability of PC. Results: A total of 1998 diseased sites in 27 patients were included in the analysis. The rates of PC1 and PC2 were 58.4% and 70.2% and were significantly correlated to smoking habits at site level (r (1) = 7.03, p = 0.008; r (1) = 36.17, p < 0.001). Tooth type, mobility, clinical attachment level (CAL) and PPD at baseline significantly affected PC. Conclusions: The present findings indicate that non‐surgical periodontal treatment is effective in PC, but its performance is influenced by baseline PPD and CAL and residual pockets may remain. [ABSTRACT FROM AUTHOR]

Background: Periodontitis is characterized by local inflammatory conditions in the periodontium, its severe form has been associated with elevated systemic inflammatory markers. However, the long‐term effects of periodontal inflammation control on systemic inflammatory markers are unclear. Objective: This study aimed to investigate the long‐term effects of periodontal therapy on the levels of peripheral venous blood inflammatory markers in patients with generalized aggressive periodontitis (GAgP), all of whom were now diagnosed as Stage III or IV Grade C periodontitis. Methods: Patients with GAgP were consecutively recruited from April 2013 to August 2014 (T0). Active periodontal treatment (APT) was provided, and follow‐ups were conducted over a 3‐ to 5‐year period (T1). Clinical parameters were assessed and fasting venous blood was collected at T0 and T1. Complete blood cell counts were obtained, and biochemical analyses were performed to evaluate the levels of serum components. The correlations between probing depth (PD) and hematological parameters were analyzed. Results: A total of 49 patients with GAgP completed APT and follow‐ups. Probing depth (PD) reduced from 5.10 ± 1.07 mm at T0 to 3.15 ± 0.65 mm at T1. For every 1‐mm reduction in PD after treatment, the neutrophil count, neutrophil‐lymphocyte ratio, and total protein concentration were reduced by 0.33 × 109/L, 0.26, and 1.18 g/L, respectively. In contrast, the albumin/globulin ratio increased by 0.10. Conclusion: This study indicated that periodontal therapy may have beneficial effects on peripheral venous blood inflammatory markers in patients with GAgP during long‐term observation. [ABSTRACT FROM AUTHOR]

Background: The aim of the present study was to evaluate the subgingival microbiome in patients with grade C molar‐incisor pattern periodontitis (C‐MIP) affecting the primary or permanent dentitions. Methods: DNA was isolated from subgingival biofilm samples from diseased and healthy sites from 45 C‐MIP patients and subjected to phylogenetic microarray analysis. C‐MIP sites were compared between children affected in the primary to those affected in the permanent dentitions. Within‐subject differences between C‐MIP‐affected sites and dentition‐matched healthy sites were also evaluated. Results: C‐MIP sites of subjects affected in the primary dentition showed partially overlapping but distinct microbial communities from C‐MIP permanent dentition sites (p < 0.05). Differences were due to increased levels in primary C‐MIP sites of certain species of the genera Capnocytophaga and Leptotrichia, while C‐MIP permanent dentition sites showed higher prevalence of Filifactor alocis. Aggregatibacter actinomycetemcomitans (Aa) was among species seen in high prevalence and levels in both primary and permanent C‐MIP sites. Moreover, both permanent and primary C‐MIP sites showed distinct microbial communities when compared to dentition‐matched healthy sites in the same subject (p < 0.01). Conclusions: Primary and permanent teeth with C‐MIP showed a dysbiotic microbiome, with children affected in the primary dentition showing a distinct profile from those affected in the permanent dentition. However, Aa was enriched in both primary and permanent diseased sites, confirming that this microorganism is implicated in C‐MIP in both dentitions. [ABSTRACT FROM AUTHOR]

Aggressive forms of periodontitis, especially in young patients, are often associated with an increased proportion of the Gram-negative bacterium Aggregatibacter actinomycetemcomitans of the microbiota of the affected periodontal sites. One of the virulence factors of A. actinomycetemcomitans is a leukotoxin (LtxA) that induces a pro-inflammatory cell death process in leukocytes. A. actinomycetemcomitans exhibits a large genetic diversity and different genotypes vary in LtxA production capacity. The genotype JP2 is a heavy LtxA producer due to a 530-base pair deletion in the promoter for the toxin genes, and this trait has been associated with an increased pathogenic potential. The present study focused on the production and release of LtxA by different A. actinomycetemcomitans genotypes and serotypes under various growth conditions. Four different strains of this bacterium were cultured in two different culture broths, and the amount of LtxA bound to the bacterial surface or released into the broths was determined. The cultures were examined during the logarithmic and the early stationary phases of growth. The JP2 genotype exhibited the highest LtxA production among the strains tested, and production was not affected by the growth phase. The opposite was observed with the other strains. The composition of the culture broth had no effect on the growth pattern of the tested strains. However, the abundant release of LtxA from the bacterial surface into the culture broth was found in the presence of horse serum. Besides confirming the enhanced leucotoxicity of the JP2 genotype, the study provides new data on LtxA production in the logarithmic and stationary phases of growth and the effect of media composition on the release of the toxin from the bacterial membrane. [ABSTRACT FROM AUTHOR]

Our research explores the interplay between Aggregatibacter actinomycetemcomitans (Aa) cytolethal distending toxin (Cdt) and the host's inflammatory response in molar/incisor pattern periodontitis (MIPP). Cdt disrupts phosphatidylinositol-3,4,5-triphosphate (PIP3) signaling, influencing cytokine expression through canonical and non-canonical inflammasome activation as well as nuclear factor-κB (NF-κB) activation, leading to inflammation in MIPP. THP-1 differentiated macrophages (TDMs) exposed to Cdt exhibited an upregulation of pro-inflammatory genes and subsequent cytokine release. We analyzed the ability of a small molecule therapeutic, LGM2605, known for its anti-inflammatory properties, to reduce pro-inflammatory gene expression and cytokine release in Cdt-exposed and Aa-inoculated TDMs. LGM2605's mechanism of action involves inhibiting NF-κB while activating the Nrf2–transcription factor and antioxidants. Herein, we show that this small molecule therapeutic mitigates Cdt-induced pro-inflammatory cytokine expression and secretion. Our study also further defines Cdt's impact on osteoclast differentiation and maturation in MIPP. Cdt promotes increased TRAP+ cells, indicating heightened osteoclast differentiation, specific to Cdt's phosphatase activity. Cathepsin K levels rise during this process, reflecting changes in TRAP distribution between control and Cdt-treated cells. Exploring LGM2605's effect on Cdt-induced osteoclast differentiation and maturation, we found TRAP+ cells significantly reduced with LGM2605 treatment compared to Cdt alone. Upon LGM2605 treatment, immunocytochemistry revealed a decreased TRAP intensity and number of multinucleated cells. Moreover, immunoblotting showed reduced TRAP and cathepsin K levels, suggesting LGM2605's potential to curb osteoclast differentiation and maturation by modulating inflammatory cytokines, possibly involving Nrf2 activation. In summary, our research reveals the intricate connections between Cdt, pro-inflammatory cytokines, and osteoclast differentiation, offering novel therapeutic possibilities for managing these conditions. [ABSTRACT FROM AUTHOR]

Background: Necrotizing periodontitis (NP) is a rare form of periodontal disease. It can manifest in immunocompromised patients and present as painful and rapidly progressing destruction with necrotic and ulcerated periodontal tissues. This case report describes a rare case of severe NP in human immunodeficiency virus (HIV)‐positive patient including medical management and periodontal treatment. Methods: A 28‐year‐old male presented to the periodontal clinic with chief complaint of severe oral pain leading to loss of chewing ability, spontaneous gingival bleeding, generalized gingival recession, tooth mobility, and dentinal hypersensitivity. Clinical and radiographic examination revealed generalized tissue necrosis with severe periodontal destruction, extensive bleeding, spontaneous suppuration, and heavy biofilm. Results: Medical history was positive for perinatal HIV infection, which was treated and patient was asymptomatic until he discontinued antiviral medications nine years ago. Following initial examination, patient was referred to the Infectious disease clinic and multidisciplinary management was initiated with comprehensive management of primary disease including systemic antiviral, antibiotic, and antifungal therapy to establish immunocompetence compatible with providing mechanical nonsurgical periodontal treatment. Conclusions: This case report highlights a severe and generalized form of NP in an HIV patient due to the cessation of antiviral therapy. Favorable course of interdisciplinary medical and periodontal therapy resulted in significant improvement in patient's systemic, oral, and periodontal health. [ABSTRACT FROM AUTHOR]

Background: This study determined the prevalence of aggressive (molar‐incisor pattern) (Ag/MI) periodontitis and assessed the associated subgingival bacterial‐herpesvirus microbiota in Pueblo Indian adolescents in the southwestern United States. Methods: The study included 240 Pueblo Indian adolescents, aged 13–20 years old, residing in three Rio Grande River villages in New Mexico and the Hopi Pueblo reservation in Arizona. Adolescents with Ag/MI periodontitis or periodontal health provided subgingival samples for culture of bacterial pathogens and for polymerase chain reaction detection of periodontal herpesviruses. Results: Ag/MI periodontitis was detected in 22 (9.2%) Pueblo Indian adolescents, with 21 exhibiting a localized molar‐incisor breakdown pattern. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, and other red/orange complex bacterial pathogens predominated in Ag/MI periodontitis, whereas periodontal health yielded mainly viridans streptococci and Actinomyces species. Periodontal herpesviruses demonstrated a 3.5 odds ratio relationship with Ag/MI periodontitis. The only adolescent with generalized Ag/MI periodontitis harbored viral co‐infection by cytomegalovirus plus Epstein–Barr virus Type 1, in addition to A. actinomycetemcomitans, P. gingivalis, and several other periodontopathic bacteria. Conclusions: Pueblo Indian adolescents showed an unusually high prevalence of early‐age Ag/MI periodontitis predominated by periodontopathic bacteria and herpesviruses suspected to be major etiologic agents of the disease. [ABSTRACT FROM AUTHOR]

The article titled "A Requiem for the Periodontal Ligament: A Nuanced Perspective" discusses the historical perspective on the role of bacterial plaque in implant failure and the need to consider other factors. It raises questions about the pathogenesis, risk factors, and incidence of peri-implantitis (PI) and explores the differences between implants and natural teeth in managing occlusal loads. The article also highlights the distinct microbiota and histopathology of PI compared to periodontitis and identifies various risk factors for PI. It concludes by discussing the limitations of the periodontal model for implants and the need for a more nuanced understanding. [Extracted from the article]

Matrix metalloproteinases (MMPs) are proteinases released by gingival cells, macrophages and neutrophils, induced by potentially pathogenic periodontal bacteria of the subgingival plaque, which play a critical role in the pathogenesis of periodontal disease. The expression of MMPs is controlled by chromosome 11. Single nucleotide polymorphisms (SNPs) are linked with variations in the secretion of MMPs, resulting in periodontal disease progression. Genetic studies aim to find the markers for early diagnosis and prevention of the related diseases. This systematic review focuses on finding the association between the MMPs and periodontitis among Indians. A literature review was performed, including studies published between January 1 2012 and May 2024 were incorporated. This systematic review included 1,046 participants in seven Indian studies, and substantial evidence was found for an association between MMP-9 (–1562C/T) and periodontitis in Indian population.

Aggressive periodontitis (AgP), classified as Stages III or IV and grade C periodontitis, is characterized by the rapid destruction of periodontal tissue. Genetic factors contribute to the pathogenesis of this disease, and familial aggregation of periodontitis is often observed. However, the mechanisms underlying the onset or progression of AgP have not been elucidated. Previously, we performed exome sequencing and identified AgP risk factors in Japanese AgP-patients. However, the small sample size limited our scope for detecting some of the true AgP genetic risk factors. To overcome this limitation, we searched for AgP-related genes more comprehensively from the whole exome sequencing data of the Japanese AgP-patients by extending the filtering criteria range. We identified seven AgP-associated suggestive genes, including the single nucleotide polymorphism (SNP) rs854560 in paraoxonase-1 (PON-1), which is correlated with AgP. However, the mechanism(s) underlying the induction of AgP pathogenesis by the SNP rs854560 PON-1 has not been elucidated. Thus, we further analyzed the functions of the SNP rs854560 PON-1 in human periodontal ligament (HPDL) cells through transfection of the wild-type PON-1 (WT) or SNP rs854560 PON-1 (mut) into HPDL cells. Real-time PCR indicated that mut had higher mRNA expression of osteogenic related-genes and showed a higher tendency of ALP activity and proliferation. The result suggested that WT PON-1 contributes to periodontal tissue homeostasis through appropriate proliferation and cytodifferentiation of HPDL cells, while SNP rs854560 PON-1 may mediate excessive calcification of periodontal tissue due to hyper proliferation of HPDL cells, thereby increasing the risk of AgP.

Purpose: This study aimed to compare insulin status and dysglycemia (prediabetes/diabetes) of patients with chronic (stage III, grade B) or aggressive periodontitis (stage III, grade C) to that of a healthy population. Materials and Methods: Patients with chronic (CP, n = 16) or aggressive periodontitis (AP, n = 15) and periodontally healthy controls (n = 32) were recruited. Body mass index was calculated. Glycemia, plasma insulin, glycated hemoglobin, C-reactive protein, and lipid levels were measured in fasting. The Homeostasis Model Assessment was used to calculate the insulin sensitivity (HOMA-%S), the beta-cell function (HOMA-%B), and their hyperbolic product (HOMA-%BxS). Results: The CP group showed statistically significantly insulin resistance with a lower HOMA-%S (p = 0.0003) and a reduced HOMA-%BxS (p = 0.049) despite a higher insulin level (p = 0.01) vs the control group, even after BMI adjustment. There was also a trend to dysglycemia (prediabetes/diabetes) in the chronic group. In patients with AP, no abnormalities in insulin status were observed and glycemic levels were comparable with controls. Additionally, patients in both AP and CP groups presented significantly higher CRP levels compared to those of the control group (p = 0.02). Conclusion: Patients with CP showed reduced insulin sensitivity, increased insulin levels but a reduced %BxS product and a trend to dysglycemia. These abnormalities were not observed in AP. [ABSTRACT FROM AUTHOR]

Aims: Aggressive periodontitis evolves rapidly to severe periodontal destruction, which involves a multidisciplinary treatment for handling the periodontal infection, reconstructing defects, and realigning migrated teeth. Orthodontic treatment improves all aspects of periodontal health including aesthetics, teeth function, and oral hygiene, therefore preventing degeneration. This systematic review intends to focus on the effect of orthodontic treatment on the evolution of aggressive periodontitis. The clinical parameters are pocket depth, decrease in inflammation, attachment gain, index of dental plaque, and bone gain. Materials and methods: This research is based on the analysis of four bibliographic databases which include PubMed, EBSCO, Science Direct, and Cochrane Library. Several search equations are used and the keywords are orthodontic treatment, aggressive periodontitis, migrated teeth, and combination treatment. Pertinent studies with a comparison of periodontal conditions before and after orthodontic treatment are selected. Several analytic parameters are used and tabulated. Results: Two hundred and seventy-one (271) studies were found and only four (04) were selected due to inclusion criteria. The analysis shows significant improvement in all clinical parameters. Conclusions: Although clinical parameters were improved after an orthodontic treatment, the results are irrelevant because of the insufficient studies with arguable statistical findings.

The purpose of this report is to discuss the case of a four-year-old African-American girl who presented with clinical and radiographic evidence of localized stage III grade C periodontitis. She had no history of systemic disease or caries. Treatment consisted of oral hygiene instructions, extraction of unsalvageable teeth, full-mouth debridement with the use of systemic antibiotics and subsequent periodontal maintenance care. The patient underwent a two-year follow-up, during which the disease was stabilized and no space loss was detected. Although this condition is uncommon, the pediatric dentist must be able to diagnose and treat periodontitis in the primary dentition early, together with a multidisciplinary team, to prevent a recurrence of this disease in the permanent dentition. [ABSTRACT FROM AUTHOR]

"Selman Waksman" first used the term "antibiotic" in 1942 to refer to any material produced by a bacterium that inhibits the growth of other micro-organisms in high dilution. The pathogenic bacteria, the patient, and the medication are the three main components of the antibiotic periodontal therapy idea. Patients with attachment loss or with aggressive types of periodontitis or those with periodontitis linked with underlying medical conditions are the best candidates for systemic antimicrobial therapy. The three main objectives of Periodontal Therapy are disrupting biofilms, suppressing potential periodontal pathogens throughout the entire oral cavity, and halting the illness. The microbial etiology of inflammatory periodontal disease provides the rationale for the use of antibiotic medication in periodontal therapy. This idea is predicated on the idea that a certain bacterium causes destructive periodontal disease and that antibiotic agents can be present in humans in doses greater than those required to kill or inhibit infections. [ABSTRACT FROM AUTHOR]

Aggregatibacter actinomycetemcomitans is a Gram-negative oral bacterium that has been primarily studied for its role in causing periodontal disease. The bacterium has also been implicated in several systemic diseases such as endocarditis and soft tissue abscesses. Leukotoxin (LtxA) is perhaps the best studied protein virulence factor from A. actinomycetemcomitans. The protein can rapidly destroy white blood cells (WBCs), helping the bacterium to subvert the host immune system. The functional receptor for LtxA is lymphocyte function associated antigen-1 (LFA-1), which is expressed exclusively on the surfaces of WBCs. Bacterial expression and secretion of the protein are highly regulated and controlled by a number of genetic and environmental factors. The mechanism of LtxA action on WBCs varies depending on the type of cell that is being killed, and the protein has been shown to activate numerous cell death pathways in susceptible cells. In addition to serving as an important virulence factor for the bacterium, because of its exquisite specificity and rapid activity, LtxA is also being investigated as a therapeutic agent that may be used to treat diseases such as hematological malignancies and autoimmune/inflammatory diseases. It is our hope that this review will inspire an increased intensity of research related to LtxA and its effect on Aggressive Periodontitis, the disease that led to its initial discovery. [ABSTRACT FROM AUTHOR]

Introduction: The disruptions in the ectodermal layer during intrauterine growth in the process of the formation of epidermal ridges can be linked to the association between dermatoglyphics and abnormalities of the tooth and periodontium. Given the genetic linkage of periodontal disease this study was hypothesized at observing the association of chronic periodontitis, aggressive periodontitis, and individuals with healthy periodontium as per the 1999 AAP classification of periodontitis with their fingerprint patterns and ridge count. Materials and Methods: Patients belonging to an age cohort of 18-50 who visited the department of periodontics and implantology were included in the study. Patients' periodontal status was determined and was enrolled in the study. A total of 114 subjects were compared, where 38 subjects belonged to the individual group of periodontal condition that are designated as Group A (healthy), Group B (chronic periodontitis), and Group C (aggressive periodontitis). A total of 1140 fingerprints were collected. They were analyzed and classified according to their patterns and also the ridges were counted. Results: The comparison between three groups showed a statistically significant difference between increased percentage frequency of radial loops (28%) in chronic periodontitis and plain whorls (26.3%) in aggressive periodontitis. There was a significant difference between ridge count among all the three groups, the highest being in healthy and the least between aggressive periodontal conditions. Conclusion: Observations of the study show that there was a difference in fingerprint pattern between patients of all the three periodontal conditions indicating a link between epidermal ridges and condition of periodontium. [ABSTRACT FROM AUTHOR]

Aim: Few genome‐wide association studies (GWAS) have been conducted for severe forms of periodontitis (stage III/IV grade C), and the number of known risk genes is scarce. To identify further genetic risk variants to improve the understanding of the disease aetiology, a GWAS meta‐analysis in cases with a diagnosis at ≤35 years of age was performed. Materials and Methods: Genotypes from German, Dutch and Spanish GWAS studies of III/IV‐C periodontitis diagnosed at age ≤35 years were imputed using TopMed. After quality control, a meta‐analysis was conducted on 8,666,460 variants in 1306 cases and 7817 controls with METAL. Variants were prioritized using FUMA for gene‐based tests, functional annotation and a transcriptome‐wide association study integrating eQTL data. Results: The study identified a novel genome‐wide significant association in the FCER1G gene (p = 1.0 × 10−9), which was previously suggestively associated with III/IV‐C periodontitis. Six additional genes showed suggestive association with p < 10−5, including the known risk gene SIGLEC5. HMCN2 showed the second strongest association in this study (p = 6.1 × 10−8). Conclusions: This study expands the set of known genetic loci for severe periodontitis with an age of onset ≤35 years. The putative functions ascribed to the associated genes highlight the significance of oral barrier tissue stability, wound healing and tissue regeneration in the aetiology of these periodontitis forms and suggest the importance of tissue regeneration in maintaining oral health. [ABSTRACT FROM AUTHOR]

Aim: WHIM (warts, hypogammaglobulinaemia, infections and myelokathexis) syndrome is a rare combined primary immunodeficiency disease caused by gain‐of‐function (GOF) mutations in the chemokine receptor CXCR4 and includes severe neutropenia as a common feature. Neutropenia is a known risk factor for periodontitis; however, a detailed periodontal evaluation of a WHIM syndrome cohort is lacking. This study aimed to establish the evidence base for the periodontal status of patients with WHIM syndrome. Materials and Methods: Twenty‐two adult WHIM syndrome patients and 22 age‐ and gender‐matched healthy volunteers (HVs) were evaluated through a comprehensive medical and periodontal examination. A mouse model of WHIM syndrome was assessed for susceptibility to naturally progressing or inducible periodontitis. Results: Fourteen patients with WHIM syndrome (63.6%) and one HV (4.5%) were diagnosed with Stage III/IV periodontitis. No WHIM patient presented with the early onset, dramatic clinical phenotypes typically associated with genetic forms of neutropenia. Age, but not the specific CXCR4 mutation or absolute neutrophil count, was associated with periodontitis severity in the WHIM cohort. Mice with a Cxcr4 GOF mutation did not exhibit increased alveolar bone loss in spontaneous or ligature‐induced periodontitis. Conclusions: Overall, WHIM syndrome patients presented with an increased severity of periodontitis despite past and ongoing neutrophil mobilization treatments. GOF mutations in CXCR4 may be a risk factor for periodontitis in humans. [ABSTRACT FROM AUTHOR]

Aggregatibacter actinomycetemcomitans is a Gram-negative bacterium associated with localized aggressive periodontitis as well as some systemic diseases. The strains of A. actinomycetemcomitans most closely associated with disease produce more of a secreted leukotoxin (LtxA) than isolates from healthy carriers, suggesting a key role for this toxin in disease progression. LtxA is released into the bacterial cytosol in a free form as well as in association with the surface of outer membrane vesicles (OMVs). We previously observed that the highly leukotoxic A. actinomycetemcomitans strain JP2 produces two populations of OMVs: a highly abundant population of small (<100 nm) OMVs and a less abundant population of large (>300 nm) OMVs. Here, we have developed a protocol to isolate the OMVs produced during each specific phase of growth and used this to demonstrate that small OMVs are produced throughout growth and lack LtxA, while large OMVs are produced only during the exponential phase and are enriched with LtxA. Our results indicate that surface-associated DNA drives the selective sorting of LtxA into large OMVs. This study provides valuable insights into the observed heterogeneity of A. actinomycetemcomitans vesicles and emphasizes the importance of understanding these variations in the context of bacterial pathogenesis. [ABSTRACT FROM AUTHOR]

Aggressive periodontitis (AgP) is characterized by rapid and progressive destruction of the periodontal tissues and eventual tooth loss. Genetic risk contributions have been explored and rare mutations in NOD2 were reported. Sequencing analysis of the coding regions of NOD2 was conducted using individuals of African ancestry, to identify the pathogenic protein-altering variants in individuals with AgP using: 1) In Silico tools and clinical variant classification system; 2) IF staining to understand the expression pattern, and 3) In vitro cell based assay to understand the variant protein function. We discovered a novel nonsense NOD2 variant (c.835G>T; p.Glu279Ter) ; a truncating protein variant that is clinically pathogenic, and the gene-product lacks domains regulating inflammatory responses. Murine studies suggest that this gene contributes to tooth development. In vitro analysis suggests a dominant-negative effect of the variant. NOD2 gene is expressed in the immune cells and periodontal tissues and regulates the inflammatory response within this tissue. This truncating variant found in one African family, which results in a dominant-negative effect, could explain the exacerbated immune response to pathogens in the pathogenesis of this periodontal disease.

The periodontal disease pathobiont Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) may exert a range of detrimental effects on periodontal diseases in general and, more specifically, with the initiation and progression of Localized Stage III Grade C periodontitis (molar–incisor pattern). In this review of the biogeography of this pathobiont, the full range of geographical scales for A. actinomycetemcomitans, from global origins and transmission to local geographical regions, to more locally exposed probands and families, to the individual host, down to the oral cavity, and finally, to spatial interactions with other commensals and pathobionts within the plaque biofilms at the micron/nanoscale, are reviewed. Using the newest technologies in genetics, imaging, in vitro cultures, and other research disciplines, investigators may be able to gain new insights to the role of this pathobiont in the unique initial destructive patterns of Localized Stage III Grade C periodontitis. These findings may incorporate the unique features of the microbiome that are influenced by variations in the geographic environment within the entire mouth. Additional insights into the geographic distribution of molar–incisor periodontal breakdown for Localized Stage III Grade C periodontitis may derive from the spatial interactions between A. actinomycetemcomitans and other pathobionts such as Porphyromonas gingivalis, Filifactor aclocis, and commensals such as Streptococcus gordonii. In addition, while the association of A. actinomycetemcomitans in systemic diseases is limited at the present time, future studies into possible periodontal disease–systemic disease links may also find A. actinomycetemcomitans and its geographical interactions with other microbiome members to provide important clues as to implications of pathobiological communications.

This review addresses the recent World Workshop Consensus Conference (WWCC) decision to eliminate Localized Aggressive Periodontitis (LAgP) in young adults as a distinct form of periodontitis. A “Consensus” implies widespread, if not unanimous, agreement among participants. However, a significant number of attendees were opposed to the elimination of the LAgP classification. The substantial evidence supporting a unique diagnosis for LAgP includes the (1) incisor/molar pattern of disease, (2) young age of onset, (3) rapid progression of attachment and bone loss, (4) familial aggregation across multiple generations, and (5) defined consortium of microbiological risk factors including Aggregatibacter actinomycetemcomitans. Distinctive clinical signs and symptoms of LAgP are presented, and the microbial subgingival consortia that precede the onset of signs and symptoms are described. Using Bradford–Hill guidelines to assess causation, well-defined longitudinal studies support the unique microbial consortia, including A. actinomycetemcomitans as causative for LAgP. To determine the effects of the WWCC elimination of LAgP on research, we searched three publication databases and discovered a clear decrease in the number of new publications addressing LAgP since the new WWCC classification. The negative effects of the WWCC guidelines on both diagnosis and treatment success are presented. For example, due to the localized nature of LAgP, the practice of averaging mean pocket depth reduction or attachment gain across all teeth masks major changes in disease recovery at high-risk tooth sites. Reinstating LAgP as a distinct disease entity is proposed, and an alternative or additional way of measuring treatment success is recommended based on an assessment of the extension of the time to relapse of subgingival re-infection. The consequences of the translocation of oral microbes to distant anatomical sites due to ignoring relapse frequency are also discussed. Additional questions and future directions are also presented.

The aim of this case series was to evaluate implants inserted in bone after guided bone regeneration (GBR). Fourteen patients with generalized aggressive periodontitis (GAP) who had lost one or two maxillary teeth in the incisor or premolar region were enrolled in the study. Due to bone resorption, the lateral width and vertical height of the bone were insufficient for implant placement. GBR was carried out in a staged approach using titanium-reinforced e-PTFE (expanded polytetrafluoroethylene) membranes. No bone grafts or bone substitute materials were used. After 6 to 8 months, turned-surface implants (n = 47) were inserted in augmented and nonaugmented bone sites and prosthetically treated with single crowns. All patients were examined during a 3- to 6-month recall schedule over a 10- to 20-year period, and clinical and radiographic examinations were performed. GBR yielded mean vertical and lateral bone gains of 4.5 and 7.0 mm, respectively. The implant survival rate was 100%, mucositis was present in 28.8% of sites, and peri-implantitis was not found. The annual bone loss at tooth sites was significantly higher than at implant sites in augmented bone (0.5% vs 0.2%, respectively; P = .000), and the adjacent teeth had significantly higher annual bone loss (0.8%; P = .000). Thus, severely periodontally compromised patients can be managed successfully in the long-term with the described clinical protocol. [ABSTRACT FROM AUTHOR]

Localized juvenile (aggressive) periodontitis starts at puberty in otherwise healthy individuals and involves the proximal surfaces of permanent incisors and first molars. The disease destroys a sizeable amount of periodontal bone within a few months despite minimal dental plaque and gingival tissue inflammation. Cytomegalovirus and Epstein–Barr virus, as well as the two main periodontopathic bacteria Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, are linked to juvenile periodontitis. Juvenile periodontitis‐affected teeth show cementum hypoplasia. We hypothesize that an active herpesvirus infection, at the time of root formation, hampers cementum formation and, at puberty, herpesvirus reactivation triggers an upgrowth of bacterial pathogens which produce rapid periodontal destruction on teeth with a defective periodontium. A pathogenic interaction between active herpesviruses and bacterial pathogens can potentially explain the etiology and incisor‐first molar destructive pattern of juvenile periodontitis. Effective treatment of juvenile periodontitis may target the herpesvirus‐bacteria co‐infection. [ABSTRACT FROM AUTHOR]

Objectives: This research was performed to investigate if there is a role for IL-39 in immunopathogenesis of both systemically healthy and diabetic periodontitis patients. Additionally, to explore if we can consider IL-39 and IL-35 as biomarkers for periodontitis activity. Materials and methods: A total of 38 periodontitis patients and 19 control volunteers were included in our study. The periodontitis patients were divided equally into (Group I), 19 patients with stage III grade C periodontitis with diabetes mellitus and (Group II), 19 patients with stage III grade B periodontitis and systemically healthy. Gingival crevicular fluid levels of each interleukin were measured pre- and postoperatively for all periodontitis patients as well as control subjects using ELISA. Results: Our study results showed that the highest level for IL-39 was in diabetic periodontitis patients that decreased significantly postoperatively. However, the highest level for IL-35 was revealed in control group while the lowest value was registered in diabetic periodontitis patients and statistically increased after periodontal treatment. Conclusions: Based on the results of our research, both investigated biomarkers may have a potent role in pathogenesis of periodontitis. Clinical relevance: We could consider both interleukins as accurate diagnostic markers for periodontitis patients, regardless of diabetes mellitus association, as well as promising markers that can aid in the prevention and treatment of periodontitis patients worldwide. [ABSTRACT FROM AUTHOR]

To evaluate and compare the associations of VEGFA serum levels and SNPs (rs1570360, rs699947, rs3025033, and rs2146323) with periodontitis in study participants grouped by gender. The study enrolled 261 patients with periodontitis and 441 healthy controls as a reference group. Patients underwent periodontal examination and radiographic analysis to confirm the periodontitis diagnosis. Blood samples were collected, and the DNA salting-out method was used for DNA extraction from peripheral venous blood. Genotyping of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) was performed using real-time polymerase chain reaction (RT-PCR) and serum level analysis was done for 80 individuals − 40 periodontitis-affected patients and 40 reference group subjects. The analysis of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) showed that the rs3025033 GG genotype was less frequent in the periodontitis group than in the reference group (1.6% vs. 5.7%,p = 0.008). VEGFA serum levels were not statistically significantly different between periodontitis patients and reference group subjects (554.29 (522.38) ng/ml vs. 581.32 (348.16) ng/ml, p = 0.786). Individuals carrying rs1570360, rs699947, rs3025033, and rs2146323 haplotype A-A-G-A had decreased risks of periodontitis, while rare haplotype of VEGFA (rs1570360, rs699947, rs3025033, and rs2146323) was associated with increased odds of periodontitis (OR= 0.42; 95% CI: 0.20–0.85; p < 0.017; OR= 4.08; 95% CI: 1.86–8.94; p < 0.0001, respectively). The rs3025033 GG genotype and the rs1570360, rs699947, rs3025033, and rs2146323 A-A-G-A haplotypes may play a protective role in the development of periodontitis, but a less common haplotype of the same VEGFA polymorphism may be associated with the risk of developing periodontitis. [ABSTRACT FROM AUTHOR]

Background and Objectives: Stage IV grade C localized periodontitis (pre-puberal localized aggressive periodontitis/LPP) is a rare form of inflammatory periodontal disease occurring in clinically healthy individuals (no/small calculus/dental plaque traces), due a hyper-aggressive auto-immune response to high amounts of bacteria present in the oral cavity. Case Presentation: This case report describes a 4-year-old Caucasian girl with localized gingival inflammation and advanced bone loss around the temporary lower left canine. The first diagnostic assumption was hypophosphatasia, and the patient was sent for further genetic and metabolic investigations (which turned out to be negative). The LPP diagnosis was made during the family's summer holidays due to her parents' concerns about persistent gingival inflammation and tooth mobility. Results: The diagnosis of LPP was supported by clinical oral examination results, earlier X-rays, earlier blood tests, and a periodontal bacterial test. The treatment was limited to avoid spreading inflammation to other teeth (via topical antibiotic treatment) due to our limited time frame, while the main problem of excessive amounts of periodontal bacteria in the oral cavity was not addressed. The tooth was eventually lost. Conclusions: The ability to early recognize radiological and clinical LPP signs correlated with understanding of its pathological auto-immune mechanism is extremely important for expanding treatment options, since bone preservation and reducing amounts of bacteria are strictly correlated with therapeutic speed. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate miRNA expression profiles in individuals with periodontitis which is a chronic inflammatory condition affecting the integrity of the periodontal attachment. miRNAs play a crucial role in gene regulation through various mechanisms, making them potential diagnostic markers and therapeutic targets for various diseases. Materials and methods: A total of 25 individuals with aggressive periodontitis and 25 controls were included in the study. Gingival tissues were collected for miRNA isolation and cDNA synthesis. miRNAs associated with periodontitis, including hsa-miR-185-5p, hsa-miR-17, hs-miR-146a, hs-miR-146b, hs-miR-155, hs-miR-203, hs-miR-205, hs-miR-223, and hsa-miR-21-3p, were analyzed using a combination of miRTarBase database analysis and literature mining was performed. Real-time PCR was used to assess the expression patterns of the target miRNAs, and the data were analyzed using the REST program. Results: The study revealed upregulated expression levels of hsa-miR-223-3p, hsa-miR-203b-5p, hsa-miR-146a-5p, hsa-miR-146b-5p, and hsa-miR-155-5p in individuals with periodontitis. Conversely, downregulated expression was observed for hsa-miR-185-5p, hsa-miR-21-3p, and hsa-miR-17-3p. Conclusion: The findings suggest significant differences in the expression of specific miRNAs associated with inflammation in periodontitis. MZB1 acts as a hormone-regulated adipokine/pro-inflammatory cytokine, driving chronic inflammation and influencing cellular expansion. Predominantly expressed in marginal zone and B1 B cells, specialized subsets that respond rapidly to infections, MZB1 impacts immune protein synthesis and immune cell maturation, notably targeting microRNA-185 to potentially impede T cell development. Further research is needed to elucidate the functional significance and potential implications of these miRNAs. Clinical relevance: miRNAs regulate the expression of target genes by finely tuning protein expression levels. The current findings provide compelling evidence of notable variations in the expression levels of specific miRNAs associated with inflammation in individuals affected by periodontitis; hence, miRNAs hold promise as potential therapeutic targets for periodontitis. [ABSTRACT FROM AUTHOR]

Visfatin, as a novel adipokine, is considered to play a role in periodontal inflammation. Chemerin is another newly identified adipokine that is possible to have a role in periodontitis firstly reported in our previous study. The aim of the current study is to evaluate the gingival crevicular fluid (GCF) levels of visfatin and chemerin in periodontitis and and compare these adipokine levels with before and after non-surgical periodontal treatment. Twenty-nine patients with Stage III Grade B periodontitis and eighteen healthy subjects included in this cross-sectional cohort study. Clinical periodontal parameters and GCF were obtained from all subjects. Eight weeks after the following non-surgical periodontal treatment including scaling and root planning, samples and clinical periodontal parameters were collected again in the periodontitis group. The levels of adipokines were analyzed with standard enzyme-linked immunosorbent assay. The levels of visfatin and chemerin were statistically significantly higher at periodontitis group as compared to healthy group (P < 0.001). Although, no changes were observed in visfatin levels after periodontal treatment (P > 0.05), chemerin levels were significantly decreased (P < 0.001). Also, no differences were observed as compared to the healthy group (P > 0.05). Visfatin and chemerin may play a role in the periodontal disease process. In addition, it can be considered that the decreased chemerin levels after non-surgical periodontal treatment may play an important role for developing host modulation strategies. [ABSTRACT FROM AUTHOR]

Objectives: The current study aimed to investigate the association of matrix metalloproteinase- (MMP-) 1, -2, -3, -7, and -13 gene polymorphisms with chronic periodontitis (CP) in an Iranian population. Materials and Methods: In this case–control study, 87 subjects with CP and 89 periodontally healthy subjects were allocated to case and control groups, respectively. Subjects' venous blood samples (5 cc) were collected, and DNA extraction was performed. A spectrophotometer was utilized to assess the concentration of extracted DNAs. The desired gene polymorphisms were examined using restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR) followed by electrophoresis. Statistical analyses were done using the Pearson Chi-Square test, odds ratio, and t-Test using SPSS Version 28. Results: The MMP-1 (-1607 1G/2G) rs1799750, MMP-3 (-1171 5A/6A) rs3025058, and MMP-7 (-181 A/G) rs11568818 gene polymorphisms significantly differed between case and control groups (PV = 0.019, 0.007, and 0.028, respectively). In contrast, the gene polymorphisms of MMP-2 (-1306 C/T) rs243865 and MMP-13 (-77 A/G) rs2252070 did not make a significant difference. Regarding allele frequencies, the presence of the 2G allele in the MMP-1 (-1607) rs1799750 genotype increased the CP susceptibility significantly, while subjects with the 6A allele in their MMP-3 (-1171) rs3025058 genotype showed significantly lower susceptibility to CP (PV = 0.008 and < 0.001, respectively). Conclusion: In the studied population, gene polymorphisms in the DNA sequences of MMP-1 (-1607 1G/2G) rs1799750, MMP-3 (-1171 5A/6A) rs3025058, and MMP-7 (-181 A/G) rs11568818 may have impacts on CP incidence. Clinical Relevance: Clinicians should be cautious about the association between MMP-1, MMP-3, and MMP-7 gene polymorphisms and the incidence of chronic periodontitis during periodontal treatment planning. [ABSTRACT FROM AUTHOR]

Aggressive periodontitis (AgP), Stage III or IV and Grade C according to the new periodontitis classification, is characterized by the rapid destruction of periodontal tissues in the systemically healthy population and often causes premature tooth loss. The presence of familial aggregation suggests the involvement of genetic factors in the pathogenesis. However, the genes associated with the onset and progression of the disease and details of its pathogenesis have not yet been fully identified. In recent years, the genome-wide approach (GWAS), a comprehensive genome analysis method using bioinformatics, has been used to search for disease-related genes, and the results have been applied in genomic medicine for various diseases, such as cancer. In this review, we discuss GWAS in the context of AgP. First, we introduce the relationship between single-nucleotide polymorphisms (SNPs) and susceptibility to diseases and how GWAS is useful for searching disease-related SNPs. Furthermore, we summarize the recent findings of disease-related genes using GWAS on AgP inside and outside Japan and a possible mechanism of the pathogenesis of AgP based on available literature and our research findings. These findings will lead to advancements in the prevention, prognosis, and treatment of AgP. [ABSTRACT FROM AUTHOR]

Background: Aggressive periodontitis is a severe form of periodontal disease characterized by rapid tissue destruction and tooth loss. The optimal treatment approach for managing this condition remains a topic of debate. Materials and Methods: A retrospective cohort study was conducted, involving patients diagnosed with aggressive periodontitis who received either surgical or non-surgical treatment between 2010 and 2020. Clinical and radiographic data were collected at baseline and regular intervals over a 5-year follow-up period. Surgical interventions included flap surgery, guided tissue regeneration, and bone grafting, while non-surgical treatments comprised scaling and root planning with or without adjunctive antibiotics. The primary outcomes assessed included changes in probing depth, clinical attachment level, tooth loss, and patient-reported quality of life measures. Results: A total of 120 patients were included in the study, with 60 patients in each treatment group. The surgical group demonstrated significantly greater reductions in probing depth and gains in clinical attachment level compared to the non-surgical group (P < 0.05). Tooth loss was significantly lower in the surgical group over the 5 years (P < 0.01). Patient-reported outcomes also favored the surgical group, with improved oral health-related quality of life. However, the surgical group had a higher incidence of postoperative complications. Conclusion: This study suggests that periodontal surgery yields superior long-term outcomes in the management of aggressive periodontitis compared to non-surgical treatment.