Aim: To assess the role of periodontal health in oral malodor causation and compare the two methods (organoleptic and Halimeter) of malodor measurement. Materials and Methods: A total of 240 subjects (60 subjects without any evidence of periodontal disease and 180 patients with gingivitis and periodontitis) were evaluated for periodontal and oral malodor parameters. Periodontal parameters included Plaque Index (PI), Gingival Index (GI), mSBI, calculus component of OHIS, pocket depth (PD), and clinical attachment level (CAL), and oral malodor was assessed by organoleptic scores, Halimeter readings, and Tongue Coating Index (TCI). Results: 80% of the sample when assessed organoleptically (i.e. 192 subjects) and 74.6% when assessed with Halimeter (i.e. 179 subjects) presented with varying degrees of halitosis. All the clinical parameters were significantly associated with oral malodor (P < 0.001). The amount of tongue coating and bleeding on probing played the most important role in increasing VSC concentration, followed by periodontal status, plaque indices, and calculus component. Conclusion: There was a high prevalence of halitosis in the present study population. All the clinical parameters were significantly related to oral malodor in this study, and the results indicate that determining VSC levels with Halimeter is a useful means of diagnosing halitosis objectively.

(1) Background: This systematic review aimed to evaluate the effects of laser therapy on radiographic bone level (RBL) changes in peri-implantitis defects. (2) Methods: A literature search with defined inclusion criteria was performed. PubMed, Web of Science, Cochrane Library, and Google Scholar were searched through September 2020. The evaluated primary outcomes were RBL changes. In studies that reported RBL data, corresponding secondary clinical outcomes were probing depth (PD), bleeding on probing (BOP), and clinical attachment level (CAL). (3) Results: Thirteen articles were selected for data extraction and risk of bias assessment. Eight studies showed evidence of RBL gain in the laser groups compared to baseline, but did not report the statistical significance. Eight of these 13 studies reported comparisons to control. Five of the eight studies did not show RBL gain in the laser groups compared to control. In the laser groups compared to baseline, 11 of 13 reported reduced PD, and 6 of 13 reported significantly reduced BOP. Compared to the control, eight of the eight reported reduction of PD, and three of six reported significantly reduced BOP. Statistical significance was not consistently reported. (4) Conclusions: Within the limits of this systematic review, laser treatment may promote bone gain in peri-implantitis defects, may reduce BOP and PDs, and may be comparable to mechanical therapy. However, definitive conclusions can only be made with statistically significant data, which were found lacking in the currently available studies. This systematic review was registered with the National Institute for Health Research, international prospective register of systematic reviews (PROSPERO): CRD42020207972.

Adherence and colonization of candida on denture soft liners is the most important contributing factor in development of denture stomatitis. This invitro study is undertaken to investigate whether the incorporation of tea tree oil into denture soft liners would inhibit the growth of candida albicans. Each 10 specimen disks incorporated with tea tree oil into soft liners (St) and without tea tree oil (S) were prepared. Both the tea tree oil daily. These disks were inoculated with candida albicans suspension for assessment of fungal growth and were rinsed with sterile water to remove loosely attached surface organisms. The attached yeasts were measured by inoculating them on saboraud's agar. Treated and control disks were stored in distilled water for 1, 30, 60 days and washed daily with wet cotton. Data between treated and control disks were compared by applying t-test. The mean colony forming units (CFU) per mm(2) for specimens without tea tree oil after water storage and wash with wet cotton for 1, 30 and 60 days was 7.1 × 10(6), 6.5 × 10(6), 6.8 × 10(6), respectively and for specimens with tea tree oil CFU decreased significantly to 2.1 × 10(6), 2.8 × 10(6), 3.1 × 10(6) after 1, 30 and 60 days. Treated disks were effective in controlling the growth of C.albicans for two months following water storage. Addition of tea tree oil to denture soft liner significantly reduced growth of C.albicans suggesting a new form of intra oral effective antifungal management for denture stomatitis.

Background/Objectives: Periodontal disease (PD) is a chronic inflammatory condition caused by dysbiosis of the oral microbiome. PD is linked to systemic inflammation and endothelial dysfunction, which associate it with cardiovascular disease (CVD). This systematic review explores the molecular and microbial mechanisms through which periodontal pathogens, including “Red Complex” bacteria (Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola) and Fusobacterium nucleatum, influence cardiovascular health via inflammatory pathways, immune modulation, and microbial dissemination. Methods: A systematic review was conducted following PRISMA guidelines. A literature search was conducted in the PubMed and ScienceDirect databases using relevant keywords, with strict inclusion and exclusion criteria, from the first week of September 2024 to the first week of October 2024. Studies addressing the relationship between PD and CVD were assessed for methodological rigor, relevance, and data availability. The outcomes were synthesized using a descriptive narrative approach. Out of 591 records screened, 421 full-text articles were sought for retrieval. The final review included 58 articles providing supplementary aggregated data after eligibility assessment. Results: The pathogenesis of PD involves the activation of immune cells and the release of pro-inflammatory cytokines (such as IL-1, IL-6, TNF-α, and PGE2) and chemokines (including IL-8 and MCP-1) along with oxidative stress driven by reactive oxygen species (ROS). Periodontal pathogens trigger endothelial oxidative stress and systemic inflammation via Toll-like receptors (TLRs), NF-κB signaling, and nitric oxide (NO) dysregulation, contributing to endothelial dysfunction and atherogenesis. Biomarkers, such as C-reactive protein, interleukins, and matrix metalloproteinases (MMPs), further highlight the systemic inflammatory response. Conclusions: This review underscores the significant role of periodontal pathogens and inflammatory mediators in systemic health, particularly in the progression of CVD. Although existing evidence illustrates these associations, the underlying molecular mechanisms remain inadequately understood, indicating a need for further research to advance precision medicine and therapeutic strategies.

Porphyromonas gingivalis (Pg), a Gram-negative oral pathogen, promotes and accelerates periodontitis-associated gut disorders. Intestinal epithelial barrier dysfunction is crucial in the pathogenesis of intestinal and systemic diseases. In this study, we sought to elucidate the protective role of cinnamaldehyde (CNM, an activator of Nrf2) against P. gingivalis (W83) and Pg-derived lipopolysaccharide (Pg-LPS) induced intestinal epithelial barrier dysfunction via antioxidative mechanisms in IEC-6 cells. IEC-6 (ATCC, CRL-1592) cells were pretreated with or without CNM (100 µM), in the presence or absence of P. gingivalis (strain W83, 10⁹ MOI) or Pg-LPS (1, 10, and 100 µg/mL), respectively, between 0–72 h time points by adopting a co-culture method. Intestinal barrier function, cytokine secretion, and intestinal oxidative stress protein markers were analyzed. P. gingivalis or Pg-LPS significantly (p < 0.05) increased reactive oxygen species (ROS) and malondialdehyde (MDA) levels expressing oxidative stress damage. Pg-LPS, as well as Pg alone, induces inflammatory cytokines via TLR-4 signaling. Furthermore, infection reduced Nrf2 and NAD(P)H quinone dehydrogenase 1 (NQO1). Interestingly, inducible nitric oxide synthase (iNOS) protein expression significantly (p < 0.05) increased with Pg-LPS or Pg infection, with elevated levels of nitric oxide (NO). CNM treatment suppressed both Pg- and Pg-LPS-induced intestinal oxidative stress damage by reducing ROS, MDA, and NO production. Furthermore, CNM treatment significantly upregulated the expression of tight junction proteins via increasing the phosphorylation levels of PI3K/Akt/Nrf2 suppressing inflammatory cytokines. CNM protected against Pg infection-induced intestinal epithelial barrier dysfunction by activating the PI3K/Akt-mediated Nrf2 signaling pathway in IEC-6 cells.