Orthodontic treatment in the presence of aggressive periodontitis.

INTRODUCTION: Aggressive periodontitis causes periodontal destruction, with loss of supporting alveolar bone. The common symptom is rapid attachment loss in the first molar and incisor area, in young adults. OBJECTIVE: The aim of this study was to discuss the challenges, implications and the impact of orthodontic treatment in patients affected by severe periodontal problems, specifically aggressive periodontitis. DISCUSSION: In addition to other bacteria, the main pathogen involved in aggressive periodontitis is the Aggregatibacter actinomycetemcomitans. However, the susceptibility to the disease differs among individuals, being immune deficiencies the main reason for this variability. Many orthodontists are not comfortable about performing treatments on individuals with aggressive periodontitis. CONCLUSION: Orthodontic treatment is feasible in young patients with severe and localized aggressive periodontitis, as long as the limitations imposed by the disease are respected. An interdisciplinary approach is required, with frequent periodontal follow-up before, during and after orthodontic treatment, allowing the correction of dental positions without aggravating bone loss.

Local IL-10 level as a predictive factor in generalized aggressive periodontitis treatment response.

Generalized aggressive periodontitis (GAgP) presents a reduced response to non-surgical therapy. However, it is not clear if the initial clinical, microbiological or immunological characteristics are impacting the worse response to treatment. This study aimed to identify the predictive value of clinical, microbiological and immunological patterns on the clinical response to therapy in GAgP patients. Twenty-four GAgP patients were selected, and gingival crevicular fluid (GCF) and subgingival biofilm were collected. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis and Tannerella forsythia levels were evaluated by qPCR, and IL-1ß and IL-10 concentration by ELISA. Twelve patients were treated with SRP (scaling and root planning), and twelve with SRP plus 375 mg amoxicillin and 250 mg metronidazole (8/8 hours, 7 days) (SRP + AM). The clinical changes (Probing Pocket Depth [PPD] reduction and Clinical Attachment Level [CAL] gain) 6 months post-treatment were correlated to the initial clinical, inflammatory and microbiological variables using stepwise logistic regression (α = 5%). CAL gain at 6 months was 1.16 ± 0.77 for SRP and 1.74 ± 0.57 mm for SRP + AM (P > .05). PPD reduction was 1.96 ± 0.82 for SRP and 2.45 ± 0.77 mm for SRP + AM (P < .05). In the SRP group, IL-10 showed a predictive value for clinical response. The higher the IL-10 concentration at baseline, the higher the reduction in PPD at 6 months (P = .01, r = .68). However, when antimicrobials were administered, no significant influence was detected (P > .05). It can be concluded that the IL-10 levels in GFC act as a predictor of clinical response to GAgP. Moreover, the intake of antimicrobials appears to overlap the influence of the inflammatory response on clinical response to treatment. Clinical trial registration number: NCT03933501.

One-year follow-up of the immune profile in serum and selected sites of generalized and localized aggressive periodontitis.

BACKGROUND: The local and systemic immunological profiles of important inflammatory mediators in the localized (LAgP) and generalized (GAgP) forms of aggressive periodontitis are still unknown, as well as the effect of periodontal therapy on these parameters. The aim of this prospective study was to evaluate clinical and immune responses of patients with AgP undergoing nonsurgical treatment. MATERIAL AND METHODS: Eighteen patients with GAgP, 10 with LAgP and 10 healthy participants were included in this study. AgP participants were submitted to scaling and root planing plus systemic antibiotics (amoxicillin and metronidazole). At baseline and 1-year follow-up were measured clinical parameters, such as probing depth [PD] and clinical attachment loss [CAL], and the levels of 10 immunological mediators (GM-CSF, M-CSF, MCP-1, ICAM-1, CXCL8, IL-1ß, TNF-α, IL-17, IL-4, and IL-10) in the gingival crevicular fluid (GCF) of selected sites [AgP forms: PD ≥ 6 mm or the deepest, bleeding on probing (BoP) and bone loss measured by periapical radiography; healthy individuals: PD ≤ 3 mm, no BoP, no bone loss] and serum. RESULTS: After periodontal treatment both forms of AgP presented a significant reduction of PD and CAL, an increase of GM-CSF, ICAM-1, MCP-1, TNF-α, IL-17, IL-4, and IL-10 in the GCF, as well as of GM-CSF and IL-4 in the serum, and a reduction in the serum concentration of IL-1ß. Serum levels of M-CSF, ICAM-1, and MCP-1 remained significantly below those found in healthy individuals in both forms of AgP even after therapy. An increase in the systemic or local levels of MCP-1, ICAM-1 and the anti-inflammatory profile (IL-4, IL-10) was correlated with an improvement in clinical parameters of LAgP patients. Also, a local reduction of IL-1ß levels in both forms of AgP was correlated with an increase in the clinical attachment gain. CONCLUSION: Nonsurgical periodontal therapy was successful in improving clinical parameters and modulating the immune response in both forms of AgP. However, this therapeutic approach does not seem to affect the deficient level of important serum mediators involved in mechanisms of cell transmigration.

Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

OBJECTIVE: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP). SUBJECTS AND METHODS: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR. RESULTS: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29. CONCLUSION: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals.

Orthodontic treatment in patients with aggressive periodontitis.

INTRODUCTION: Aggressive periodontitis (AP) is a condition that promotes breakdown of the periodontal tissues in a short time. In severe cases, pathologic migration of teeth and tooth loss can occur, producing esthetic and functional problems for the patient. Orthodontic treatment may be recommended to restore esthetics and masticatory function. We assessed the effects of orthodontic movement in the periodontal tissues of treated patients with AP. METHODS: Ten subjects (ages 25.0 ± 5.22 years) with AP received periodontal treatment followed by orthodontic treatment. Maintenance sessions were performed monthly under a strict dental biofilm control. They were compared with 10 periodontally healthy subjects (ages 22.9 ± 5.23 years) who received orthodontic treatment. Probing pocket depth, clinical attachment level, bleeding on probing, and dental plaque index were measured at baseline, after orthodontic treatment, and after 4 months. RESULTS: Statistical analysis showed improvement in all clinical parameters between baseline and 4 months after orthodontic treatment: probing pocket depth (0.29 mm), clinical attachment level (0.38 mm), bleeding on probing (4.0%), and dental plaque index (11%). CONCLUSIONS: The periodontal parameters of the AP patients remained stable during orthodontic treatment under strict biofilm control.

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.

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

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.

Benefits of adjunctive moxifloxacin in generalized aggressive periodontitis: a subgroup analyses in Aggregatibacter actinomycetemcomitans-positive/negative patients from a clinical trial.

AIM: The aim of the present study was to evaluate the influence of the baseline detection of Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) on the clinical outcomes of moxifloxacin (MOX) as an adjunct to full-mouth scaling and root planing (SRP) in generalized aggressive periodontitis (GAgP). METHODS: Forty patients were randomly distributed to two therapy protocols: SRP + placebo or SRP combined with MOX. A. actinomycetemcomitans was detected using culture methods. The significance of the treatment option (MOX or SRP + placebo) on the dependent variables (probing depth [PD] and clinical attachment level [CAL]), considering the interaction with the baseline detection of A. actinomycetemcomitans, was estimated. RESULTS: MOX therapy led to a higher significant PD reduction and CAL gain in A. actinomycetemcomitans-positive patients at baseline. In A. actinomycetemcomitans-positive patients, the reduction of sites ≥5 mm was higher in the MOX group. A. actinomycetemcomitans was not present in sites with PD ≥6 mm in the MOX group. The interactions of A. actinomycetemcomitans and MOX were significantly associated with CAL gain and PD reduction at 6 months. CONCLUSIONS: Adjunctive MOX trended toward better clinical responses in A. actinomycetemcomitans-positive patients at baseline. These results suggest that A. actinomycetemcomitans at baseline might modify the effect of adjunctive MOX in GAgP.

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.

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.

Predictors of clinical outcomes after periodontal treatment of aggressive periodontitis: 12-month randomized trial.

Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≥7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis.

Terapia antibiótica como adjuvante à terapia mecânica para o tratamento de periodontite agressiva generalizada / Antibiotic therapy as adjunctive to mechanical therapy for the treatment of generalized aggressive periodontitis ­ a literature review

O objetivo deste estudo foi avaliar os protocolos de antibióticos propostos em pacientes com periodontite agressiva generalizada (PAgG). Sessões de raspagem supragengival e polimento, instrução de higiene oral e quaisquer outros procedimentos de adequação foram realizados para alcançar um índice de placa < 20%. A raspagem e alisamento radicular (RAR) ou debridamento periodontal (associado ou não à desinfecção com clorexidina), e o debridamento periodontal ultrassônico em sessão única foram adotados. A azitromicina (AZT), a doxiciclina (DOX), o metronidazol (MET), a clindamicina, e a moxifl oxacina (MOX) foram alguns dos medicamentos testados. Alguns protocolos de antimicrobianos mostraram benefícios clínicos (redução do NS e PS, com ganho do NIC). Baseado na ação contra o Aa, a associação AMX + MET parecem ser a de eleição. No entanto, efeitos adversos, como o desconforto gastrointestinal, mal-estar geral, sonolência, náusea, dor de cabeça, gosto metálico ou eventos mais severos (erupção cutânea grave) foram observados. Por outro lado, apenas 0,7% dos pacientes relataram reações adversas com o AZT, que pode ser usado por um período menor (três dias). O uso do MET em concentrações menores (250 mg) não é efetivo. A MOX (apenas um comprimido por dia, custo reduzido) tem boa biodisponibilidade, longa meia-vida, boa penetração tecidual, e excelente tolerabilidade, parecendo tão efi ciente quanto o AMX+MET, e motivando a realização de novos protocolos de tratamento. Embora a análise microbiológica tenha demonstrado que a terapia medicamentosa foi superior em reduzir e/ou suprimir a carga microbiana subgengival, há tendência de recolonização bacteriana, ressaltando a necessidade da terapia periodontal de suporte.

The aim of this study was to evaluate the antibiotic protocols proposed to treat aggressive generalized periodontitis (AgGP) patients. Supragingival scaling and root planing, oral hygiene instructions, and other aid tools were performed to reach < 20% plaque score. The root scaling and planning or periodontal debridement (associated or not to chlorhexidine), and the ultrasonic periodontal debridement (single session) were adopted. The azithromycin (AZT), doxycycline (DOX), metronidazole (MET), clindamycin, and moxifl oxacin (MOX) were some of the investigated agents. Some antimicrobial protocols demonstrated clinical benefi ts (BoP and PD reductions, as well as CAL improvements). Based on the action against Aa, the AMX + MET association seems to be the therapy of choice. However, adverse effects, such as gastrointestinal discomfort, malaise, numbness, nausea, headache, metallic taste, or more severe reactions (cutaneous rash) were observed. On the other hand, only 0.7% of patients reported unpleasant symptoms with AZT, which can be used by a shorter period (three days). The use of MET in lower concentrations (250 mg) is not effective. The MOX (1 tablet once a day, reduced cost) seems to be as effi cient as AMX + MET, motivating the generation of new treatment protocols. Although the microbiological analysis had demonstrated that the antibiotic therapy was superior in reducing and/or eliminate the subgingival bacterial load, there is a trend for microbial recolonization, which emphasizes the need for periodontal supportive therapy.

Full-mouth ultrasonic debridement associated with povidone iodine rinsing in GAgP treatment: a randomised clinical trial.

OBJECTIVE: This study evaluated the clinical, immunological and microbiological results of full-mouth ultrasonic debridement (FMUD) with 10 % povidone iodine (PVPI) as the cooling liquid in the treatment of generalised aggressive periodontitis (GAgP). MATERIAL AND METHODS: Twenty-eight patients presenting GAgP were randomly assigned to one of the following groups for evaluation: FMUD + SS (n = 14)--single session of FMUD with 0.9 % saline solution as cooling agent and FMUD + PVPI (n = 14)--single session of FMUD with PVPI solution as cooling agent. Probing depth (PD), relative clinical attachment level (RCAL), relative position of gingival margin, plaque index (FMPI) and bleeding score (FMBS), immunological (interleukin-10 and interleukin-1ß concentrations in gingival crevicular fluid) and microbiological (Aa and Pg amounts) parameters were evaluated at baseline, first, third and sixth months after treatment. RESULTS: The two groups presented reduction of FMPI and FMBS and had statistically significant PD reductions, RCAL gains and gingival recession (p < 0.05). Both therapies reduced Pg levels in deep and in moderate pockets (p < 0.05). FMUD + PVPI reduced Aa levels in deep pockets. However, no inter-group differences in clinical, immunological and microbiological parameters were observed (p > 0.05). CONCLUSIONS: It could be concluded that 10 % PVPI used as an irrigant solution in FMUD decreased Aa levels in deep pockets but had no additional benefits when compared with saline solution irrigation in terms of clinical, microbiological and immunological results. CLINICAL RELEVANCE: The FMUD is a valid option for the treatment of GAgP, but the use of 10 % PVPI did not improve the results of the periodontal therapy.

Predictors of clinical outcomes after periodontal treatment of aggressive periodontitis: 12-month randomized trial

Abstract Little is known about the factors that may be used in clinical practice to predict the therapeutic response of aggressive periodontitis patients. The aim of this study was to determine predictors of clinical outcomes after non-surgical treatment of aggressive periodontitis. A total of 24 patients (aged 13-26 years) received oral hygiene instructions, as well as subgingival scaling and root planing. Twelve subjects received systemic azithromycin at random. Clinical variables were assessed at baseline, 3, 6, 9, and 12 months. Baseline microbiological assessment was performed by checkerboard DNA-DNA hybridization. Multivariable models used generalized estimating equations. There were significant improvements in the entire sample in regard to pocket depth, clinical attachment level and bleeding on probing. Significant predictors of a reduction in mean pocket depth were: use of azithromycin, non-molar teeth, generalized disease and baseline pocket depth. Absence of plaque predicted a 0.22 mm higher attachment gain, whereas a baseline pocket depth ≥7 mm predicted a 1.36 mm higher attachment loss. Azithromycin, plaque, and baseline pocket depth were significant predictors of bleeding on probing. The concomitant presence of all three red complex species predicted a 0.78 mm higher attachment loss. It may be concluded that dental plaque, tooth type, disease extent, baseline pocket depth, and use of azithromycin were significant predictors of the clinical response to treatment for aggressive periodontitis in young individuals. Moreover, the presence of multiple periodontal pathogens may predict challenges in achieving a favorable outcome for aggressive periodontitis.

Generalized aggressive periodontitis: microbiological composition and clinical parameters in non-surgical therapy / Periodontitis agresiva generalizada: composición microbiológica y parámetros clínicos en la terapia no quirúrgica

The aim of this study was to determine the variations in periodontal parameters and microbiological composition in periodontal pockets at the baseline and 3 and 6 months posttreatment in patients with Generalized Aggressive Periodontitis (GAP) undergoing nonsurgical periodontal treatment combined with chlorhexidine and systemic antibiotics. Medical and dental history was taken from 10 subjects, average age 30.62.7 years, diagnosed with GAP. A nonsurgical periodontal treatment combined with 0.12% chlorhexidine, 875 mg amoxicillin and 500 mg metronidazole every 12 hours for ten days was conducted. At each visit, the following measurements were recorded: bacterial plaque (BP), bleeding on probing (BOP), probing depth (PD), clinical attachment level (CAL), hypermobility, and furcation lesions, and a sample of subgingival plaque was taken from the site of the deepest probing depth of each sextant to identify Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, Prevotella intermedia and Aggregatibacter actinomycetemcomitans using molecular biology techniques. After 6 months, the Wilcoxon test showed an increase of 0.97 mm in CAL (p=0.0047) and 2.54 mm in PD (p=0.009). A healthy site was defined as having a PD <5 mm, negative BOP and no pathogenic bacteria detected at 6 months, indicating significant improvement (p=0.008), with OR (95% CI) =4.7 (1.102220.11). With the treatment protocol used in this study, 6 months after treatment, patients had an approximately 4fold higher possibility of presenting PD <5 mm and periodontal pockets without periodontal pathogenic bacteria.

En este trabajo, nos propusimos determinar las variaciones de los parámetros periodontales y la composición microbiológica de las bolsas periodontales al inicio, a los 3 y 6 meses después del tratamiento en pacientes con periodontitis agresiva generalizada (GAP), sometidos a tratamiento periodontal no quirúrgico combinado con clorhexidina y antibióticos sistémicos. Se elaboró historia médica y dental en 10 sujetos, con una edad media de 30,6 2,7 años, con diagnóstico de GAP. Se les practicó tratamiento periodontal no quirúrgico combinado con clorhexidina al 0,12%, 875 mg de amoxicilina y 500 mg de metronidazol. Los antibióticos se prescribieron cada 12 horas durante diez días. Se registraron: la placa bacteriana (BP), sangrado al sondaje (BOP), la profundidad de sondaje (PD), el nivel de inserción clínica (NIC), hipermovilidad y lesiones de furcación. En cada visita, se tomaron las mediciones, y se tomó una muestra de la placa subgingival en sitio de la mayor profundidad al sondaje en cada sextante para identificar mediante técnica de biología molecular: Porphyromonas gingivalis, Treponema denticola, forsythia Tannerella, Prevotella intermedia, y Aggregatibacter actinomycetemcomitans. Después de 6 meses, el análisis de la prueba de Wilcoxon mostró un aumento de 0,97 mm de CAL (p = 0,0047) y 2,54 mm en la PB (p = 0,009). Se definió sitio sano, cuando se determinó un PD <5 mm, BOP negativo, y no se detectaron bacterias patógenas a los 6 meses, lo que indicó una mejora significativa (p = 0,008), con (IC 95%) = 4,7 (1,1022 a 20,11). Con el protocolo de tratamiento presentado, es posible especular que a los 6 meses después del tratamiento, un paciente puede tener aproximadamente 4 veces más posibilidades de presentar una PD<5 mm y bolsillos periodontales sin bacterias patógenas.

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

A periodontite agressiva localizada e a periodontite agressiva generalizada são caracterizadas por uma rápida perda de inserção e destruição óssea, sem história médica significante e com acometimento de indivíduos de aproximadamente 30 anos de idade. A perda de inserção pode resultar em problemas estéticos e funcionais complexos, necessitando tratamentos envolvendo a periodontia e principalmente a ortodontia para atingir bons resultados. A maioria dos trabalhos da literatura encontrados sobre esse assunto são de relatos de casos clínicos únicos e poucos são os casos controle e ensaios clínicos randomizados de alta qualidade. Para identificar as melhores evidências científicas e incorporá-las à prática, foi realizado um trabalho científico que contribui para elucidar as melhores abordagens clínicas a serem tomadas frente a periodontite agressiva no tratamento ortodôntico. A revisão de literatura incluindo apenas casos clínicos foi a melhor forma encontrada de substantivamente contribuir para o conhecimento das abordagens clínicas em relação a pacientes com periodontite agressiva e que realizaram tratamento ortodôntico

Periodontite agressiva avançada localizada, combinada com gengivite ulcerativa necrosante: dez anos de acompanhamento de um tratamento multidisciplinar / Severe localized aggressive periodontitis combined with necrotizing ulcerative gingivitis: a 10-year follow-up of a multidisciplinary treatment

Este relato de caso descreve o tratamento de um caso de periodontite agressiva avançada localizada, combinada com gengivite ulcerativa necrosante. A paciente apresentava migração patológica dos incisivos superiores com inclinação para vestibular, que exigiu uma abordagem multidisciplinar. Após a conclusão do tratamento periodontal, a terapia ortodôntica foi realizada. O tratamento desta paciente vem sendo conduzido com sucesso ao longo dos últimos dez anos.

Periodontite agressiva: conceito e considerações clínicas / Aggressive periodontitis: concept and clinical considerations

A periodontite agressiva (PAg) é uma das formas mais severas da doença periodontal (DP), tendo como característica o início precoce, a rápida instalação, a perda de inserção e a destruição óssea por agentes etiológicos diversificados, como presença de periodontopatógenos altamente virulentos, em contrapartida à quantidade inconsistente de biofilme bacteriano e à susceptibilidade genética do hospedeiro. O sucesso da intervenção terapêutica é dependente de um diagnóstico precoce, seu tratamento não possui protocolos específicos, mas há uma busca por respostas e tratamentos mais eficientes no controle da doença. Diante disso, esse estudo teve por objetivo realizar uma revisão de literatura sobre a PAg, abordando protocolos de tratamento, sua etiologia microbiana, susceptibilidade do indivíduo e envolvimento imunológico e genético associado à doença.