Effect of non-surgical periodontal treatment on gingival crevicular fluid hypoxia inducible factor-1 alpha, vascular endothelial growth factor and tumor necrosis factor-alpha levels in generalized aggressive periodontitis patients.

BACKGROUND: Hypoxia-inducible angiogenic pathway involving hypoxia inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and tumor necrosis factor-alpha (TNF-α) may regulate several biological processes related to inflammation. The present study aimed to assess the effect of non-surgical periodontal treatment on gingival crevicular fluid (GCF) HIF-1α, VEGF, and TNF-α levels in generalized aggressive periodontitis (G-AgP). METHODS: Twenty G-AgP patients and 20 periodontally healthy individuals were included. G-AgP patients received scaling and root planning (SRP), per quadrant at a 1-week-interval, performed with ultrasonic and periodontal hand instruments. GCF samples were collected and clinical periodontal parameters including probing depth, clinical attachment level, gingival index and plaque index were recorded at baseline, 1 and 3 months after treatment. Biomarker levels in GCF were analyzed by ELISA. RESULTS: At baseline all clinical parameters and GCF HIF-1α, VEGF, and TNF-α levels were significantly higher in G-AgP patients compared to healthy control (P < 0.05). All clinical parameters improved over the 3-month-period in G-AgP patients (P < 0.05). GCF HIF-1α levels in G-AgP reduced at 1 and 3 months post-treatment, however, this did not reach to statistical significance (P > 0.05). GCF VEGF and TNF-α levels remained unchanged throughout the study period (P > 0.05). CONCLUSIONS: Within the limitations of the present study, although HIF-1α seems to possess a potential diagnostic value for G-AgP, it might not be a proper predictor of clinically favorable treatment outcome. SRP plus different adjunctive therapies could provide better information about the prognostic role of hypoxia-inducible angiogenic pathway in G-AgP.

Tooth loss in aggressive periodontitis: Results 25 years after active periodontal therapy in a private practice.

AIM: To assess tooth loss in patients with aggressive periodontitis (AgP) 10-35 years after active periodontal therapy (APT) in a private practice and to detect possible factors influencing tooth loss. MATERIAL AND METHODS: In 100 patients with AgP, tooth loss was recorded over a median follow-up period of 25.5 years after APT, retrospectively. Patient- and tooth-level factors were assessed with a Cox frailty regression model. RESULTS: Of 2,380 teeth, 227 were lost during a median follow-up time of 25.5 years (2.3 ± 3.6 teeth/patient, range 0-17 teeth), resulting in a mean tooth loss rate of 0.09 teeth/patient/year. At patient-level, statistically significant factors for tooth loss were smoking (p = .039) and the baseline diagnosis generalized AgP (p < .001). Influencing factors at tooth-level were location in the maxilla (p = .003), baseline bone loss (p < .001), molars (p < .001) and premolars (p < .001) as well as abutment teeth (p = .009). CONCLUSION: Tooth loss occurred rarely in patients with AgP treated in a private practice over a long-time period. Annual tooth loss rates are comparable with those described in university settings. Smoking, generalized form of AgP, location/type of tooth, baseline bone loss and abutment status could be detected as factors impacting upon tooth loss.

Six-month clinical outcomes of non-surgical periodontal treatment with antibiotics on apoptosis markers in aggressive periodontitis.

OBJECTIVE: Extrinsic and intrinsic pathways of apoptosis are involved in generalized aggressive periodontitis (GAgP). The aim of this study was to evaluate 6-month clinical outcomes relative to apoptosis of one-stage full-mouth disinfection (OSFMD) and systemic antibiotics (SA) in the treatment of GAgP. METHODS: Twenty-six patients with GAgP were included in this prospective follow-up intervention study. Gingival crevicular fluid (GCF) was collected from patients at baseline and 3 and 6 months after periodontal therapy, which consisted of OSFMD and SA (amoxicillin and metronidazole, 500 mg each for 7 days). The levels of p53, caspase-3, TNF-α, TRAIL, IL-1ß, and IL-10 in GCF were measured via ELISA. RESULTS: Periodontal parameters were improved at 3 and 6 months compared to baseline (p < 0.05). p53 was decreased up to 6 months (p < 0.05). TRAIL, TNF-α, and IL-10 were similar at baseline and 3 and 6 months. Caspase-3 and IL-1ß were decreased at 3 months (p < 0.05), but similar at 6 months compared to baseline (p > 0.05). CONCLUSION: Although OSFMD plus SA improves clinical periodontal parameters up to 6 months, this treatment protocol differentially regulates the apoptosis markers caspase-3 at 3 months and p53 at 6 months without influencing TRAIL in GCF.

Outcomes After 25 Years of Periodontal Treatment and Maintenance of a Patient Affected by Generalized Severe Aggressive Periodontitis.

This report describes the long-term outcomes of nonsurgical periodontal therapy and supportive periodontal treatment (SPT) of a 21-year-old patient affected by generalized aggressive periodontitis at multiple teeth with a compromised prognosis. After 25 years of SPT, no teeth had been extracted and no periodontal pockets associated with bleeding on probing were present. Radiographic analysis showed an improvement in infrabony defects, demonstrating long-term improvement is possible with nonsurgical periodontal treatment provided that smoking is not present and the patient is included in a strict SPT.

Inflammatory serum markers up to 5 years after comprehensive periodontal therapy of aggressive and chronic periodontitis.

AIM: The aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study. METHODS: Twenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months. RESULTS: Clinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl-1; 12 weeks: 5.34 ± 1.40 nl-1; 60 months: 7.73 ± 2.89 nl-1; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement. CONCLUSION: Despite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy. CLINICAL RELEVANCE: Systemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.

Localised aggressive periodontitis in a 3-year-old-boy.

BACKGROUND: Localised aggressive periodontitis (LAgP), characterised by rapid attachment and bone loss, which may occur in children and adolescents, without clinical evidence of systemic disease. CASE REPORT: Three-year-old boy was referred with excessive mobility of 83 and exfoliation of 73. Clinical examination revealed acceptable oral hygiene. Blood tests were performed to evaluate PMNs activity and the parents were advised to apply 0.2% chlorhexidine twice a day. One month later 83 was still excessively mobile. Blood tests were normal. TREATMENT: A full mouth scaling and curettage were performed under general anaesthesia. Since 83 had been spontaneously exfoliated one day earlier, a biopsy was taken from its socket. The biopsy examination revealed granulation tissue with actinomyces colonies. A course of amoxicillin 250 mg three times a day for 7 days was prescribed. Cultures from periodontal pockets of the child's family members were found negative to Aggregatibacter actinomycetem comitans (Aa). FOLLOW-UP: Examination 3 months later, no tooth mobility was observed and the cultures from the periodontal pockets were negative to Aa. Thereafter, the child was periodically reviewed every 3 months for 26 months with no signs of periodontal disease. CONCLUSION: Amoxicillin combined with curettage around the involved teeth may be effective in LAgP treatment.

Tratamento ortodôntico em pacientes com periodontite agressiva: considerações clínicas / Orthodontic treatment in patients with aggressive periodontitis: clinical considerations

O objetivo desse trabalho foi confrontar as abordagens dos tratamentos envolvendo periodontite agressiva e ortodontia através de uma revisão de literatura baseada em artigos de condutas clínicas. Foi realizada uma busca na base de dados PubMed, retroativa a 10 anos e utilizando palavras-chave Mesh. Ao final da seleção, resultaram 13 artigos de casos clínicos e um artigo com uma série de casos. A maioria envolveu pacientes jovens e mulheres, e todos realizaram tratamento periodontal e ortodôntico para controle da periodontite agressiva. A perda óssea severa não contraindica o uso de aparelho ortodôntico, e a movimentação dentária associada com um intenso controle periodontal apresenta-se como uma forma de sucesso no tratamento da doença.

The aim of this study was to elucidate treatment approaches involving aggressive periodontitis and orthodontics through a literature review based on articles of clinical procedures. A search was conducted in PubMed database using MeSH key words and limited to the past 10 years. The appropriate studies were selected and resulted in 13 papers of single case reports and one paper including four case reports. The majority of the cases involved young patients and women, and all underwent orthodontic and periodontal treatment to control aggressive periodontitis. Severe bone loss does not contraindicate the use of braces and tooth movement together with an appropriate periodontal control presents a way to successfully treat the disease.

Biomarker levels in gingival crevicular fluid of generalized aggressive periodontitis patients after non-surgical periodontal treatment.

OBJECTIVES: The aim of this study was to assess the effects of non-surgical periodontal treatment on gingival crevicular fluid (GCF) cytokines in patients with generalized aggressive periodontitis (GAgP), in relation to clinical parameters. MATERIALS AND METHODS: Data were obtained from 16 GAgP patients and 15 periodontally healthy controls. Periodontal parameters and GCF biomarker levels were evaluated at baseline and repeated 3 and 6 months after treatment for GAgP subjects. Moderate and deep pocket sites were analyzed separately. The amount of interleukin (IL)-1ß, IL-9, tumor necrosis factor (TNF)-α, platelet-derived growth factor (PDGF-bb), and vascular endothelial growth factor (VEGF) were measured using a highly specific and sensitive multiplex bead immunoassay. RESULTS: At baseline, cytokine levels in the moderate and deep pocket sites of GAgP patients were higher than those of the healthy control sites. In GAgP group, periodontal treatment led to improvement in all examined clinical parameters and resulted in a statistically significant reduction in the total amounts of IL-1ß, VEGF, and TNF-α, in comparison to baseline, already 3 months after therapy in both moderate and deep pocket sites and of PDGF-bb in deep sites (p < 0.01). At the concentration level, only IL-1ß and VEGF were affected. CONCLUSION: Non-surgical treatment of GAgP provided significant clinical benefits leading to a marked decrease in the GCF levels of some pro-inflammatory and pro-angiogenic cytokines, but not of IL-9 and PDGF-bb. CLINICAL RELEVANCE: Although the periodontal therapy successfully decreased clinical signs of inflammation, the GCF levels of some inflammatory cytokines were still elevated.

Moderate- to long-term therapeutic outcomes of treated aggressive periodontitis patients without regular supportive care.

BACKGROUND AND OBJECTIVE: Risk for deterioration in treated aggressive periodontitis (AgP) individuals remained unclear. This retrospective cohort study investigated 7-26 years of periodontal outcomes and oral health-related quality of life (OHRQoL) of young adults with advanced periodontitis. MATERIAL AND METHODS: Eighty-nine previously treated patients with AgP were re-examined. Clinical and radiographic parameters before treatment discontinuation and at re-examination were compared. OHRQoL at re-call was assessed with the short-form Oral Health Impact Profile (OHIP-14S). RESULTS: None of the subjects adhered to suggested periodontal therapy and maintenance after discharge. Mean percentage of sites with probing pocket depth (PPD) ≥6 mm at re-examination was 4.5 ± 5.9%. A total of 182 teeth had been lost over time. Tooth loss rate was 0.14/patient/year. From 68 subjects with documented favorable treatment outcomes, higher percentage of sites with PPD ≥6 mm at re-examination and higher radiographic proximal bone loss was associated with current smoking status. Patients with AgP with <20 teeth at re-call had worse OHRQoL than those with ≥20 teeth. Patients with higher full-mouth mean PPD also reported poorer OHRQoL. CONCLUSION: Treatment in patients with AgP who smoke and neglect proper supportive care, risk periodontal disease progression. Substantial tooth loss and higher full-mouth mean PPD led to poorer OHRQoL in this cohort.

Diagnóstico y tratamiento de la periodontitis agresiva / Diagnosis and treatment of aggressive periodontitis

La periodontitis agresiva es una enfermedad de baja prevalencia, multifactorial, de avance rápido, sin compromiso sistémico, con alteraciones inmunológicas, con fuerte influencia genética, agregación familiar y generalmente de instalación temprana. Tiene dos formas: una localizada, y otra generalizada. No está debidamente aclarado, si se trata de una enfermedad periodontal diferente a otras o si es la expresión fenotípica de una periodontitis crónica en pacientes susceptibles. Su protocolo diagnóstico incluye una historia médica dental, examen clínico periodontal y examen radiológico. El tratamiento de la periodontitis agresiva incluye principalmente, control de higiene bucal, raspaje y alisado radicular, complementado con terapia antibiótica sistémica y local. La terapia quirúrgica depende de los casos. La terapia de mantenimiento es imprescindible para lograr mejores resultados. El objetivo de este artículo fue revisar los protocolos diagnósticos y terapéuticos y proponer un flujograma de tratamiento en base a evidencias científicas recientes.

Aggressive periodontitis is a low-prevalence, multifactorial disease, of rapid progression and with no systemic compromise. It presents immunological alterations, a strong genetic influence, familial aggregation and early onset. It can be localized or generalized. It is not clear whether it is an independent periodontal disease, or if it is the phenotypic expression of chronic periodontitis in susceptible patients. Its diagnostic protocol includes a dental medical history, a clinical periodontal examination and a radiological examination. Treatment usually includes improving oral hygiene, dental scaling and root planing, as well as systemic and local antibiotic therapy. Surgical therapy will depend on each individual case. Maintenance therapy is essential to achieve better results. The aim of this paper is to review diagnostic and therapeutic protocols, and to propose a treatment flowchart based on the latest scientific evidence

Local application of IGFBP5 protein enhanced periodontal tissue regeneration via increasing the migration, cell proliferation and osteo/dentinogenic differentiation of mesenchymal stem cells in an inflammatory niche.

BACKGROUND: Periodontitis is a widespread infectious disease ultimately resulting in tooth loss. The number of mesenchymal stem cells (MSCs) in patients with periodontitis is decreased, and MSC functions are impaired. Rescuing the impaired function of MSCs in periodontitis is the key for treatment, especially in a manner independent of exogenous MSCs. Our previous study found that overexpressed insulin-like growth factor binding protein 5 (IGFBP5) could promote exogenous MSC-mediated periodontal tissue regeneration. Here, we investigate the role of IGFBP5 protein in MSCs and periodontal tissue regeneration independent of exogenous MSCs in an inflammatory niche. METHODS: TNFα was used to mimic the inflammatory niche. Lentiviral IGFBP5 shRNA was used to silence IGFBP5 and recombinant human IGFBP5 protein (rhIGFBP5) was used to stimulate the periodontal ligament stem cells (PDLSCs) and bone marrow stem cells (BMSCs). The effects of IGFBP5 on PDLSCs were evaluated using the scratch-simulated wound migration, Transwell chemotaxis, alkaline phosphatase (ALP) activity, Alizarin red staining, Cell Counting Kit-8, Western blot, Real-time PCR, Co-IP and ChIP assays. The swine model of periodontitis was used to investigate the functions of IGFBP5 for periodontal regeneration and its anti-inflammation effect. RESULTS: We discovered that 0.5 ng/ml rhIGFBP5 protein enhanced the migration, chemotaxis, osteo/dentinogenic differentiation and cell proliferation of MSCs under the inflammatory condition. Moreover, 0.5 ng/ml rhIGFBP5 application could rescue the impaired functions of IGFBP5-silenced-MSCs in the inflammatory niche. Furthermore, local injection of rhIGFBP5 could promote periodontal tissue regeneration and relieve the local inflammation in a minipig model of periodontitis. Mechanistically, we found that BCOR negatively regulated the expression of IGFBP5 in MSCs. BCOR formed a protein complex with histone demethylase KDM6B and raised histone K27 methylation in the IGFBP5 promoter. CONCLUSIONS: This study revealed that rhIGFBP5 could activate the functions of MSCs in an inflammatory niche, provided insight into the mechanism underlying the activated capacities of MSCs, and identified IGFBP5 as a potential cytokine for improving tissue regeneration and periodontitis treatment independent of exogenous MSCs and its potential application in dental clinic.

Long-term treatment costs for aggressive periodontitis in a German population.

AIM: This study assessed the long-term annual costs for treating aggressive periodontitis (AgP) patients. METHODS: A cohort of compliant AgP patients was retrospectively evaluated. Costs for active periodontal therapy (APT, including scaling and root planing, open flap debridement, root resections, but not pocket elimination or regenerative surgery) and supportive periodontal therapy (SPT, including also costs for restorative, endodontic, prosthetic and surgical treatments) were estimated from a mixed payer perspective in Germany. The impact of tooth- and patient-level factors on annual costs was assessed using mixed modelling. RESULTS: A total of 52 patients (mean [SD] age: 35.2/6.8 years), with 26.5 (4.0) teeth (38% with bone loss >50%) were treated. Mean follow-up (retention) time was 16.9 (5.4) years. Total treatment costs per patient and per tooth were 6,998 (3,807) and 267 (148) Euro, respectively. Approximately 87% of the costs were generated during SPT, 13% during APT. Annual patient- and tooth-level costs were 536 (209) and 20.1 (65.0) Euro, respectively. Annual tooth-level costs were significantly increased in patients aged 34 years or older, male patients, former or current smokers, teeth with furcation involvement degree II/III, and bone loss 50%-70%. CONCLUSIONS: Annual treatment costs for treating AgP patients were similar to those found for chronic periodontitis patients. Certain parameters might predict costs.

The Effects of Diode Laser Therapy as an Adjunct to Scaling and Root Planing in the Treatment of Aggressive Periodontitis: A 1-Year Randomized Controlled Clinical Trial.

OBJECTIVE: The aim of this study was to investigate and compare the clinical, microbial, and inflammatory effects of a diode laser as an adjunct to scaling and root planing (SRP) versus SRP alone for the treatment of generalized aggressive periodontitis (GAgP). METHODS: Using a split-mouth design, 31 patients with GAgP were enrolled in the study. The maxillary right and left quadrants were randomly assigned to SRP+diode laser or SRP alone. Patients were examined on a regular basis for clinical, microbiological, and inflammatory mediator changes over a 1-year period. Clinical attachment level (CAL) was the primary outcome variable chosen. In addition, subgingival biofilm samples and gingival crevicular fluid (GCF) inflammatory mediators were analyzed at each follow-up session. RESULTS: Compared to baseline, both treatments demonstrated an improvement in periodontal parameters at 1 year. However, SRP+diode laser produced a significant improvement in probing depth (PD; 2.56 ± 0.44 vs. 3.36 ± 0.51 mm, p < 0.05) and CAL (3.47 ± 0.25 vs. 4.11 ± 0.26 mm, p < 0.05) values compared to SRP alone. Similarly, in the SRP+diode laser group, the bacteria of orange complex group were significantly reduced at 30 and 60 days compared to SRP alone. Moreover, SRP+diode laser determined a reduction in mean GCF level of interleukin (IL)-1ß and IL-1ß/IL-10 ratio at 15 and 30 days compared to SRP alone (p < 0.05). CONCLUSIONS: At 1 year, SRP+diode laser yielded a significant reduction in some clinical parameters, while microbial and inflammatory mediator changes were not significantly reduced compared to SRP alone.

Non-Surgical Therapy Reduces Presence of JP2 Clone in Localized Aggressive Periodontitis.

BACKGROUND: Previous studies have provided substantial evidence of the association of Aggregatibacter actinomycetemcomitans, and its highly leukotoxic JP2 genotype, with localized aggressive periodontitis (LAgP). The present study aims to evaluate presence of JP2 in individuals with LAgP after periodontal treatment. METHODS: Sixty African-American patients with LAgP, aged 5 to 25 years, were examined. At baseline, probing depth (PD), clinical attachment level (CAL), bleeding on probing, and plaque index were measured, and subgingival plaque was collected from LAgP diseased and healthy sites for each participant. Patients received whole-mouth ultrasonic debridement, scaling and root planing, and a 7-day prescription of amoxicillin and metronidazole. Participants were reevaluated and resampled and received regular maintenance therapy at 3, 6, and 12 months after treatment. Polymerase chain reaction was used to detect presence of the JP2 genotype before and after treatment. RESULTS: At baseline, the JP2 sequence was identified in 75% of LAgP diseased sites and in 56.67% of healthy sites. At 3, 6, and 12 months after treatment, the number of patients was 40, 31, and 31, respectively, and JP2 detection decreased to 17.5%, 6.45%, and 3.23%, respectively, in diseased sites (P <0.001) and to 2.5%, 3.23%, and 0%, respectively, in healthy sites (P <0.001). Clinical parameters of disease were also significantly reduced after therapy (P <0.001). Additionally, significant correlations were observed between JP2 presence and mean PD (P <0.002) and CAL (P <0.001), after therapy. CONCLUSION: Periodontal therapy was successful in reducing clinical parameters of LAgP and subgingival presence of JP2 in diseased and healthy sites.

Clarithromycin as an Adjunct to One-Stage Full-Mouth Ultrasonic Periodontal Debridement in Generalized Aggressive Periodontitis: A Randomized Controlled Clinical Trial.

BACKGROUND: The aim of the present study is to evaluate the periodontal clinical and microbiologic responses and possible adverse effects of clarithromycin (CLM) combined with periodontal mechanical therapy in the treatment of patients with generalized aggressive periodontitis. METHODS: Forty patients were selected and randomly assigned into one of two groups: 1) CLM (n = 20): one-stage full-mouth ultrasonic debridement (FMUD) associated with CLM (500 mg, every 12 hours for 3 days); and 2) placebo (n = 20): FMUD associated with placebo pills. Clinical and microbiologic parameters were evaluated at baseline and 3 and 6 months postoperatively. RESULTS: Both treatments presented statistically significant clinical and microbiologic improvements. However, the CLM group presented lower means of probing depth for pockets ≥7 mm at 6 months (4.0 ± 1.7 mm) compared with the placebo group (4.7 ± 1.3 mm) (P = 0.04). In addition, the CLM group also presented greater reduction of Porphyromonas gingivalis (Pg) DNA counts at 6 months (P = 0.0001). CONCLUSION: Results from this study suggest both treatments are effective; however, adjunct use of CLM to FMUD leads to better reduction of deep pockets and Pg at 6 months compared with FMUD alone.

IL-6 and IL-10 gene polymorphisms in patients with aggressive periodontitis: effects on GCF, serum and clinic parameters.

Genetic variations observed in cytokines affect periodontitis susceptibility. The aim of this study was to investigate interleukin(IL)-6(-174) and IL-10(-597) gene polymorphisms in generalized aggressive periodontitis (GAgP) patients. Also, we aimed to evaluate the effects of IL-6 and IL-10 gene polymorphisms on the clinical outcomes of non-surgical periodontal therapy and cytokine levels in gingival crevicular fluid(GCF) and serum. Fifty-three patients with GAgP and 50 periodontally healthy individuals were included in this study. Clinical parameters, GCF and blood samples were collected at baseline and at 6-week. Non-surgical periodontal therapy was performed in patients with GAgP. Gene analysis were determined by PCR-RFLP(polymerase chain reaction-restriction fragment length polymorphism) and cytokine levels were determined by enzyme-linked immunosorbent assay(ELISA).GAgP patients showed significant improvement on clinical parameters after periodontal therapy(p<0.05). In the GAgP group, IL-6 GG genotype and G allele frequency were higher than in the control group. GCF IL-6 level was also significantly lower at 6-week in the GAgP group. Higher GCF IL-10 levelswere observed in patients carrying the IL-6 GG genotype than in those carrying the GC+CC genotype at baseline. In conclusion, IL-6(-174) and IL-10(-597) gene polymorphisms were found to be associated with GAgP and genotype distribution did not affect the outcome of non-surgical periodontal therapy, while patients with IL-6(-174) GG genotype had higher levels of GCF IL-10 levels.

IL-6 and IL-10 gene polymorphisms in patients with aggressive periodontitis: effects on GCF, serum and clinic parameters

Abstract Genetic variations observed in cytokines affect periodontitis susceptibility. The aim of this study was to investigate interleukin(IL)-6(-174) and IL-10(-597) gene polymorphisms in generalized aggressive periodontitis (GAgP) patients. Also, we aimed to evaluate the effects of IL-6 and IL-10 gene polymorphisms on the clinical outcomes of non-surgical periodontal therapy and cytokine levels in gingival crevicular fluid(GCF) and serum. Fifty-three patients with GAgP and 50 periodontally healthy individuals were included in this study. Clinical parameters, GCF and blood samples were collected at baseline and at 6-week. Non-surgical periodontal therapy was performed in patients with GAgP. Gene analysis were determined by PCR-RFLP(polymerase chain reaction-restriction fragment length polymorphism) and cytokine levels were determined by enzyme-linked immunosorbent assay(ELISA).GAgP patients showed significant improvement on clinical parameters after periodontal therapy(p<0.05). In the GAgP group, IL-6 GG genotype and G allele frequency were higher than in the control group. GCF IL-6 level was also significantly lower at 6-week in the GAgP group. Higher GCF IL-10 levelswere observed in patients carrying the IL-6 GG genotype than in those carrying the GC+CC genotype at baseline. In conclusion, IL-6(-174) and IL-10(-597) gene polymorphisms were found to be associated with GAgP and genotype distribution did not affect the outcome of non-surgical periodontal therapy, while patients with IL-6(-174) GG genotype had higher levels of GCF IL-10 levels.

Adjunct Antimicrobial Therapy and Periodontal Surgery to Treat Generalized Aggressive Periodontitis: A Case Report.

Here we report a case of generalized aggressive periodontitis treated with periodontal therapy including adjunct antimicrobial therapy and periodontal surgery. The patient was a 22-year-old woman who presented with the chief complaint of gingival recession. Baseline examination revealed generalized plaque deposition and gingival inflammation. Thirty-nine percent of the sites had a probing depth (PD) of 4-6 mm and 2% a PD of ≥7 mm; 63% exhibited bleeding on probing (BOP). Radiographic examination revealed vertical bone loss in the molars and horizontal bone loss in other teeth. Microbiological examination of subgingival plaque revealed the presence of Aggregatibacter actinomycetemcomitans and Tannerella forsythia. Oral health-related quality of life was assessed as a measure of patient-reported outcome. Based on a clinical diagnosis of generalized aggressive periodontitis, initial periodontal therapy and adjunct antimicrobial therapy were implemented. After reducing inflammation and subgingival bacteria, open flap debridement was performed for teeth with a PD of ≥4 mm. Reevaluation showed no sites with a PD of ≥5 mm, a minimal level of BOP, and a marked reduction in the level of the targeted periodontal pathogens. The patient's oral health-related quality of life was slightly worsened during supportive periodontal therapy (SPT). Implementation of adjunct antimicrobial therapy targeting periodontal pathogens and subsequent periodontal surgery resulted in improvement in periodontal and microbiological parameters. This improvement has been adequately maintained over a 2-year period. However, additional care is necessary to further improve the patient's oral health-related quality of life during SPT.

Clinical and Immunoinflammatory Evaluation of One-Stage Full-Mouth Ultrasonic Debridement as a Therapeutic Approach for Smokers With Generalized Aggressive Periodontitis: A Short-Term Follow-Up Study.

BACKGROUND: This study aims to evaluate the effect of one-stage full-mouth ultrasonic debridement (OSFMUD) on clinical and immunoinflammatory parameters in smokers with generalized aggressive periodontitis (GAgP). METHODS: Fourteen smoking and 14 non-smoking patients with GAgP were selected. After initial supragingival therapy, patients were treated by OSFMUD. Full-mouth parameters evaluated were: 1) plaque index (PI); 2) bleeding scores (BS); 3) probing depth (PD); and 4) clinical attachment level (CAL). Clinical evaluation was performed, and gingival crevicular fluid (GCF) was collected for selected sites (ss) at baseline and 1, 3, and 6 months. GCF was analyzed via enzyme-linked immunosorbent assay for: 1) receptor activator of nuclear factor-κ B ligand (RANKL); 2) osteoprotegerin (OPG); 3) interleukin (IL)-6; and 4) tumor necrosis factor (TNF)-α, whereas secreted osteoclastogenic factor of activated T-cells (SOFAT) was evaluated by Western blotting. RESULTS: Significant reduction (P <0.05) was observed between baseline and 6 months for: 1) PI; 2) BS; and 3) PD, with no difference between smoking and non-smoking patients (P >0.05). Regarding CAL, only non-smoking patients showed a significant decrease (P <0.05). Significant reduction (P <0.05) was observed in both groups for: 1) PIss; 2) PDss; 3) bleeding on probing; and 4) relative CAL. Smoking and non-smoking patients presented significantly decreased levels of IL-6 and TNF-α over time (P <0.05); however, no difference was observed between groups (P >0.05). RANKL was significantly different (P <0.05) only for non-smokers at 6 months, whereas OPG was not significant (P >0.05). SOFAT expression was significantly lower (P <0.05) after OSFMUD for non-smokers only. CONCLUSION: Considering the clinical and immunoinflammatory parameters evaluated in this short-term follow-up study, it can be concluded that OSFMUD can be used as an alternative treatment for smokers with GAgP.