Full-mouth disinfection effects on gingival fluid calprotectin, osteocalcin, and N-telopeptide of Type I collagen in severe periodontitis.

BACKGROUND: To compare the effects of full-mouth disinfection (FMD) and full-mouth ultrasonic debridement (FMUD) on clinical, microbiological and biochemical parameters with conventional quadrant-wise scaling and root planning (Q-SRP) in severe chronic periodontitis. METHODS: In the present prospective randomized controlled clinical trial with three parallel arms (#NCT04038801), 60 chronic periodontitis patients were randomly assigned to three study groups by a consecutive number in ascending order: FMD (n = 20), FMUD (n = 20), and Q-SRP (n = 20). All measurements and treatments were performed by the same investigator. At baseline, gingival crevicular fluid (GCF) and subgingival plaque were collected and clinical periodontal parameters were recorded. Ultrasonic debridement was completed within 24 hours in FMD and FMUD groups. Chlorhexidine gluconate was used for FMD. Q-SRP was performed by hand instruments per quadrant at 1-week-intervals. Clinical measurements and sampling were repeated at 1, 3, and 6 months after treatment. Real-time PCR was used for quantitative analysis of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, and total bacteria count. GCF Calprotectin, osteocalcin, and N-telopeptide of type I collagen (NTx) levels were analyzed by ELISA. The changes of GCF biomarker levels after treatment between groups were the primary outcomes. RESULTS: No harm was observed. All treatment strategies resulted in significant improvements in all clinical parameters (P < 0.05), with no significant differences between study groups at all time-points (P ˃ 0.05). Aggregatibacter actinomycetemcomitans was significantly decreased in FMD compared to FMUD and Q-SRP at 6 months (P < 0.05). Although GCF NTx total amounts increased in all groups during the study period, this increase was less prominent in full-mouth groups at three time points after treatment (P < 0.05). CONCLUSIONS: Present results represent the short-term effects. Full-mouth treatment approaches offered limited beneficial effects on microbiological and biochemical parameters over quadrant-wise approach. All three treatment strategies can be recommended in the management of severe chronic periodontitis.

Use of Fractal Analysis for the Discrimination of Trabecular Changes Between Individuals With Healthy Gingiva or Moderate Periodontitis.

BACKGROUND: The aim of this study is to evaluate the capability of fractal analysis to discriminate the changes in the trabecular structure of interdental bone between individuals with healthy gingiva or moderate periodontitis using digital images. METHODS: Two groups of patients were included according to the probing depth, bleeding on probing, and clinical attachment level. The first group (n = 50) consisted of individuals with healthy gingiva, whereas the other group consisted of patients with moderate periodontitis (n = 50). Periapical images obtained with a storage phosphor plate system during clinical examination were used for the fractal dimension (FD) calculations. Two rectangular regions of interest (ROIs) were placed at mandibular posterior interdental bone areas. The mean of the two ROIs was used to calculate mean FD by using the box-counting method. Student t test was used for the comparison of the FDs of the two groups (P = 0.05). RESULTS: The mean FD of patients with periodontitis was 0.83, whereas it was 1.02 for the patients with healthy gingiva. A significant difference was obtained in the mean FD values of healthy individuals and patients with moderate periodontitis (P <0.05). CONCLUSION: Fractal analysis can quantitatively discriminate the trabecular integrity alterations induced by periodontitis and therefore can be recommended for the diagnosis and monitoring of changes in trabecular architecture associated with periodontitis.

Gene polymorphisms of matrix metalloproteinase-2, -9 and -12 in periodontal health and severe chronic periodontitis.

AIM: Matrix metalloproteinases (MMPs) are involved in periodontal tissue remodeling and degradation. MMP polymorphisms could alter transcription and function of these enzymes. The aim of this study was to investigate MMP-2, MMP-9 and MMP-12 gene polymorphisms in relation to susceptibility to severe chronic periodontitis (CP). METHODS: Genomic DNA was obtained from peripheral blood of 87 severe CP patients and 107 periodontally healthy subjects. MMP-2 -735C/T, MMP-9 -1562C/T and MMP -12357Asn/Ser gene polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism. Probing depth, clinical attachment loss, supragingival plaque accumulation and bleeding on probing were recorded. The data were analyzed by chi-square, logistic regression and Mann-Whitney-U-tests. RESULTS: The genotype distributions and allele frequencies of MMP-2, MMP-9 and MMP-12 genes were similar in CP and healthy subjects (p>0.05). Differences between rare allele carriage rates of CP and healthy groups regarding MMP-2, MMP-9 and MMP-12 gene polymorphisms were not significant (p>0.05). However, T allele carriers of MMP-9 -1562 gene had less risk for CP (OR=0.36; 95% CI=0.16-0.81). CONCLUSION: These data suggest that MMP-2 -735C/T, MMP-9 -1562C/T and MMP-12 357Asn/Ser polymorphisms are not associated with susceptibility to severe CP in Turkish population. However, T allele of MMP-9 -1562 gene might be associated with decreased susceptibility to severe CP.

Matrix metalloproteinase-2, -9, and -12 gene polymorphisms in generalized aggressive periodontitis.

BACKGROUND: Matrix metalloproteinases (MMPs) are involved in periodontal tissue remodeling and degradation. Polymorphisms in the promoter region of the MMP-2 and -9 genes and in the coding region of the MMP-12 gene could affect transcription and the function of these enzymes. The aim of the present study was to determine the association between the aforementioned MMP polymorphisms and generalized aggressive periodontitis (GAgP). METHODS: Genomic DNA was obtained from the peripheral blood of 92 subjects with GAgP and 157 periodontally healthy subjects. MMP-2 -735C/T, MMP-9 -1562C/T, and MMP-12 357Asn/Ser polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism. Probing depth, clinical attachment loss, supragingival plaque accumulation, and bleeding on probing were recorded. The data were analyzed by chi(2), logistic regression, and Mann-Whitney U tests. RESULTS: The genotype distributions, allele frequencies, and rare allele carriage of MMP-2 and MMP-12 genes were similar in GAgP and healthy subjects (P >0.05). T allele frequency and T allele carriage of the MMP-9 -1562 C/T polymorphism were significantly lower in the GAgP group than in the healthy group (P <0.05). In addition, logistic regression analysis revealed a protective effect for MMP-9 -1562 T allele carriers (odds ratio = 0.52; P = 0.04). CONCLUSIONS: MMP-2 -735C/T and MMP-12 357Asn/Ser polymorphisms are not related to GAgP. Conversely, the MMP-9 -1562 gene T allele might be associated with a decreased risk for GAgP in the Turkish population.

Tissue plasminogen activator and plasminogen activator inhibitor-1 gene polymorphisms in patients with chronic periodontitis.

BACKGROUND: Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) are involved in the pathogenesis of periodontitis by controlling proteolytic events in the extracellular matrix. This study was designed to investigate the association of t-PA and PAI-1 gene polymorphisms with chronic periodontitis (CP). METHODS: One hundred eighty-nine subjects were included. Genomic DNA was obtained from the peripheral blood of 84 patients with CP and 105 periodontally healthy subjects. Polymerase chain reaction and endonuclease digestion was used to genotype the 4G/5G polymorphism in the promoter region of the PAI-1 gene and the Alu-repeat insertion (I)/deletion (D) polymorphism in intron 8 of the t-PA gene. RESULTS: The genotype distributions and allele frequencies of t-PA polymorphism were not different between patients with CP and healthy subjects (24.7% I/I, 45.7% I/D, and 29.6% D/D and 30.3% I/I, 45.5% I/D, and 24.2% D/D, respectively; P >0.05). The t-PA D allele frequency was similar in patients with CP (52.4%) and healthy subjects (46.5%). PAI-1 genotype distribution in patients with CP (30.9% 4G/4G, 35.8% 4G/5G, and 33.3% 5G/5G) and healthy subjects (36.2% 4G/4G, 41.9% 4G/5G, and 21.9% 5G/5G) was also similar. The 4G allele frequency was not different between patients with CP (48.8%) and healthy subjects (57.1%) (P >0.05). The 4G allele frequency in non-smoking CP patients was significantly lower than in non-smoking, healthy subjects (chi(2) = 4.201; P = 0.040). Non-smoking CP patients also had a significantly lower percentage of 4G-positive genotypes compared to non-smoking healthy subjects (chi(2) = 5.046; P = 0.025). CONCLUSIONS: t-PA or PAI-1 genotypes are not associated with susceptibility to CP in Turkish subjects. Conversely, the 4G allele of the PAI-1 gene could be related to a decreased susceptibility to CP in non-smokers.

Gingival crevicular fluid transforming growth factor-beta1 in several forms of periodontal disease.

BACKGROUND: Transforming growth factor-beta(1) (TGF-beta(1)) has significant effects on periodontal host response regulation. Limited knowledge on the role of TGF-beta(1) in various periodontal disease types and particularly in advanced periodontitis forms warranted the present study. The aim of the present study was to evaluate the gingival crevicular fluid (GCF) TGF-beta(1) levels in patients with different forms of periodontal disease. METHODS: GCF TGF-beta(1) levels were investigated in 32 chronic periodontitis (CP), 30 generalized aggressive periodontitis (G-AgP), 15 gingivitis patients and 16 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, plaque and bleeding on probing. TGF-beta(1) levels were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg) and concentration (pg/microl). RESULTS: G-AgP and CP groups had significantly elevated GCF TGF-beta(1) total amount compared to healthy group (p<0.008). Moreover, GCF TGF-beta(1) total amount of G-AgP group was significantly higher than that of gingivitis group (p<0.008). G-AgP and CP groups had similar GCF TGF-beta(1) total amount (p>0.008). Significant correlation was found between GCF TGF-beta(1) total amount and all clinical periodontal parameters (p<0.05). CONCLUSIONS: The results of the present study suggest contribution of TGF-beta(1) to the pathogenesis of advanced chronic and aggressive periodontitis. TGF-beta(1) may thus be one of the components modulating exaggerated host response together with other major mediators of inflammation.

Adjunctive subantimicrobial dose doxycycline: effect on clinical parameters and gingival crevicular fluid transforming growth factor-beta levels in severe, generalized chronic periodontitis.

BACKGROUND: At present there is limited data concerning the efficacy of non-surgical periodontal therapy supplemented with subantimicrobial dose doxycycline (SDD) in the treatment of severe, generalized periodontitis. The purpose of the present study was to evaluate the effect of adjunctive SDD therapy on clinical periodontal parameters and gingival crevicular fluid (GCF) transforming growth factor-beta1 (TGF-beta1) levels in patients with severe, generalized chronic periodontitis over a 6-month period. METHODS: Thirty-five patients with severe, generalized periodontitis and 11 periodontally healthy subjects were included in the present study. Patients received full-mouth supragingival debridment at baseline and randomized to take either SDD b.i.d. or placebo b.i.d. for 3 months. Patients received root planing and oral hygiene instruction once a week for four consecutive weeks. Clinical measurements including probing depth (PD), clinical attachment level, papilla bleeding index and plaque index and GCF sampling were performed at baseline, 3 and 6 months. The GCF TGF-beta1 levels were analysed by enzyme-linked immunosorbent assay. RESULTS: Thirteen patients in both study groups completed the 6-month trial. Following scaling and root planing (SRP) plus SDD and SRP plus placebo therapy significant improvements in clinical periodontal parameters of both groups were observed (p<0.025). In the SDD group a significantly higher percentage (%73.4) of deep pockets resolved (PD reduction > or =3 mm from baseline) when compared with placebo group (%49.7) at 6 months (p<0.05). At baseline there were no significant differences in GCF TGF-beta1 levels between three groups. Both total amount and concentration of GCF TGF-beta1 in SDD and placebo groups increased when compared with baseline at 3 months. However, only GCF TGF-beta1 levels of SDD group was significantly higher than baseline (p<0.025) and placebo group (p<0.017) at 3 months. At 6 months GCF TGF-beta1 levels of both groups were similar to baseline levels (p<0.025). CONCLUSIONS: These data indicate that combination of SDD with non-surgical therapy improves clinical parameters of periodontal disease and increases GCF TGF-beta1 levels together with a decrease in prevalence of residual pockets in patients with severe, generalized chronic periodontitis. Increased GCF TGF-beta1 levels following SDD therapy might suggest a novell pleiotrophic mechanism for tetracyclines to inhibit connective tissue breakdown.