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Clinical and morphological manifestation of periodontitis is associated with persistent inflammation of the gingiva, loss of connective tissue attachment, formation of a periodontal pocket and loss...

Background: Periodontitis is a chronic inflammatory disruption of the supportive periodontal tissue. It is known that the chronic periodontitis is initiated by the increased level of specific bacteria, but the progression of the disease is defined by characteristics of the host response to the bacterial load. There is evidence that individual genetic, systemic and environmental risk factors can influence the course of the disease. Some genes and intergenic relations are in connection with the modification of the periodontal disease, and so they change the clinical course, the severity and the prognosis of the decease. Purpose: The aim of the current investigation is to establish the presence of IL-8 gene polymorphism and serum levels to IL- 8 in patients with chronic periodontitis. Material and methods: In the recent study, 35 patients (24 females and 11 males) are included with diagnosis moderate to severe periodontitis. Periodontal important parameters such as PD, CAL and Bone loss are included. The level of IL- 8 in a patient’s serum is tested by ELISA (enzyme-linked immunosorbent assay). The presence of IL- 8 polymorphism in loci rs4073 (-251A/T) and rs2227307 (-396T/G) is established by polymerase chain reaction (PCR). Results: The analysis of the current assay recognized a statistically significant correlation between: HI and PBI- severity and HI and BOP; a significant correlation between PBI- severity and PD average and Bone loss; the strong correlation between BOP and Bone loss; the significant correlation between PD 3- 5mm and PD ≥ 7mm and CAL average, also a strong correlation between PD ≥ 7mm and Bone loss. The results have shown that the biggest interrelationship observed between the presence of GT/AT genotype and TT/TT genotype and distribution of PD 5-7 mm and PD ≥ 7 mm (p

The purpose of this investigation was to assess the acute effects of partial range of motion (pROM) exercises, on the accuracy of soccer penalty kicks on goal. This method limits the joint from moving through the complete length of a motion, creates an occlusion effect, and thus causes the type 1 muscle fibers to work anaerobically. Thirty-six soccer players, with 5-8 years of soccer playing experience, were pretested for accuracy then retested ( rtt = 0.92 ) and divided into random groups from the Associação Banco do Brasil Futebol Clube—Group A, Paraná Futebol Clube—Group P, and Coritiba Futebol Clube—Group C. Groups were composed of 12 people performing full range of motion (fROM) exercises or pROM exercises. Both groups performed 5 sets of back squats at 50% of body weight in sets of 40 seconds with metronome tempo of 56 bpm for an average of 10-12 repetitions per 40-second set. Blood samples were collected post-warm-up, after the 3rd set, and following the 5th set for both groups, within 3–5 minutes of cessation of exercise. Athletes performing fROM exercises showed increased blood lactate from 2.69 ± 0.2 to 4.0 ± 1.2 mmol/L ( p < 0.05 ), and in pROM, blood lactate increased from 2.48 ± 0.42 to 10.29 ± 1.3 mmol/L ( p < 0.001 ). In fROM, accuracy decreased from 42.96 ± 13.39 % to 41.37 ± 17.25 % ( p > 0.1 ), a slight decrease, while in the pROM groups, accuracy decreased from 45.42 ± 14.93 % to 24.53 ± 10.2 % ( p < 0.001 ). The calculations demonstrating average percentages of accuracy are presented in the tables. These findings support that pROM exercises significantly increase blood lactate resulting in a reduction in soccer kick accuracy. This decrease in accuracy directly correlates to the accumulation of lactic acid and hydrogen ions (H+) and demonstrates that pROM strength training should not be utilized prior to a sport-specific session in order to avoid interference with the development of special skills.

During puberty there are increased levels of sex hormones, which can affect the oral environment. At this period, there is a peak prevalence of periodontal pathology believed to be related to alteration in the subgingival microflora. This study investigated the interaction between sex hormones isolated in the saliva, and the subgingival microflora in children undergoing puberty. The study included 60 children aged 10–14 years who were monitored: 30 without gingivitis (up to 25% Papillary Bleeding Index—PBI) and good oral hygiene, and 30 children with plaque-induced gingivitis (over 50% PBI). All patients were registered with a periodontal status using a medical card developed for this purpose. For the study of sex hormones (oestradiol, progesterone and testosterone), samples of unstimulated saliva were taken under fasting condition in the morning and were tested by using labelled immunological analysis and liquid chromatography with mass spectrometry [LC-MS (MS(QQQ)]. Gingival sulcus from six teeth was taken with paper pins to test nine control strains (pooled sample) by real-time polymerase chain reaction (PCR). The results showed that, when comparing children with gingivitis with healthy children, only the oestradiol hormone had elevated values. In the children with gingivitis, the composition of the subgingival microflora was much more varied and complex, with a tendency to increase the species diversity of microorganisms from the red complex. The oestradiol levels in saliva correlated with the total number of subgingival microorganisms, as well as with some species of microorganisms, Capnocytophaga gingivalis, Peptostreptococcus micros, Treponema denticola and Tannerella forsythia.

International audience; Objective: To investigate the impact of baseline and time-varying factors on the risk of serious adverse events (SAEs) in patients during long-term certolizumab pegol (CZP) treatment.Methods: Safety data were pooled across 34 CZP clinical trials in rheumatoid arthritis (RA), axial spondyloarthritis (axSpA), psoriatic arthritis (PsA), and plaque psoriasis (PSO). Cox proportional hazards modeling was used to investigate the association of baseline patient characteristics with risk of serious infectious events (SIEs), malignancies, and major adverse cardiac events (MACEs). Cox modeling for recurrent events assessed the impact of time-varying body mass index (BMI), systemic corticosteroid (CS) use, and disease activity on SIE risk in RA and SAE risk in PSO.Results: Data were pooled from 8747 CZP-treated patients across indications. Cox models reported a 44% increase in SIE risk associated with a baseline BMI of 35 kg/m2 or more versus a baseline BMI of 18.5 kg/m2 to less than 25 kg/m2 . Baseline systemic CS use, age of 65 years or more, and disease duration of 10 years or longer also increased SIE risk. Older age was the only identified risk factor for malignancies. The risk of MACEs increased 107% for BMI of 35 kg/m2 or more versus BMI of 18.5 kg/m2 to less than 25 kg/m2 and increased 51% for men versus women. Higher disease activity, older age, systemic CS use, BMI of 35 kg/m2 or more, and baseline comorbidities were SIE risk factors in RA. Age and systemic CS use were risk factors for SAEs in PSO.Conclusion: Age, BMI, systemic CS use, and disease activity were identified as SIE risk factors in CZP-treated patients. Risk of malignancies was greater in older patients, whereas obesity and male sex were MACE risk factors.

The aim of the present study was to evaluate the adjunctive effect of hyaluronic acid (HA) gel in the treatment of residual periodontal pockets over a 12-month period. Periodontal patients presenting at least one residual periodontal pocket 5–9 mm of depth in the anterior area were recruited from six university-based centers. Each patient was randomly assigned to subgingival instrumentation (SI) with the local adjunctive use of HA for test treatment or adjunctive use of local placebo for control treatment at baseline and after 3 months. Clinical parameters ( )probing depth (PD), bleeding on probing (BoP), plaque index (PI), recession (REC), clinical attachment level (CAL)) and microbiological samples for the investigation of the total bacterial count (TBC) and presence of specific bacterial species (Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, Fusobacterium nucleatum) were taken at baseline and every 3 months, until study termination. PD was determined as the primary outcome variable. From a total of 144 enrolled, 126 participants (53 males, 73 females) completed the entire protocol. Both treatments resulted in statistically significant clinical and microbiological improvements compared to baseline. Although the local application of HA showed a tendency for better results, there was a lack of statistically significant differences between the groups.

Multifactorial nature of chronic periodontitis is well known. The data indicate that the bacteria of subgingival biofilm (with their presence at high levels, too), as well as the immune response of the organism, genetic components and environmental factors play a significant role in the development of periodontal destructive disease. On the one hand the strong relationship between microorganisms from the “red complex” has been proved. On the other hand the initiation and progression of chronic periodontitis has been verified, as well. The presence of bacterial metabolic products and other substances (lipopolysaccharides, enzymes and toxins) results in increased expression of proinflammatory cytokines and release of active agents leading to the development of a local tissue lesion. Thus, the negative (destructive) side of the immune response is expressed and associated with the immunopathological nature of periodontitis. Literary data testify the importance of interleukin-8 (IL-8) in regulating the inflammatory response to bacterial infection and suggest its association with susceptibility to periodontitis.

Background: Certolizumab pegol (CZP) is an anti-TNF drug approved for rheumatoid arthritis (RA), axial spondyloarthritis (axSpA), psoriatic arthritis (PsA), psoriasis (PSO) and Crohn’s disease (CD). Older age, comorbidity burden and corticosteroid (CS) use have been linked to increased risk of serious infectious events (SIEs) in CZP-treated patients (pts) with RA.1 However, the impact of overall disease burden on the risk of serious adverse events (SAEs) has not been fully examined for other CZP indications. High body mass index (BMI) has been associated with systemic inflammation and greater comorbidity risk.2,3 Greater disease burden in these pts may lead to increased CS use – a known risk factor for SAEs.1 Objectives: To examine the contribution of BMI and CS use to the risk of SIEs, malignancies and major adverse cardiovascular events (MACE) in CZP-treated pts across indications. Methods: Safety data were pooled across 49 CZP clinical trials (27 RA, 1 axSpA, 1 PsA, 5 PSO, 15 CD). SAEs of potential concern were medically reviewed by an external expert committee using predefined case rules. Incidence rates (IR) were calculated per 100 pt–years (PY). Multivariate Cox modeling was used to estimate relative risk (hazard ratio [HR]) of time to first SIE, malignancy or MACE by baseline BMI ( Results: Across indications, 11,317 pts received CZP (21,695 PY total exposure; max: 7.8 years [yrs]; exposure for RA: 13,542 PY; axSpA: 978 PY; PsA: 1,316 PY; PSO: 1,481 PY; CD: 4,378 PY). Mean BMI was 27.8 kg/m2 in RA, 27.6 kg/m2 in axSpA, 29.8 kg/m2 in PsA, 30.1 kg/m2 in PSO, and 24.0 kg/m2 in CD. Overall, 4,132 pts (37%) took CS at baseline, more so in RA (46%) and axSpA (51%). Across indications, IRs were 0.82/100 PY for all malignancies (IR for malignancies excluding non-melanoma skin cancer [NMSC] was 0.66/100 PY), 0.47/100 PY for MACE, and 3.62/100 PY for SIEs. According to the Cox model, age ≥45 yrs, disease duration Conclusion: In CZP-treated pts across indications, malignancy risk was not influenced by BMI or CS use. As expected, obesity and CS use increased the risk of MACE. The SIE risk associated with CS use was compounded in obese pts, which may reflect the contribution of comorbidities, disease activity or other factors not examined here. References [1] Curtis J. Arthritis Res Ther 2017;19:276; 2. Perez de Heredia F. Proc Nutr Soc 2012;71:332–8; 3. Harpsoe M. Int J Epidemiol 2014;43:843–55. Acknowledgement: We thank the patients who participated. This study was funded by UCB Pharma, medical writing by Emma Phillips, Costello Medical, UK. Disclosure of Interests: Vivian Bykerk Grant/research support from: Mallinckrodt, BMS, Crescendo Biosciences, Sanofi/Regeneron., Consultant for: Amgen, Pfizer, UCB, Scipher, Sanofi/Genzyme/Regeneron, Andrew Blauvelt Grant/research support from: AbbVie, Aclaris, Akros, Allergan, Almirall, Amgen, Boehringer Ingelheim, Celgene, Dermavant, Dermira Inc, Eli Lilly and Company, Galderma, Genentech/Roche, GlaxoSmithKline, Janssen, LEO, Meiji, Merck Sharp & Dohme, Novartis, Pfizer, Purdue Pharma, Regeneron, Revance, Sandoz, Sanofi Genzyme, Sienna Pharmaceuticals, Sun Pharmaceuticals, UCB Pharma, Valeant, Vidac, Consultant for: AbbVie, Aclaris, Akros, Allergan, Almirall, Amgen, Boehringer Ingelheim, Celgene, Dermavant, Dermira Inc., Eli Lilly and Company, Galderma, Genentech/Roche, GlaxoSmithKline, Janssen, LEO, Meiji, Merck Sharp & Dohme, Novartis, Pfizer, Purdue Pharma, Regeneron, Revance, Sandoz, Sanofi Genzyme, Sienna Pharmaceuticals, Sun Pharmaceuticals, UCB Pharma, Valeant, Vidac., Speakers bureau: Janssen, Regeneron, Sanofi Genzyme, Jeffrey Curtis: None declared, Cecile Gaujoux-Viala Consultant for: Speaking and/or consulting fees from AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Merck-Serono, Medac, Nordic Pharma, Novartis, Pfizer, Roche, Sandoz, Sanofi and UCB Pharma., Speakers bureau: Speaking and/or consulting fees from AbbVie, Amgen, Bristol-Myers Squibb, Celgene, Eli Lilly, Gilead, Janssen, Merck-Serono, Medac, Nordic Pharma, Novartis, Pfizer, Roche, Sandoz, Sanofi and UCB Pharma., Tore K. Kvien Grant/research support from: AbbVie, BMS, MSD, Pfizer, Roche and UCB., Consultant for: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi, Mylan and UCB, Speakers bureau: AbbVie, Biogen, BMS, Boehringer Ingelheim, Celgene, Celltrion, Eli Lilly, Hospira, Merck-Serono, MSD, Novartis, Oktal, Orion Pharma, Pfizer, Roche, Sandoz, Sanofi and UCB, William Sandborn Shareholder of: Stock options from Escalier Biosciences, Gossamer Bio, Oppilan Pharma, Precision IBD, Progenity and Ritter Pharmaceuticals, Grant/research support from: Research grants from Atlantic Healthcare Limited, AbbVie, Amgen, Celgene/Receptos, Genentech, Gilead Sciences, Janssen, Lilly and Takeda, Consultant for: Consulting fees from AbbVie, Allergan, Amgen, Boehringer Ingelheim, Celgene, Conatus, Cosmo, Escalier Biosciences, Ferring, Genentech, Gilead, Gossamer Bio, Janssen, Lilly, Miraca Life Sciences, Nivalis Therapeutics, Novartis Nutrition Science Partners, Oppilan Pharma, Otsuka, Paul Hastings, Pfizer, Precision IBD, Progenity, Prometheus Laboratories, Ritter Pharmaceuticals, Robarts Clinical Trials (owned by Health Academic Research Trust or HART), Salix, Shire, Seres Therapeutics, Sigmoid Biotechnologies, Takeda, Tigenix, Tillotts Pharma, UCB Pharma and Vivelix, Kevin Winthrop Consultant for: Gilead, Galapagos, Eli Lilly and Company, Abbvie, Pfizer, GSK, Christina Popova Employee of: Employee of UCB Pharma., Xavier Mariette Grant/research support from: Servier, Consultant for: AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Janssen, Pfizer, UCB Pharma

SUMMARY: Chronic periodontitis is a multifactorial disease that is characterized by attachment loss and loss of alveolar bone. Periodontal pathogens from the subgingival microbiota are suggested as a major etiological factor for the periodontitis. The host inflammatory response against bacteria and their virulence factors underlies the current understanding of the pathogenesis of chronic periodontitis. The destructive immune response was shown to be associated with an extremely increased production of inflammatory cytokines in periodontal tissues. The expression of several cytokines likeIL-1β and IL-6 is responsible for alveolar bone resorption, and loss of connective tissue attachment in chronic periodontitis. Authors reported a reduction in the levels of inflammatory cytokines after successful periodontal therapy. Measuring the levels of inflammatory factors may be diagnostic approach to assess the effectiveness of the therapy of periodontitis.

Background:Durability over time varies according to the safety, tolerability and efficacy of a drug.1However, durability may vary between patient (pt) subgroups,1,2and physicians should consider pt characteristics when making treatment decisions. Certolizumab pegol (CZP) is an anti-tumour necrosis factor (anti-TNF) agent approved for the treatment of chronic inflammatory diseases, including rheumatoid arthritis (RA) and plaque psoriasis (PSO).3However, little is known about the impact of pt baseline characteristics on long-term CZP durability.Objectives:To investigate the durability of CZP and reasons for discontinuation over 3 years (yrs) in subgroups of pts with RA or PSO using pooled clinical trial data.Methods:27 RA and 3 PSO clinical trials were pooled for indication-specific analyses. Kaplan-Meier curves were calculated to estimate CZP durability for pt subgroups by age, gender, disease duration, prior anti-TNF use and geographic region. Reasons for CZP discontinuation were investigated.Results:6927 RA and 1112 PSO pts were included; mean ages were 53.0 yrs (standard deviation [SD]: 12.2 yrs) and 45.4 (13.0) yrs, respectively. 79.3% RA pts were female (of all patients, 19.4% were women of childbearing age [18–Table 1.CZP durability at 3 years,[a] by patient subgroup% patientsRAPSOAll49.270.1Age, yrs 18–52.166.3 45–49.468.3 ≥6543.369.4Gender Female49.364.1 Male48.269.2 WoCBA51.162.0 Male aged 18–56.568.3Prior anti-TNF use Yes49.360.1 No49.668.5Disease duration, yrs 43.239.6 1–52.663.6 5–51.464.4 ≥1048.769.7Region Asia-Pacific58.5 Central Europe61.578.8 Eastern Europe54.2 Latin America57.1 N America36.653.9 W Europe33.867.7 Rest of the world66.3[a] For PSO, the 3 year analysis was calculated with Week 144 data. CZP: certolizumab pegol; N: North; PSO: psoriasis; RA: rheumatoid arthritis; TNF: tumour necrosis factor; W: Western; yrs: years.Conclusion:Overall, CZP durability was similar to that reported for other anti-TNFs with some differences between indication and subgroups.1Factors influencing durability included age, disease duration and geographic region. Gender differences were observed in the 18–45 yrs age group, however, both male and female CZP durability was higher than in older RA pts.References:[1]Neovius M. Ann Rheum Dis 2015;74:354–60;2.Lie E. Ann Rheum Dis 2015;74:970–8;3.EMA. CIMZIA SmPC 2019. Available at:https://www.ema.europa.eu[Last accessed 09/01/20].Acknowledgments:This study was funded by UCB Pharma. Editorial services were provided by Costello Medical.Disclosure of Interests:Vivian Bykerk: None declared, Alice B Gottlieb Grant/research support from:: Research grants, consultation fees, or speaker honoraria for lectures from: Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB., Consultant of:: Research grants, consultation fees, or speaker honoraria for lectures from: Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB., Speakers bureau:: Research grants, consultation fees, or speaker honoraria for lectures from: Pfizer, AbbVie, BMS, Lilly, MSD, Novartis, Roche, Sanofi, Sandoz, Nordic, Celltrion and UCB., Kristian Reich Grant/research support from: Affibody; Almirall; Amgen; Biogen; Boehringer Ingelheim; Celgene; Centocor; Covagen; Eli Lilly; Forward Pharma; Fresenius Medical Care; GlaxoSmithKline; Janssen; Kyowa Kirin; LEO Pharma; Medac; Merck; Novartis; Miltenyi Biotec; Ocean Pharma; Pfizer; Regeneron; Samsung Bioepis; Sanofi Genzyme; Takeda; UCB; Valeant and Xenoport., Consultant of: Affibody; Almirall; Amgen; Biogen; Boehringer Ingelheim; Celgene; Centocor; Covagen; Eli Lilly; Forward Pharma; Fresenius Medical Care; GlaxoSmithKline; Janssen; Kyowa Kirin; LEO Pharma; Medac; Merck; Novartis; Miltenyi Biotec; Ocean Pharma; Pfizer; Regeneron; Samsung Bioepis; Sanofi Genzyme; Takeda; UCB; Valeant and Xenoport., Speakers bureau: Affibody; Almirall; Amgen; Biogen; Boehringer Ingelheim; Celgene; Centocor; Covagen; Eli Lilly; Forward Pharma; Fresenius Medical Care; GlaxoSmithKline; Janssen; Kyowa Kirin; LEO Pharma; Medac; Merck; Novartis; Miltenyi Biotec; Ocean Pharma; Pfizer; Regeneron; Samsung Bioepis; Sanofi Genzyme; Takeda; UCB; Valeant and Xenoport., Yoshiya Tanaka Grant/research support from: Asahi-kasei, Astellas, Mitsubishi-Tanabe, Chugai, Takeda, Sanofi, Bristol-Myers, UCB, Daiichi-Sankyo, Eisai, Pfizer, and Ono, Consultant of: Abbvie, Astellas, Bristol-Myers Squibb, Eli Lilly, Pfizer, Speakers bureau: Daiichi-Sankyo, Astellas, Chugai, Eli Lilly, Pfizer, AbbVie, YL Biologics, Bristol-Myers, Takeda, Mitsubishi-Tanabe, Novartis, Eisai, Janssen, Sanofi, UCB, and Teijin, Kevin Winthrop Grant/research support from: Bristol-Myers Squibb, Consultant of: AbbVie, Bristol-Myers Squibb, Eli Lilly, Galapagos, Gilead, GSK, Pfizer Inc, Roche, UCB, Christina Popova Employee of: UCB Pharma, Nicola Tilt Employee of: UCB Pharma, Andrew Blauvelt Consultant of: AbbVie, Aclaris, Almirall, Arena, Athenex, Boehringer Ingelheim, Bristol-Myers Squibb, Dermavant, Dermira, Eli Lilly, FLX Bio, Forte, Galderma, Janssen, Leo, Novartis, Ortho, Pfizer, Regeneron, Sandoz, Sanofi Genzyme, Sun Pharma, and UCB Pharma, Speakers bureau: AbbVie

Background: Periodontitis is a chronic inflammatory disruption of the periodontal supportive tissues. There are the numerous evidences for his bacterial etiology. Though the occurrence of periodontal bacteria is considered to be the main cause of periodontitis, certain characteristics of the individual immune response may also have influence on the disease development and progression, and on the treatment outcomes. There are some reports that attempt to identify genetic factors associated with periodontitis including polymorphisms of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) genes. We were interested from the distribution of several genotypes of the cytokines: interleukin-6 - (G-174C) and (G-597A), lymphotoxin- α (A+252G), and tumour necrosis factor-alpha (G-308A) in patients with chronic periodontitis. Aim: To investigate the association of chronic periodontitis with certain gene polymorphisms of interleukin-6 (IL-6), Lymphotoxin- α, and tumor necrosis factor-alpha (TNF-α). Material and methods: The study included 30 patients with moderate or severe chronic periodontitis, and 10 persons with healthy periodontium. Total genomic DNA was extracted from the buccal epithelial cells. TNF-A (G-308A), IL-6 (G-174C), IL-6 (G-597A) and LT-A (A+252G) genes polymorphisms were analyzed by Polymerase chain reaction (PCR). Results: Outcomes showed a large variety in genotype’s distribution in the investigated groups. No important difference was observed in the distribution of IL-6, TNF-α and LT-α genotypes between chronic periodontitis patients and controls in this study be reason of the small studied group. However, a significant difference in the LT-α was observed – a prevalence of the genotype GG in patients with severe periodontitis. In relation with IL-6 (G-597A) and IL-6 (G-174C) genotyping – in both of them in patients with severe periodontitis was occurred most frequently the genotype GG. In patients with periodontitis the frequency of genotype GG of TNF-α (G-308A) was significantly increased. Conclusion: The assessment IL-6 (G-597A) and IL-6 (G-174C), and TNF-α (G-308A) revealed that genotype GG was moderate associated with chronic periodontitis in Bulgarian individuals. As a result of these findings we may suppose that the G allele may play an important role in the development and progression of periodontal disease in this population. The frequency of LT-A (A252G) was significantly greater in severe periodontitis patients in this study.

Today, it is known that pathogenic bacteria are the key factors for the initiation of periodontal disease, but the host response and the severity of clinical expression are largely determined by genetic susceptibility and environmental factors. There is evidence that the individual response to the environment and variations in the immune response in periodontitis are associated with genetic factors. Of particular interest are the polymorphisms of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) genes and the factors that determine the production of these cytokines, since they play an important role in the pathophysiology of inflammation and in particular, in periodontal diseases. The identification of a specific IL-1 family genotype which correlates with the severity of periodontitis, demonstrates that it is genetic mechanisms that determine the intensity of immunoinflammatory response in different individuals (and hence, the severity of periodontal disease) due to...

INTRODUCTION: Antibiotic use in chronic periodontitis may result in improvement in periodontal status, although many questions regarding the indications for this therapy remain unanswered. The polymicrobial etiology of the periodontal infection hinders the choice of the proper antibiotic agent. Furthermore the indiscriminate use of antibiotics could lead to high levels of resistance and to various adverse reactions. In the recent years a various molecular diagnostics protocols were proposed in order to facilitate the decision for adjunctive antibiotic administration. OBJECTIVE: The aim of this study is to compare the microbiological effectiveness of adjunctive antibiotic administration with the mechanical periodontal therapy. METHODS: 30 patients with severe chronic periodontitis were enrolled in this study and were divided in 3 groups: Control group – with mechanical debridement only. Test group 1 – with combined adjunctive antibiotic administration using Amoxicillin+ Metronidazole. Test group 2 – with target antibiotic administration according to the resuts from the Real Time PCR identification. RESULTS: The prevalence of all the isolated microorganisms (exept. E.nodatum and C.gingivalis) in Test Group 2 demonstrates statistically significant reduction compared with the other treatment approaches. Almost complete elimination was registered for the consensus pathogens from the red and orange complexes (above 99% and 100% for P.intemedia). CONCLUSION: The adjunct antibiotic treatment targeted with Real-Time PCR identification demonstrates almost complete elimination of the putative periodontal pathogens in the deep periodontal pockets in patients with severe chronic periodontitis. This result suggests slower recolonisation of these habitats thus limiting the risk for progression of the periodontal destruction.

INTRODUCTION: The periodontal pathology is of great social importance due to the vast distribution in the human population. The adjunctive antibiotic administration could improve the healing in such cases but the latest data of the continuingly growing antibiotic resistance requires more precise approaches of antibiotic selection. The contemporary molecular diagnostic methods could offer the required precision for the microbiological identification in order to achieve better control of the periodontitis. OBJECTIVE: The aim of this study is to compare the microbiological effectiveness of adjunctive antibiotic administration with the mechanical periodontal therapy. METHODS: 30 patients with severe chronic periodontitis were enrolled in this study and were divided in 3 groups: Control group – with mechanical debridement only. Test group 1 – with combined adjunctive antibiotic administration using Amoxicillin+ Metronidazole. Test group 2 – with target antibiotic administration according to the resuts from the Real Time PCR identification. RESULTS: A considerable improvement of the periodontal status was reported in all treatment groups. The most positive results were in the group with target antibiotic administration were all tested clinical parameters showed the best improvement with statistically significant changes in sites with PD7mm and CAL>5mm. CONCLUSION: The adjunctive antibiotic administration demonstrates better clinical effectiveness concerning the reduction of the severely affected sites in cases with severe generalized chronic periodontitis compared to the mechanical therapy alone. From all examined groups the target approach has statistically significant better results. These results suggest that this approach is recommended in cases with high prevalence of deep pockets.

This review examines literature data concerning the bacterial findings in chronic periodontitis depending on pocket depth, and presents the latest published information on the presence of proinflammatory factors in periodontal environment. It has been found that chronic periodontitis affects as much as 80% of the middle-aged population; by comparison, the prevalence of aggressive periodontitis reaches up to 1-1.5%. It is accepted that this social disease is multifactorial in etiology, but the evidence in the literature suggests that the levels of specifi c Gram-negative organisms in subgingival plaque biofilm play a major role in the initiation and progression of the disease. Of the many bacterial species inhabiting the periodontal environment, three types - Porphyromonas gingivalis (PG), Treponema denticola (TD), Tannerella forsythia (TF) - are strongly associated with the initiation and progression of periodontitis. Microbiological studies suggest that Porphyromonas gingivalis should be considered a major etiologic agent. Currently, Porphyromonas gingivalis is strongly associated with the pathogenesis of chronic periodontitis. On the other hand, the presence of Aggregatibacter actinomycetemcomitans in patients with chronic periodontitis may be related to the severity of the disease and thus modify the therapeutic plan. The increased amount of periodontal pathogens in the subgingival area can activate a cascade of defense mechanisms of the body associated with the production of factors causing infl ammation and destruction, which suggests a correlation between the bacterial findings and the body response implemented by enhancing the local cytokine expression. Studies in the literature show that the presence of certain micro-organisms in the periodontal environment is associated to increased levels of proinflammatory cytokines in the gingival fluid and gingival tissue. These levels have been associated with destructive tissues response. There is little evidence in the literature on the correlation of the levels of periodontal pathogens of sites with different pocket depth with periodontal disease activity defined by the degree of the proinflammatory cytokine expression such as tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6 ).

INTRODUCTION: Chronic periodontitis is defined as an inflammatory disease of the supporting tissues of teeth caused by microorganisms in the dental biofilm, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation and gingival recession. Treatment of chronic periodontitis aims at arresting the inflammation and stopping the loss of attachment by removal and control of the supra- and subgingival biofilm and establishing a local environment and microflora compatible with periodontal health. The AIM of this study was to evaluate the effectiveness of non-surgical therapy (scaling and root planning) in the treatment of moderate chronic periodontitis. MATERIALS AND METHODS: The study included 30 patients aged between 33 and 75 years, of which 46.7% women and 53.3% men, diagnosed with moderate and, at some sites, severe periodontitis. They were treated with non-surgical periodontal therapy methods (scaling and root planning and curettage if indicated). Additionally, chemical plaque control with rinse water containing chlorhexidine was applied. The diagnostic and reassessment procedures included measuring the periodontal indices of 601 periodontal units before and after the therapy. The indices measured were the papillary bleeding index (PBI), the hygiene index (HI), the probing pocket depth (PPD) and the clinical attachment level (CAL). RESULTS: Significant reduction of plaque and gingival inflammation was found in all treated patients; we also found a statistically significant reduction of periodontal pockets with clinically measured depth ⋋ 5 mm (PD ⋋ 5 mm). Pockets with PD > 5 mm did not show statistically significant lower incidence rates probably due to the initially small percentage of deep pockets in the patients studied. There was a statistically significant reduction of all sites with attachment loss, the highest significance found at sites where the attachment loss was greater than 5 mm. CONCLUSION: The results of the study suggest that nonsurgical periodontal therapy is effective in managing the moderate chronic periodontitis. Given a good patient compliance, the antimicrobial periodontal therapy can be quite efficient in arresting the inflammatory process and reducing the depth of periodontal pockets; it can also achieve a stable attachment loss level and obviate the need to use a surgical periodontal treatment modality.

The understanding of the pathogenesis of periodontitis makes various progresses in the last decades. Today it is well known that the synthesis of high levels of pro-inflammatory mediators from gingival tissues in response to periodontal pathogens results in destruction of soft and hard periodontal tissues and clinical expression of periodontal disease. The occurrence of increased IL-6, IL-1β, TNFα and PGE2 levels in GCF or gingival tissue is capable to indicate risk of progression of destruction in specific periodontal site. Detection of gene expression of numerous major cytokines in high levels in gingival tissues and crevicular fluid may be indicator for activity of periodontitis and provides the rationale for the additional periodontal therapy. The current conception of the pathogenesis of periodontitis suggests that additional host modulation approach may inhibit the production of pro-inflammatory mediators in periodontal tissues and thus may enhance the treatment result.

The width of the attached gingiva is defined as a distance between the depth of the gingival sulcus or gingival/periodontal pocket to the mucogingival junction. Authors suggest that a minimal amount of attached gingiva is necessary to ensure the gingival health. When the buccal bone plate and gingival tissues are thin and the position of the tooth is too vestibular gingival margin often displaces apically, and gingival recession develops. In the presence of gingival recession and reduced vestibular depth oral hygiene procedures are embarrassed.The definition of class III gingival recession is marginal lack of tissue extended to/or beyond the mucogingival junction with bone and soft tissue loss interdentally or malpositioning of the tooth.Prognosis for class III and IV gingival recession is that only partial coverage can be expected after root coverage procedures - FGG (free gingival graft) or connective tissue graft (CTG). Adjunctive surgical techniques would be helpful to achieve better aesthetic outcomes.

Periodontal diseases are inflammatory and destructive diseases of the dentogingival complex associated with specific periodontal pathogens inhabiting periodontal pockets. Periodontal diseases lead to damage of the periodontal tissues supporting the teeth (bone and connective tissue) and affect the quality of life of the affected individuals: poor alimentation, tooth loss, social and financial problems. Although it is generally considered that the disease has multifactorial etiology, data show that some specific Gram-negative microorganisms in the subgingival plaque biofilm play a major role in the initiation and progression of periodontitis. Porphyromonas gingivalis, Treponema denticola and Tannerella forsythia form a consortium in the subgingival biofilm and are regarded as the principal periodontopathogenic bacteria. Other microorganisms that have been implicated as predominant species in the disease process are: Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, Prevotella intermed...

BACKGROUND: Successful prevention and treatment of periodontitis is contingent upon effective control of the periodontopathic microbiota. Periodontal pathogens reside in deep subgingival sites but also colonize supragingival plaque, tongue dorsum and other oral sites. Antimicrobial agents administered systemically or locally can help suppress periodontal pathogens in periodontal sites and in the entire mouth. MATERIALS AND METODS: Thirty patients with generalized severe chronic periodontitis with 567 periodontal pockets >5mm were included in the presented study. The mechanical periodontal treatment was performed with ultrasonic device P5 Newtron in four visits. Subgingival irrigation of the periodontal pockets in the right two quadrants (split-mouth study) were performed with 10% povidone-iodine solutions. Full mouth periodontal status evaluation was recorded again on the last visit. RESULTS: The results from this study show significant improvement of the clinical parameters of periodontitis in all treated patients and in almost all periodontal sites. In the regions treated with subgingival irrigation with 10% povidone-iodine solution superior reduction of the probing depth, more attachment gain and better reduction of the gingival inflammation were recorded in comparison with regions treated with SRP only. CONCLUSION: This study demonstrates positive effect of the subgingival irrigations with 10% povidoneiodine in cases of severe chronic periodontitis. This results are rationale for future studies on the effectiveness of the iodophore solutions in the treatment of the disease and on the clinical significance of the investigated treatment.

SUMMARY Literature data relate certain Gram-negative anaerobe microorganisms with advanced destructive periodontal lesion. There are some references which reported higher levels of periodontal pathogens by the red and orange complex in deep periodontal pockets. The aim of this study is to determine the presence of most important periodontal pathogens and Candida spp. in deep periodontal pockets in patients with severe chronic periodontitis. The results of this study indicate the presence of high levels of periodontal pathogens in a strong connection with periodontal disease in deep periodontal pockets of patients studied.

Introduction: Currently accepted understanding about the role of the host inflammatory response in the progression of destructive periodontal diseases is the basis of therapeutic approaches with NSAIDs. Reduced levels of IL-1 and PGE2 in crevicular fluid and gingival tissues are measured in patients with adjunctive host modulation therapy in comparison with conventional mechanical therapy alone in numerous studies. The healing in patients with this additional therapy demonstrates successful elimination of gingival inflammation with pocket depth reduction and attachment level improvement. Aim: To investigate the effectiveness of additional host modulation therapy with NSAID (Aulin) in patients with chronic periodontitis. Material and methods: The study involves 14 adult patients suffering moderate to advanced periodontitis, instructed for strict daily plaque control (including personal hygiene involving interdental brushes and dental floss) and antimicrobial mouth rinsing with 0.2% chlorhexidine (Corsodyl) and is treated with scaling and root planning. On the 5th day of the treatment the patients are put on adjunctive systemic administration of NSAID (Aulin) for 14 days, twice daily x100 mg. The efficiency of the therapy is measured at its 6th week with the same clinical parameters – PD, CAL, HI, and PBI. Results: The results of the treatment depict significant shift in the distribution of shallow and deep periodontal pockets. The shallow pockets (1-3mm) in the initial status of the patients are 23.8% from all measured pockets and at the end of the applied treatment this number rises up to 75.7%. The initial level of the deep periodontal pockets (≥5mm) is 9.8% and decreases to 0.5% after treatment. The quantity of pockets with moderate depth (35mm) decreases from 66.5% to 38.7% at the end of the evaluated treatment. Conclusion: Within the limits of this pilot study we may conclude that the additional host modulation therapy