Background and Objective: Aggressive periodontitis is a destructive disease that leads to a quick and extensive periodontal tissue loss. Mast cells are known to play important roles in allergic reactions, host defense against bacterial infections, local homeostasis, inflammation, and angiogenesis. The aim of the present study was to evaluate the relationship between mast cell numbers and Aggressive periodontitis.Materials and Methods: A descriptive analytical and blind study was designed and gingival specimens from 19 moderate to advanced Aggressive periodontitis sites (case group) and 18 gingivitis sites (control group) was taken during flap and crown lengthening surgeries. Toluidine blue and Hematoxylin Eosin staining were done for mast cell counting and inflammation assessment, respectively. Inflammatory and mast cells in 5 micron sections were assessed by two trained observers utilizing light microscopy. ANOVAs and T test with an alpha error level less than 5% were used to analyze the data.Results: The mean values of the mast cell numbers were 7.6±10.8 and 9.8±13.0 in Aggressive periodontitis and gingivitis sites, respectively. There were no statistically significant differences among the mast cell counts, clinical attachment loss, or pathologic inflammation (P> 0.05).Conclusions: The present study indicates that mast cell numbers were not significantly different between Aggressive periodontitis and gingivitis. Further studies are required to evaluate dynamic aspects of host defense.

Aim: Several studies, rerealed that in pathogenesis of Aggressive periodontitis, neutrophil dysfunction especially chemotaxis defects may have some role. But in other studies, there is no report of neutrophil chemotaxis defect in patients with Aggressive periodontitis. In this regard, this study was designed to assess the chemotaxis of peripheral blood neutrophils in patients with Aggressive periodontitis. Materials and Method: For this purpose, we studied the neutrophil chemotaxis of 27 patients with Aggressive periodontitis which intum included: 12 patients with LJP; 7 patients with GJP; and 8 patients with RAP. Also,we included 10 normal subjects in our study as control group. The chemotaxis test was performed as leading&ont assay by using 3 micrometer filters and LPS-activated serum as chemotactic factor. Results: Statistical analysis by Kruskal WaIlis and Mann-Whitney U tests showed that the random migration of neutrophils in the case group (Aggressive periodontitis patients) is significantly lower than control group (P<0.015) but in the case of netrophil chemotaxis, no significant difference was seen. The net chemotaxis of LJP group was significantly higher than control group (P<0.009). Conclusion: These results showed that there is no defect in the chemotaxis of peripheral blood neutrophils of Iranian patients with Aggressive periodontitis. So it is likely that the neutrophil dysfunction is not important in the pathogenesis of Aggressive periodontitis in Iranian patients. Of course more studies are needed in order to emphasize the above hypothesis.

Background &Aim: Aggressive periodontitis is a disease characterized by rapid destruction of supporting structure of teeth in young adult. The main causative factor in periodontal disease is the bacterial plaque, however, genetic is considered one of the main predisposing factors of the disease. Efforts to find genetic markers of this disease are one of the most active fields of periodontal research. The major histocompatiblity complex genes in human have been investigated to find correlation between the presence of specific MHC genes as possible genetic marker of certain diseases. MHC investigations on Aggressive periodontitis have shown inconclusive results. The aim of this study was to address the question as to whether there is a significant association between Aggressive periodontitis and HLADQB1- 0201 sub group.Methods & Materials: This was a case-control study. Data collection was performed by direct examination of samples and the study population was selected among patients referring to Periodontitic Department of Mashed Dental School, as well as periodontal practices and clinics in the city of Mashed. Sampling was a convenience sampling method through witch 59 individuals including of 30 subjects with Aggressive periodontitis and 29 periodontal healthy subjects were selected and the method of examination was PCR-ssp. X2 test was used to test the presence of significant association.Results: 14 persons of cases were positive for allele 0201 and 16 persons were negative for the allele, while 10 persons of the controls were positive and 19 persons were negative for the allele.Conclusion: These findings indicate that the prevalence of HLA- DQB1 allele 0201 is greater among subjects with periodontitis as compared to periodontal healthy subject. However, this association is not statistically significant.

Background: Interleukin-29 (IL-29) is one of the cytokines which has immunomodulatory properties and might play a role in the pathogenesis of periodontal diseases. The aim of this study was an immunohistochemical analysis of IL-29 in gingival tissues of chronic and Aggressive periodontitis. Materials and Methods: In this cross-sectional study based on clinical evaluation and inclusion and exclusion criteria, 20 patients with generalized chronic periodontitis, 13 patients with generalized Aggressive periodontitis, and 20 periodontally healthy individuals were enrolled. Gingival tissue samples were obtained during periodontal flap and crown lengthening surgery in periodontal patients and healthy individuals, respectively. Tissue samples were examined to determine the level of IL-29 expression by immunohistochemistry. The data were analyzed using SPSS and paired t-test, ANOVA test, and Tukey’ s test (P < 0. 05). Results: A total of 53 participants (34 females and 19 males) were enrolled in this study. IL-29 expression in the connective tissue of the patient groups was more than the healthy one (P < 0. 001). In the Aggressive periodontitis group, there was a significant increase of IL-29 expression compared to the other two groups, but there was no significant difference between the chronic periodontitis and healthy groups. Conclusion: According to the results of this study, IL-29 expression was increased in the gingival tissue of Aggressive and chronic periodontitis. IL-29 local expression in Aggressive periodontitis is higher than the chronic periodontitis and healthy groups, which could suggest the role of IL-29 in the etiopathogenesis of Aggressive periodontitis.

Background: Visfatin, also known as nicotinamide phosphoribosyltransferase, has been suggested as a pro‑ inflammatory and immunomodulating marker for periodontitis. The aim of this study was an immunohistochemical analysis of visfatin in gingival tissues of patients with chronic periodontitis and Aggressive periodontitis. Materials and Methods: In this cross‑ sectional study based on clinical evaluation and inclusion and exclusion criteria. Twenty patients with generalized chronic periodontitis, 13 patients with generalized Aggressive periodontitis, and 20 periodontally healthy individuals enrolled. Gingival tissue samples were obtained during periodontal flap surgery and crown lengthening surgery in periodontal patients and healthy group, respectively. Tissue samples were transferred to a pathology laboratory to determine the degree of inflammatory infiltration by hematoxylin and eosin staining and the level of visfatin expression by immunohistochemistry. The data were analyzed using SPSS version 20 statistical software and paired t‑ test, Mann– Whitney test, and Spearman rank correlation coefficient. P < 0. 05 was considered statistically significant. Results: Inflammation grading and visfatin expression were significantly higher in periodontally diseased gingiva compared to the control group (P < 0. 05). However, no significant difference was found between two diseased groups. The relationship between inflammation grading and visfatin expression in Aggressive periodontitis group was statistically significant, positive and relatively strong (P = 0. 025, r = 0. 617). However, no significant relationship has been found between visfatin expression and inflammation grading in the chronic periodontitits and control groups (P > 0. 05). Conclusion: Visfatin expression was increased in gingival tissues of chronic periodontitis and Aggressive periodontitis patients. Hence, visfatin may have a role in the etiopathogenesis of chronic periodontitis and Aggressive periodontitis.

Introduction: GAgP is a multifactorial disease, which occurs in presence of bacteria and is influenced by genetic and environmental factors; leading to periodontal tissue dysfunction among subjects younger than 30 years. Proinflammatory cytokines are involved in immune response to periodontal pathogens through associating in inflammation phenomenon. It is supposed that gene polymorphisms of cytokines play a role in immune response and therefore in periodontal pathogenesis. In this study we assessed the gene polymorphisms of most important proinflammatory cytokines: Interleukin (IL)-1b +3954 C/T, IL-1a -889 C/T & Tumor necrosis factor-a (TNF-a) -308 G/A.Materials & Methods: In this case-control study approved by ethical committee of Mashhad University of Medical Sciences, after obtaining arm venous blood samples from patients (n=65) and healthy individuals (n=60) referring to Mashhad dental school, the DNA was extracted in Bu-Ali Research Institute. Restriction fragment length polymorphism polymerase chain reaction (PCR-RFLP) procedure was performed for determining polymorphisms. Data were analyzed by SPSS software V.15.Results: IL1b: CT, CC & TT genotypes in patients were 39.6%, 60.4% & 0.0% and in healthy individuals 41.7%, 50% & 8.3%, respectively. IL1a: CT, CC & TT genotypes in patients were 44.6%, 46.2% & 9.2% and in healthy individuals were 46.5%, 51.2% & 2.3%, respectively. TNFα: GA, GG & AA genotypes in patients were 44.8%, 41.4% & 13.8% and in healthy individuals were 46.7%, 50% & 3.3%, respectively. None of the differences was statistically significant.Conclusion: The lack of any association between the IL-1a, IL-1b, TNF-a polymorphisms and GAgP in the population presented here, brings into doubt the usefulness of these candidate genes as markers of susceptibility to this form of periodontitis.