Background/Aim. Mast cells are mononuclear cells originating from bone marrow. They produce various biologically active substances, which allow them to actively participate in immune and inflammatory processes associated with periodontal disease. The study focused on distribution and density of mast cells in healthy gingiva as well as in different stages of periodontal disease. Methods. The material used for this purpose was gingival biopsies taken from 96 patients classified into 4 groups: healthy gingiva, gingivitis, initial and severe periodontal disease. Toluidine blue staining according to Spicer was utilized for identifying mast cells. Results. Basing on our study, the density of mast cells in the gingival tissue increases with the progression of the infection, which means they are more numerous in gingivitis compared to healthy gingiva, as well as in periodontal disease compared to gingivitis. Conclusion. Increase in the number of mast cells in the infected gingiva can be correlated with an increased influx of inflammatory cells from blood circulation into the gingival stroma, as well as with the collagen lysis, since these cells produce substances with collagenolytic potential. Based on the distribution of mast cells, it could be concluded that in the evolution of periodontal disease there are significant dynamic alterations in migration and localization of these cells.

Background and objectives: Atherosclerotic cardiovascular disease (ASCVD) remains a major global cause of mortality, with chronic infections and systemic inflammation, including those arising from periodontal pathogens, contributing to vascular pathology. This study aims to investigate the presence of bacterial DNA from oral cavity microorganisms in atherosclerotic plaques of patients with abdominal aortic aneurysm (AAA) and to explore correlations with oral health indices and clinical variables. Materials and Methods: Forty patients (mean age 61 ± 6 years; 60% male) with periodontitis and AAA were included. Subgingival biofilm and arterial plaque samples were analyzed using PCR for A. actinomycetemcomitans, P. gingivalis, P. intermedia, T. forsythensis, and T. denticola. Dental indices (PI, GI, SBI, and PPD) were determined in all patients, and concordance of the findings was assessed by Cohen’s κ, and correlations were evaluated using Spearman’s coefficient. Results: P. gingivalis exhibited the highest concordance between oral and arterial plaques, followed by T. forsythensis and A. actinomycetemcomitans. T. denticola DNA was not detected in aortic samples. Positive correlations found between A. actinomycetemcomitans and P. gingivalis with dental indices were found to be statistically significant. Conclusions: The detection of periodontal pathogens, particularly P. gingivalis and T. forsythensis, in both oral and arterial plaques supports their potential role in atherosclerotic and aneurysmal changes. The findings highlight the relevance of periodontal health in cardiovascular risk prevention and the need for longitudinal studies to reveal causal mechanisms.

Parodontalna bolest (parodontopatija) je hronična inflamatorna bolest u čiju patogenezu su uključene različite ćelije urođenog i stečenog imuniteta, među kojima i makrofagi. Makrofagi su profesionalni fagociti čija je osnovna uloga ingestija i destrukcija mikroorganizama. Pored fagocitoze, ove ćelije su angažovane u produkciji proinflamatornih citokina i u prezentaciji antigena T-ćelijama, te se smatraju ključnim ćelijama urođenog imunskog odgovora. U našem istraživanju praćena je gustina i distribucija makrofaga u zdravoj i inflamiranoj gingive sa ciljem da se proceni njihov značaj u patogenezi parodontopatije. Materijal su činile gingivalne biopsije 96 pacijenata svrstanih u 4 grupe: zdrava gingiva, gingivitis, početna parodontopatija i uznapredovala parodontopatija. Za identifikaciju makrofaga korišćena je imunohistohemijska tehnika bojenja zasnovana na upotrebi monoklonskog antitela anti-CD68. Prema našem istraživanju gustina makrofaga je veća u gingivitisu i parodontopatiji u odnosu na zdravu gingivu. Između gingivitisa i parodontopatije nije nađena značajna razlika u gustini makrofaga. Grupisanje makrofaga u blizini delimično liziranih kolagenih vlakana u parodontopatiji ukazuje na njihovu kolagenolitičku aktivnost. Povećanje broja makrofaga u inflamiranoj gingivi može se dovesti u vezu i sa resorpcijom kosti jer se ove ćelije mogu diferencirati u osteoklaste.

Collagen is a major constituent of the gingival extracellular matrix, which crucially affects the histoarchitecture of the gingival tissue. Collagen type I dominates the gingival tissue, while type II, III and IV are present to a lesser extent. Changes in distribution and density occur in the inflamed gingiva. The aim of the study was to examine the organization and density of the collagen in healthy and inflamed gingiva. The material for the study consisted of the gingival biopsies performed in 96 patients aged from 13 to 70 years. The gingival specimens were classified into 4 groups: healthy gingiva, gingivitis, moderate periodontal disease and severe periodontal disease. The samples of the gingival tissues were stained by the method of Van Gieson’s Stain, while the VD of the collagen was measured bz the use of multipurpose testing system M42. In healthy gingival collagen are thick and receptive to color. In gingivitis collagen is mostly preserved structure, but reduced volume; in the periodontitis collagen bundles are reduced, short, thin, disorganized, often fragmented and less susceptibility to color. In healthy gingiva collagen fibers occupy 58.6 ± 5.1% of the volume of lamina propria; in gingivitis significantly lower (44.2 ± 6.2%); in moderate periodontitis 32.7 ± 8.5% and in the progressed periodontitis only 28.7 ± 9.7%. Based on our results, we concluded that in periodontal disease occurs collagenolysis. Quantitative evaluation of gingival collagen volume density may reflect the clinical severity of periodontal disease.

Photobiomodulation (PBM) may improve diabetic wound repair, but the temporal relationship between local angiogenic signaling and tissue-level healing remains incompletely defined. We examined previously unreported tissue vascular endothelial growth factor (VEGF) and histopathological outcomes from 72 ulcer-bearing male Wistar rats from a previously reported experimental cohort, using a balanced 2 × 2 × 3 design comprising metabolic status, PBM treatment, and healing day (3, 7, or 10; n = 6 per cell). Tissue VEGF was quantified by ELISA and normalized to total protein; histopathological outcomes included exploratory inflammation/injury and tissue repair composite scores. In the factorial log-VEGF model, diabetes × day (p = 0.0017) and LLLT × day (p = 0.0010) interactions demonstrated phase-dependent responses. On day 3, PBM-treated animals had an adjusted VEGF ratio of 2.13 versus untreated animals (95% CI 1.63–2.78; Holm-adjusted p < 0.001), whereas diabetic animals had lower VEGF than healthy animals (ratio 0.50, 95% CI 0.39–0.66; adjusted p < 0.001). VEGF concentrations converged by day 10. PBM remained associated with a higher exploratory tissue repair score after adjustment for healing day, diabetes status, and contemporaneous VEGF, whereas VEGF itself was not independently associated with repair. These findings demonstrate phase-dependent differences in tissue VEGF and suggest that contemporaneous VEGF concentrations do not fully explain treatment-associated variation in exploratory histopathological repair scores.