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Background: Parkinson's disease (PA) affects 1% of the global population above 60 years. PA pathogenesis involves severe neuroinflammation that impacts systemic and local inflammatory changes. We tested the hypothesis that PA is associated with periodontal tissue inflammation promoting a greater systemic inflammatory burden. Methods: We recruited 60 patients with Stage III, Grade B periodontitis (P) with and without PA (n = 20 for each). We also included systemically and periodontally healthy individuals as controls (n = 20). Clinical periodontal parameters were recorded. Serum, saliva, and gingival crevicular fluid (GCF) samples were collected to measure the inflammatory and neurodegenerative targets (YKL‐40, fractalkine, S100B, alpha‐synuclein, tau, vascular cell adhesion protein‐1 (VCAM‐1), brain‐derived neurotrophic factor (BDNF), neurofilament light chain (NfL). Results: Parkinson's patients in this study had mild to moderate motor dysfunctions, which did not prevent them from performing optimal oral hygiene control. Periodontal parameters and GCF volume were significantly higher in the P and P+PA groups than in the control group. PA was associated with significantly increased bleeding on probing (BOP) compared to P‐alone (p < 0.05), while other clinical parameters were similar between P and P+PA groups. In saliva and serum, YKL‐40 levels were higher in the P+PA group than in P and C groups (p < 0.001). GCF NfL levels from shallow sites were significantly higher in the P+PA group compared to the C group (p = 0.0462). GCF S100B levels from deep sites were higher in the P+PA group than in healthy individuals (p = 0.0194). Conclusion: The data suggested that PA is highly associated with increased periodontal inflammatory burden—bleeding upon probing and inflammatory markers—in parallel with PA‐related neuroinflammation. [ABSTRACT FROM AUTHOR]

Background: Resolvins are endogenous mediators of the resolution of inflammation. They are derived from omega‐3 polyunsaturated fatty acid precursors. Resolvin D1 (RvD1) and Resolvin E1 (RvE1) are the best‐characterized members for actively promoting periodontal regeneration in experimental animal models. Here, we evaluated the efficacy of RvD1 and RvE1 on cementoblasts, the key cells involved in dental cementum regeneration and the attachment of the tooth to the alveolar bone. Methods: Immortalized mouse cementoblasts (OCCM‐30) were treated with different concentrations (0.1‐1000 ng/mL) of RvD1 and RvE1. Cell proliferation was measured using an electrical impedance‐based real‐time cell analyzer. Mineralization was evaluated with von Kossa staining. The mRNA expression of mineralized tissue‐associated markers of bone sialoprotein (BSP), Type I collagen (COL I), osteocalcin (OCN), osteopontin (OPN), runt‐related transcription factor 2 (RunX2), alkaline phosphatase (ALP), osteoprotegerin (OPG), receptor activator of nuclear factor kappa B (NF‐κB) (RANK), receptor activator of NF‐κB ligand (RANKL), and extracellular matrix‐degrading enzymes [matrix metalloproteinase (MMP)‐1, MMP‐2, MMP‐3, MMP‐9, and their tissue inhibitors (TIMP‐1, TIMP‐2)], RvE1 receptor (ChemR23) and RvD1 receptor (ALX/PFR2), cytokines (tumor necrosis factor‐alpha {TNF‐α}, interleukin {IL}‐1β, IL‐6, IL‐8, IL‐10, IL‐17), oxidative stress enzymes [superoxide dismutase (SOD), glutathione peroxidase (GPX), and cyclooxygenase‐2 (Cox‐2)] were analyzed using quantitative polymerase chain reaction (qPCR). Results: Both RvD1 and RvE1 (10‐100 ng/mL) significantly increased the proliferation of cementoblasts and mineralized nodules at all concentrations (p < 0.05). RvE1 increased BSP, RunX2, and ALP compared with the RvD1 dose and time‐dependently, while RvD1 and RvE1 differentially regulated COL‐I. RvE1 increased OPG mRNA expression, whereas RANK‐RANKL mRNA expression decreased by RvE1. MMP‐2, MMP‐3, MMP‐9, TIMP‐1, and TIMP‐2 expressions were reduced by RvE1 compared with RvD1. Treatment of cementoblasts with RvD1 and RvE1 differentially affected cytokine and oxidative stress enzymes while significantly increasing their receptor expressions (ChemR23 and ALX/PFR2). Conclusions: RvD1 and RvE1 regulate proliferation, mineralization, and gene expression in cementoblasts using similar pathways while differentially affecting tissue degradation, suggesting a targeted therapeutic approach for cementum turnover during periodontal regeneration. [ABSTRACT FROM AUTHOR]

Background: The resolution of inflammation is an active process mediated by specialized lipid mediators called lipoxins and resolvins. Periodontal ligament fibroblasts (PDLFs) play a significant role in periodontal regeneration. The purpose of the current study was to determine the impact of resolvin D1 (RvD1) on human PDLF cell wound healing and proliferation, receptor expression (G-protein-coupled receptor 32 [GPR32] and formyl peptide receptor 2 [ALX/FPR2]), and cytokine expression and release.Methods: PDLFs were stimulated with interleukin-1β (IL-1β) (500 pg/ml) with and without RvD1 (100 nM). RvD1 receptor expression was determined by quantitative real-time polymerase chain reaction (qPCR), immunofluorescence microscopy, and fluorescence-activated cell sorting. Wound closure was measured by a scratch assay, and proliferation was determined by bromodeoxyuridine incorporation. Interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein-1, cyclooxygenase-2, matrix metalloproteinases-1, -2, and -3 (MMP-1, -2, and -3), tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and -2), prostaglandin E2, and osteoprotegerin (OPG) gene expression and production were measured using qPCR and Western blotting, multiplex immunoassay, and enzyme-linked immunosorbent assay.Results: PDLF expressed GPR32 and ALX/FPR2. RvD1 reversed IL-1β-induced inhibition of wound healing and proliferation of PDLF. IL-1β also induced the production of proinflammatory cytokines and MMPs. This effect was reversed by RvD1. RvD1 reversed IL-1β-induced inhibition of TIMP-1, TIMP-2, and OPG.Conclusion: The data suggested that RvD1 has a pro-wound healing, proliferative, and anti-inflammatory impact on the PDLF that favors periodontal regeneration. [ABSTRACT FROM AUTHOR]

Background: Sex hormone therapy has strict recommendations in the treatment of postmenopausal symptoms, in which testosterone (TES) replacement may play a potential role. However, it remains unclear whether TES affects the course of chronic inflammation and alveolar bone loss in females. Herein, we investigated the role of androgen receptor and TES on the inflammatory response and alveolar bone resorption associated with ligature-induced periodontal disease in female rats.Methods: Fifty female Holtzman rats were divided in five groups (n = 10/group): androgen receptor antagonist (flutamide); estrogen receptor antagonist (fulvestrant); TES supplementation; aromatase inhibitor (anastrozole); and TES plus anastrozole. Periodontitis was induced by ligatures around the lower first molars for 2 weeks. Twenty animals (n = 10/group) were used as untreated ligated or non-ligated controls. Bone loss and the number of osteoclasts were measured through radiographic and immunohistochemical analysis, respectively. Inflammatory cytokines, chemokines and bone markers were measured by multiplex immunoassay and ELISA in serum samples and periodontal tissues.Results: The blockage of androgen receptor significantly increased radiographic bone loss and tissue levels of IL-1α (P <0.05), IL-1β (P <0.001) and IL-10 (P <0.01) compared with the periodontitis group. Testosterone supplementation significantly increased EGF levels in tissue samples, whereas when combined with aromatase inhibitor anastrozole significantly increased both EGF and VEGF (P <0.05). None of the treatment conditions significantly impacted the number of osteoclasts compared with the periodontitis group.Conclusions: Androgen receptor activation is an important factor in the regulation of several inflammatory markers, and its blockage significantly increases bone loss. [ABSTRACT FROM AUTHOR]

Background: Neutrophil function is critical for initiation and progression of infecto-inflammatory diseases. Key quorum-sensing plaque bacteria, such as Fusobacterium nucleatum, act as bridging species between early and late colonizer pathogens, such as Porphyromonas gingivalis, as the biofilm ages and periodontal inflammation increases. This study is designed to determine impact of different F. nucleatum strains on neutrophil function.Methods: Cells of human promyelocytic leukemia cell line-60 were differentiated into neutrophil-like cells and cultured with F. nucleatum strains of subspecies (ssp.) nucleatum ATCC 25586, ssp. polymorphum ATCC 10953, and ssp. vincentii ATCC 49256. Neutrophil phagocytosis of F. nucleatum strains and neutrophil apoptosis were analyzed by flow cytometry. Superoxide generation was measured by cytochrome C reduction in the presence and absence of N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) (1 μM) stimulation. Proinflammatory cytokine release was determined after 2, 6, and 24 hours of culture in the presence/absence of different F. nucleatum strains. Expression of Toll-like receptor (TLR)2, TLR4, and nuclear factor (NF)-kappa B mRNA levels were analyzed using real-time quantitative polymerase chain reaction. Each experiment was repeated at least three times in triplicate. Data were analyzed using analysis of variance followed by post hoc Bonferroni correction.Results: All strains of F. nucleatum significantly increased phagocytic capacity of neutrophils. Neutrophil phagocytosis of F. nucleatum ssp. polymorphum was significantly greater than that of F. nucleatum ssp. vincentii and ssp. nucleatum (P <0.001). F. nucleatum ssp. nucleatum and ssp. polymorphum significantly blocked fMLP-induced superoxide generation (P <0.001). Although F. nucleatum vincentii also reduced superoxide generation (25%), the impact was not as strong as that of ssp. nucleatum (83%) and ssp. polymorphum (100%). All F. nucleatum strains stimulated significant increase in neutrophil apoptosis compared with control (P <0.001) and significantly increased expression of NF-κB mRNA in neutrophils (P <0.05). Levels of interleukin-8 and tumor necrosis factor-α produced by neutrophils were significantly increased in all F. nucleatum groups compared with control (P <0.001).Conclusions: These findings suggest that different strains of F. nucleatum impact neutrophil function in different ways. Two of three subspecies blocked neutrophil superoxide generation in response to a secondary stimulus, preventing oxidative killing by neutrophils. The direct role of bridging species in pathogenesis of periodontitis may be greater than previously suspected in which they create a favorable environment for pathogenic transition of the dental ecosystem. [ABSTRACT FROM AUTHOR]

Background: Diacylglycerol (DAG), levels of which are tightly regulated by diacylglycerol kinases (DGKs), is a lipid mediator linked to key biologic functions. Members of the DGK family undergo alternative splicing, generating the protein diversity necessary to control different intracellular DAG pools. DGKα function is altered in polymorphonuclear neutrophils (PMNs) of patients with localized aggressive periodontitis (LAgP), suggesting a genetic basis. Here, the authors assess DGKα spliced transcripts in human LAgP neutrophils. Methods: In an expression library of a patient with LAgP, PMNs were screened for different DGKα transcripts. Realtime polymerase chain reaction and in vitro expression assays were performed to assess the fate of different transcripts on protein translocation and superoxide production in human leukemia cells (HL-60) and COS-7 cells. Results: A DGKα transcript that lacks exon 10 (DGKαΔl0) and generates a premature stop codon and a truncated protein was identified as being upregulated in LAgP neutrophils. In vitro assays revealed that DGKαΔl0 translocation occurred even in the absence of important regulatory motifs. Transfection of HL-60 neutrophil-like cells with the DGKαΔl0 spliced variant induced an increase in the stimulated production of superoxide anion replicating the phenotype of LAgP PMNs. Conclusion: DGKαΔl0 can act as a dominant-negative transcript that can modulate superoxide production and provides an example of genetic regulation of the inflammatory response that may be relevant to human inflammatory diseases such as LAgP. [ABSTRACT FROM AUTHOR]

Background: Chronic periodontitis (CP) is an inflammatory disease in which cytokines play a major role in the progression of disease. Anti-inflammatory cytokines (interleukin 4 [IL-4] and IL-10) were reported to be absent or reduced in diseased periodontal tissues, suggesting an imbalance between the proinflammatory and anti-inflammatory mediators. This study tests the hypothesis that there is cellular crosstalk mediated by proinflammatory and anti-inflammatory cytokines and that blocking proinflammatory cytokine (tumor necrosis factor-α [TNF-α] and IL-1) production will enhance anti-inflammatory cytokine (IL-4 and IL-10) production from peripheral blood mononuclear cells (PBMCs) in response to Porphyromonas gingivalis. Methods: PBMCs were isolated from individuals diagnosed with CP or healthy individuals and cultured for 24 hours. Concanavalin A (ConA) was used as an activator of lymphocyte function. Live and heat-killed P. gingivalis or lipopolysaccharide from P. gingivalis were used as the bacterial stimulants. TNF-α and IL-1 production was neutralized by specific antibodies against TNF-α and IL-Iα or IL-β. Culture supernatants were evaluated by enzyme-linked immunosorbent assay for TNF-α, IL-1β, IL-4, and IL-10 production. Results: Live P. gingivalis did not result in any significant IL-10 or IL-4 release, whereas heat-killed P. gingivalis led to a significant increase in IL-10 levels compared with unstimulated or live P. gingivalis-stimulated cells from both healthy individuals or those with CP. Overall, PBMCs from patients with CP produced significantly lower IL-10 in response to ConA and P. gingivalis, suggesting chronic suppression of the anti-inflammatory cytokine production. Blocking the proinflammatory cytokine response did not result in any substantial change in IL-10 or IL-4 response to live P. gingivalis. Blocking the proinflammatory cytokine response restored IL-10 production by cells from CP in response to P. gingivalis lipopolysaccharide. Conclusions: These findings suggest that PBMCs from patients with CP have suppressed anti-inflammatory cytokine production that can, in part, be restored by neutralizing proinflammatory cytokines. Monocytes are an important source of IL-10 production, and monocyte-derived IL-10 might play a regulatory role in the pathogenesis of CP. [ABSTRACT FROM AUTHOR]

Background: The aim of this study is to evaluate the effects of metronidazole-amoxicillin combination on clinical and microbiologic parameters in patients with generalized aggressive periodontitis. Methods: Twenty-eight patients were randomly included. The test group (n = 12) received amoxicillin-metronidazole combination and scaling and root planing; the control group (n = 16) received scaling and root planing alone. In addition to the clinical examinations, sub-gingival plaque samples were analyzed for total cultivable bacteria and the presence of Porphyromonas gingivalis, Tannerella forsythia (previously T. forsythensis), Treponema denticola, Prevotella intermedia, Prevotella nigrescens, Prevotella pallens, and Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans) using polymerase chain reaction. Results: All clinical parameters improved significantly compared to baseline (P<0.05) in both groups. There was a statistically significant reduction of pockets and clinical attachment gain in the combined group compared to the control group (P<0.05). Total counts of bacteria also decreased significantly at 3 and 6 months in both groups (P<0.05). T. denticola and T. forsythia were the most prevalent bacteria throughout the study. T. denticola showed a continuous decrease over 6 months in the test group, whereas no change was seen in the control group beyond 3 months. P. gingivalis decreased significantly at 3 months (P <0.05), whereas T. forsythia was the only pathogen decreased below detection limits by the combination therapy with a significant difference compared to the control group (P<0.05). Conclusions: The results from this study suggest that combined amoxicillin and metronidazole use as an adjunct to scaling and root planing leads to better clinical healing compared to mechanical treatment alone. The polypharmaceutical approach used results in a significant and substantial decrease in T. forsythia and prevents its recolonization for 6 months, suggesting that T. forsythia may determine the long-term stability of periodontal treatment outcomes. [ABSTRACT FROM AUTHOR]

Background: Hormonal changes during puberty, pregnancy, and menopause may impact periodontal tissues by altering the host response. There are only a few studies that examined gingival changes during the menstrual cycle. This longitudinal and prospective study aims to investigate clinical and laboratory markers of gingival inflammation in women at different phases during their menstrual cycles. Methods: Twenty-seven females were included in this study. Subjects were given oral hygiene instructions before the study, and their plaque index scores were recorded once a week for 2 months. The duration and regularity of the menstrual cycle were also checked at the same time. The gingival index and bleeding on probing (BOP) were recorded. Probing depths were measured to assess the periodontal condition of the subjects. Gingival crevicular fluid (GCF) was collected to analyze the levels of interleukin (IL)-113 and tumor necrosis factor-alpha on the first menstruation day (MD), estimated ovulation day (OD), and estimated predominant progesterone secretion day (PgD). These exact menstrual cycle days were determined according to serum progesterone and estradiol levels. Results: BOP and IL-1β levels in GCF showed significant increases from the MD to PgD under optimal plaque control. Among the 12 subjects that had premenstrual symptoms, six subjects reported oral complaints during the premenstrual period, whereas apthous lesions were more frequent during the menstruation period. Conclusion: These results demonstrate that the fluctuation of sex steroid hormones impact gingival inflammation during menstruation. [ABSTRACT FROM AUTHOR]

Background: It has been recently shown that monounsaturated fatty acids inhibit endothelial activation and reduce tissue responsiveness to cytokines. The present study has been planned to investigate topical application of a novel monounsaturated fatty acid complex (1-tetradecanol complex) for prevention of Porphyromonas gingivalis-induced periodontitis in rabbits. Methods: Experimental periodontitis was induced in New Zealand white rabbits with silk sutures tied a round the mandibular second premolars bilaterally, followed by the topical application of 109 colony forming units (CFU) of P. gingivalis. 1-Tetradecanol complex (1-TDC) was topically applied at 1 - and 10-mg/ml concentrations in five animals in each group, whereas control animals received olive oil vehicle (five animals) three times per week for 6 weeks, Negative controls included ligature alone (14 animals) or ligature + P. gingivalis (non treatment; 15 animals). Rabbits were sacrificed after 6 weeks, and mandibular block sections were obtained; tissues were decalcified and embedded in paraffin. Thin sections (5 µm) were stained with hematoxylin and eosin or tartrate-resistant acid phosphatase. Macroscopic and histologic evaluation of samples was followed by the characterization of cellular inflammatory infiltrate and quantitative histomorphometric measurements. Results: Treatment with both concentrations of 1-TDC and vehicle resulted in significant prevention of macroscopic periodontal inflammation and bone loss (75%; P <0.05) compared to the non-treatment (ligature + P. gingivalis) group, where significant periodontal tissue destruction characterized by attachment and bone loss was detected. However, there was no statistically significant difference between the vehicle and both 1-TDC groups. Histologically, 1-TDC inhibited inflammatory cell infiltration and prevented osteoclastogenesis, whereas treatment with vehicle did not show the same effect as in the 1-TDC groups; the difference between vehicle and the higher concentration of 1-TDC (10 mg/ml) was statistically significant. Conclusion: Topical application of an esterified monounsaturated fatty acid complex (1-TDC) was found promising in preventing bone loss, inflammatory cell infiltration, and connective tissue destruction in the rabbit periodontitis model. [ABSTRACT FROM AUTHOR]

Background: Neutrophil apoptosis may play a critical role in the resolution of inflammation by stimulating anti-inflammatory cytokine generation from monocytes. In this study, we investigated the effect of apoptotic neutrophils on interleukin (IL)-10 and IL-1beta production from monocytes in response to Porphyromonas gingivalis lipopolysaccharide.Methods: Peripheral blood neutrophils from healthy individuals were isolated by sodium diatrizoate density gradient centrifugation. In order to induce apoptosis, neutrophils were cultured for 24 hours in modified Dulbecco's medium supplemented with 10% autologous serum. Cell apoptosis was quantified by Annexin V positivity and loss of CD16 expression on the cell surface. Peripheral blood mononuclear cells were isolated from the same subjects; monocytes were purified by magnetic cell sorting and cultured with or without apoptotic or fresh neutrophils. Lipopolysaccharide from Porphyromonas gingivalis was used for cell stimulation. IL-1beta and IL-10 levels in supernatants were determined by enzyme-linked immunosorbent assay (ELISA).Results: IL-10 generation was significantly increased in monocytes cultured with apoptotic neutrophils compared to monocytes alone or cocultured with fresh neutrophils (P <0.05). IL-1beta was suppressed both in resting and lipopolysaccharide-stimulated monocytes in the presence of apoptotic neutrophils compared to monocytes alone or monocytes cultured with fresh neutrophils at all time points (P <0.05).Conclusion: Neutrophil apoptosis provides a signal to monocytes, changing the phenotype of the monocyte resulting in the production of anti-inflammatory cytokines and suppression of proinflammatory cytokines in response to lipopolysaccharide. [ABSTRACT FROM AUTHOR]

Background: Periodontopathic clinical markers are poorly understood in the pediatric population. Several studies have proposed Porphyromonas gingivalis (P. gingivalis) and an antibody response to the microorganism as factors in periodontal tissue destruction in children. The objective of this study was to examine the prevalence of P. gingivalis in dental plaque and of serum immunoglobulin G (IgG) antibody levels to P. gingivalis, and their relationship to periodontal clinical measures in children. Methods: Thirty-one subjects, aged 20 to 163 months, participated in this study. Clinical measures examined included gingivitis, plaque, alveolar bone height, age, gender, ethnicity, medical status, caries, and IgG antibody levels to P. gingivalis. Five ml of blood was collected for serum analysis, and IgG antibody levels to P. gingivalis were determined by using enzyme-linked immunosorbent assay. Plague samples were examined for the presence of P. gingivalis by DNA-DNA checkerboard. Data were analyzed on a person-level basis for relationships to serum IgG antibody levels to P. gingivalis and on a site-specific level for relationships to the presence of P. gingivalis in plaque. Results: A majority (77%) of the subjects were systemically healthy, non-white (74%), and did not have detectable P. gingivalis in their plaque. Fifty-two percent of the subjects had positive serum IgG antibody levels to P. gingivalis. Based on univariate linear regression, factors related to IgG antibody levels to P. gingivalis (P<0.05) included age, average gingival index (GI), average probing depth, and number of teeth with alveolar bone crest to cemento-enamel junction (ABC-CEJ) distances >2 mm. When all clinical measures were considered together, only age remained statistically significantly related to serum IgG antibody levels to P. gingivalis. Conclusions: Age is one of the most important factors in the development of the immune response to putative microorganisms such as P. gingivalis in children. The role of IgG as a time-sensitive measure of periodontal health in children needs to be investigated further. [ABSTRACT FROM AUTHOR]

Background: Behçet's disease (BD) pathogenesis involves severe outcomes such as blindness, central nervous system manifestations, and deep venous thrombosis that impacts systemic and local inflammatory changes. We tested the hypothesis that BD negatively affects gingival health and increases the severity of gingivitis., Methods: The study included 37 BD patients with gingivitis without any sign of periodontitis. Systemically healthy 19 patients with gingivitis (G) and 20 periodontally and systemically healthy individuals (C) were recruited as controls. BD patients were further grouped as stable and unstable based on their responses to BD treatment. Clinical periodontal parameters were measured to determine the impact of BD on gingival health. Serum and saliva levels of ELA-2 (neutrophil elastase-2), SLPI (secretory leukocyte protease inhibitor), α1-AT (alpha1-anti-trypsin), VEGF (vascular endothelial growth factor), IL-6 (interleukin-6), IL-8 (interleukin-8), and TNF-α (tumor necrosis factor alpha) were analyzed using multiplex immunoassay to measure the systemic and local inflammatory impact of BD., Results: Plaque index (PI), probing pocket depth (PPD), and bleeding on probing (BOP) were significantly higher in the BD group than in the controls (p < 0.05). IL-6 was higher in both serum and saliva in the BD group than in the G group (p < 0.05). ELA-2 levels in saliva were higher in the stable BD group than in the controls, while TNF-α and SLPI were statistically significantly higher in BD than in the control (p < 0.05). Salivary α1-AT level was statistically lower in the BD group compared to the control group., Conclusion: Our study suggested that the gingival inflammatory profile was impaired in patients with BD., (© 2024 American Academy of Periodontology.)

Background: Subgingival dental plaque is an ecosystem playing a key role in supporting both oral health and systemic health. Menopause-related changes have the potential to disrupt its balance, which is crucial to postmenopausal well-being. Our study explored how circulating estradiol levels correlate with subgingival microbial composition using checkerboard DNA-DNA hybridization in premenopausal and postmenopausal women. We also demonstrated that combining this method with 16S ribosomal RNA (rRNA) sequencing insights remains valuable for examining subgingival ecology., Methods: We assessed 40 bacterial species in 77 premenopausal and 81 postmenopausal women using checkerboard DNA-DNA hybridization and measured serum estradiol with enzyme-linked immunosorbent assay (ELISA). Women were categorized by subgingival dysbiosis severity using a modified Subgingival Microbial Dysbiosis Index (mSMDI). Six women from each normobiotic and dysbiotic subgroup across premenopausal and postmenopausal women underwent 16S rRNA sequencing analysis., Results: DNA checkerboard analysis revealed that most observed variability in individual bacterial proportions is associated with periodontitis. Two species, Leptotrichia buccalis and Streptococcus constellatus, exhibited differences related to estradiol levels within the premenopausal group (p = 0.055 and p = 0.009, respectively). 16S rRNA sequencing confirmed the mSMDI's validity in categorizing normobiotic and dysbiotic states. Menopausal status was not associated with a dysbiotic shift in the subgingival microbiome despite significantly more attachment loss in postmenopausal compared to premenopausal women., Conclusions: Our results indicate that decreased estradiol levels or increased attachment loss during menopause are not associated with changes in species abundance or dysbiotic shifts in women. The mSMDI may be a useful tool for classifying subgingival ecology based on its normobiotic or dysbiotic inclination., (© 2024 American Academy of Periodontology.)

Background: This study was designed to test the hypothesis that the leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the receptor for resolvin E1 (ERV1) prevents age- and diabetes-associated alveolar bone loss., Methods: LepR-deficient transgenic (TG) mice were cross-bred with those overexpressing ERV1 (TG) to generate double-TG mice. In total, 95 mice were divided into four experimental groups: wild type (WT), TG, LepR deficient (db/db), and double transgenic (db/db TG). The groups were followed from 4 weeks up to 16 weeks of age. The natural progression of periodontal disease without any additional method of periodontitis induction was assessed by macroscopic and histomorphometric analyses. Osteoclastic activity was measured by tartrate-resistant acid phosphatase (TRAP) staining., Results: At 4 weeks, ERV1 overexpression prevented weight gain. From Week 8 onward, there was a significant increase in the weight of db/db mice with or without ERV1 overexpression compared to the WT mice, accompanied by an increase in glucose levels. By 8 weeks of age, the percentage of bone loss in the LepR deficiency groups was significantly greater compared to WT mice. ERV1 overexpression in the db/db TG mice prevented early alveolar bone loss; however, it did not impact the development of diabetic bone loss in aging mice after the onset of weight gain and diabetes., Conclusions: The findings suggest that the overexpression of ERV1 prevents LepR-associated alveolar bone loss during the early phases of periodontal disease by delaying weight gain, diabetes onset, and associated inflammation; however, LepR deficiency increases susceptibility to naturally occurring inflammatory alveolar bone loss as the animal ages, associated with excess weight gain, onset of diabetes, and excess inflammation., (© 2024 American Academy of Periodontology.)

Background: Hormonal changes during puberty, pregnancy, and menopause may impact periodontal tissues by altering the host response. There are only a few studies that examined gingival changes during the menstrual cycle. This longitudinal and prospective study aims to investigate clinical and laboratory markers of gingival inflammation in women at different phases during their menstrual cycles., Methods: Twenty-seven females were included in this study. Subjects were given oral hygiene instructions before the study, and their plaque index scores were recorded once a week for 2 months. The duration and regularity of the menstrual cycle were also checked at the same time. The gingival index and bleeding on probing (BOP) were recorded. Probing depths were measured to assess the periodontal condition of the subjects. Gingival crevicular fluid (GCF) was collected to analyze the levels of interleukin (IL)-1beta and tumor necrosis factor-alpha on the first menstruation day (MD), estimated ovulation day (OD), and estimated predominant progesterone secretion day (PgD). These exact menstrual cycle days were determined according to serum progesterone and estradiol levels., Results: BOP and IL-1beta levels in GCF showed significant increases from the MD to PgD under optimal plaque control. Among the 12 subjects that had premenstrual symptoms, six subjects reported oral complaints during the premenstrual period, whereas apthous lesions were more frequent during the menstruation period., Conclusion: These results demonstrate that the fluctuation of sex steroid hormones impact gingival inflammation during menstruation.