Objectives: The objective of was to investigate the predictive value of single nucleotide polymorphism (SNP) in the promoter region of the cytokine interleukin(IL)-1β С(-511)Т; IL-6 G(-174)C; tumour necrosis factor(TNF)-α G(-238)A; matrix metalloproteinase(MMP)-9 С(-1562)T; urokinase plasminogen activator (uPA) С(-422)T; and urokinase plasminogen activator receptor (uPAR) T(-516)C gene as a risk modulator for the development of gingival recessions in adults. Methods: A total of 42 patients (age 270-35) with gingival recession were divided into groups: group I comprised 1, 2 Miller class (n = 22), with subgroup Ia (n = 17) with thin gingival biotype and Ib (n = 5) with thick gingival biotype; group II comprised 3, 4 Miller class (n = 20), with subgroups IIa (n = 6) with thin gingival biotype, and IIb (n = 14) with thick gingival biotype. Clinical measurements included vertical recession depth (VRD), clinical attachment level (CAL), keratinised gingival width (KGW), gingival biotype (GB), visible plaque index (PI) and papilla bleeding index (PBI). All subjects were without comorbidity and did not take any drugs. Gingival biopsy material was obtained during surgical gingival recession covering for DNA extraction. Genotyping was done using polymerase chain reaction in real time (RT-PCR) with analysis of melting curves by DT-96 DNA-Technology[tm] system. Statistical analysis for genotyping was presented by SNPStats[tm] 2006 software. Results: Patients in group Ia (1,2 Miller class recession with thin gingival biotype) expressed significantly more wildtype genotypes in genes (СС) IL-1β С(-511)Т (pwere not statistically significant. It was noticed that male patents aged under 40 [expressed?] high rates of mutant alleles in which genes for 1, 2 Miller class recession with thick biotype (group IIa). Conclusion: Carrying the mutant allele T gene uPA С(-422 )T in the promoter region appears to be a risk factor for developing gingival recession and is a potential predictor for more severe clinical phenotypes.

Objectives: Evaluate the bone formation in periodontal fenestration defects in rats applying bone marrow mesenchymal stem cells (MSC) with or without Enamel Matrix Derivate (EMD). Methods: Periodontal fenestration defects of 2 mm in height, 4 mm in width and 1 mm in depth were created in the mandible of isogenic rats. The animals were allocated into 6 groups and further divided into 3 subgroups for euthanasia at 15, 30 or 60 days postoperative (n=6 for each subgroup). Control Group (C) was the spontaneous healing. In the Propylene Glycol Alginate Group (PGA) 25µl of the vehicle was applied in the defect. The Enamel Matrix Derivate Group (EMD) received 25 µl of Emdogain™. Mesenchymal stem cells (MSC) were collected from the iliac crest of 2 isogenic rats, isolated with Ficoll and cultured in flasks. The cells were separated by flow cytometry to obtain a cell population of CD45-90+ MSC. In the mesenchymal stem cell groups (MSC, MSC-PGA and MSC-EMD) a pellet with 1,2 x 106 cells was applied in each defect, but in MSC-PGA and MSC-EMD groups the pellet was mixed with 25µl of PGA or EMD, respectively. After euthanasia the mandibles were fixed and scanned by computed microtomography apparatus. Bone volume, bone density, trabecular number and thickness were analyzed by SigmaPlot™. The normality of data was checked and ANOVA One-Way test was used, with a significance level of 5%. Results: Bone volume was increased in all groups in all times (p 0.05). In 60 days all groups were similar and had higher volume than PGA (p 0.05) and higher than C, PGA and MSC (p 0.05). MSC-E also had higher number than C and MSC (p 0.05) but statistically larger than C, EMD and PGA (p > 0.05). In 60 days C and EMD had higher thickness than MSC, MSC-PGA and MSC-EMD (p Conclusion: The adhesion of stem cells to EMD resulted in more bone volume in periodontal regeneration defects only in the period of 30 days. However, the bone density and the trabecular number and thickness were either similar or inferior to EMD alone.