1α,25-dihydroxyvitamin D3 promotes early osteogenic differentiation of PDLSCs and a 12-year follow-up case of early-onset vitamin D deficiency periodontitis.

Periodontitis is a chronic periodontal disease that contributes to tooth loss. In recent years, many animal studies have reported that vitamin D (VitD) deficiency results in chronic periodontitis. However, no studies have reported cases of early-onset periodontitis with VitD deficiency. This study reports a 5-year-old male patient with early-onset periodontitis, VitD deficiency and VitD receptor (VDR) mutation. The patient was treated with VitD and calcium, and received systematic periodontal treatment. During the 12-year treatment, the periodontal conditions of this patient were stable. Our in vitro study found that VitD could promote the expression of alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), bone morphogenetic protein 2 (BMP2), bone gamma-carboxyglutamate protein (BGLAP), and VDR in the early osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Meanwhile, VitD could downregulate mRNA expression levels of Interleukin-6 (IL-6), Interleukin-8 (IL-8), Interleukin-1ß (IL-1ß) and protein levels of IL-6 in the tumor necrosis factor-α (TNF-α) -induced inflammation of PDLSCs. Therefore, sufficient VitD supply can be a potential treatment for VitD deficiency induced early-onset periodontitis.

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents.

It has previously been shown that the presence of Aggregatibacter actinomycetemcomitans in subgingival plaque is significantly associated with increased risk for clinical attachment loss. The highly leukotoxic JP2 genotype of this bacterium is frequently detected in adolescents with aggressive forms of periodontitis. The aims of the study were to quantify the levels of JP2 and non-JP2 genotypes of A. actinomycetemcomitans in saliva of Moroccan adolescents with the JP2 genotype earlier detected in the subgingival plaque. The salivary concentrations of inflammatory proteins were quantified and linked to the clinical parameters and microbial findings. Finally, a mouth rinse with leukotoxin-neutralizing effect was administrated and its effect on the levels the biomarkers and A. actinomycetemcomitans examined. The study population consisted of 22 adolescents that previously were found to be positive for the JP2 genotype in subgingival plaque. Periodontal registration and sampling of stimulated saliva was performed at baseline. A mouth rinse (active/placebo) was administrated, and saliva sampling repeated after 2 and 4 weeks rinse. The salivary levels of JP2 and non-JP2 were analyzed by quantitative PCR and inflammatory proteins by ELISA. Both the JP2 and the non-JP2 genotype were detected in all individuals with significantly higher levels of the non-JP2. Enhanced levels of the JP2 genotype of A. actinomycetemcomitans was significantly correlated to the presence of attachment loss (≥3 mm). Salivary concentrations of inflammatory biomarkers did not correlate to periodontal condition or levels of A. actinomycetemcomitans. The use of active or placebo leukotoxin-neutralizing mouth rinse did not significantly interfered with the levels of these biomarkers. Saliva is an excellent source for detection of A. actinomycetemcomitans on individual basis, and high levels of the JP2 genotype were significantly associated with the presence of clinical attachment loss.

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.

Functional Polymorphisms of CTLA4 Associated with Aggressive Periodontitis in the Chinese Han Population.

BACKGROUND/AIMS: CTLA4 has been identified functioning as a protein receptor which functions as an immune checkpoint, downregulating the immune system. Susceptibility to aggressive periodontitis (AgP) is influenced by gene polymorphisms related to the immune response. In this study, we focused on SNPs in the 3'-UTR of CTLA4 among Chinese AgP patients, and investigated any further relationships between the SNPs and miRNAs. METHODS: This case-control study included 120 AgP patients and 150 healthy controls. Genotyping was used to detect allele distribution. Cell transfection and the dual luciferase reporter assay were performed to investigate the potential functions of SNPs located in the 3'UTR of CTLA4. RESULTS: The data show that patients with a history of smoking were more susceptible compared to controls, exhibiting deeper probing depth, greater attachment loss and more sites of bleeding on probing. The results of genotyping analysis revealed that individuals with the GA and AA genotypes, and with the A carrier had a decreased risk (P = 0.015, P = 0.03). Furthermore, patients with the G allele might be regulated by miR-105, which caused a down-regulation of CTLA4. The carriers of the GG genotype exhibited the worst results of attachment loss and bleeding on probing. CONCLUSION: These findings show that rs56102377 in the 3'-UTR of CTLA4 may act as a protective factor by disrupting the regulatory role of miR-105 in CTLA4 expression. Thus, our study highlighted a potential role of these polymorphisms as genetic susceptibility biomarkers of periodontitis in Chinese Han populations.

Comparative analysis of immune cell subsets in peripheral blood from patients with periodontal disease and healthy controls.

Periodontitis is a chronic inflammatory disease caused by the colonization of teeth by the bacterial plaque biofilm and the resultant host immune responses in adjacent periodontal tissues. Disease severity can vary dramatically between patients with periodontitis, with some subjects displaying inflammation without bony destruction (gingivitis), while others experience chronic progressive or rapidly aggressive gingival connective tissue damage and bone loss. To determine whether peripheral immune dysregulation is associated with periodontitis, we performed extensive analysis of immune cell subsets in peripheral blood from patients with chronic or aggressive periodontitis versus periodontally healthy control subjects. Peripheral blood mononuclear cells (PBMC) from patients with chronic periodontitis or aggressive periodontitis and from periodontally healthy controls were analysed by 8-10-colour flow cytometry for the frequencies of various lymphocyte subsets, including interleukin (IL)-17-, interferon (IFN)-γ-, tumour necrosis factor (TNF)-α- and IL-10-producing cells, and the frequencies and phenotype of monocytes. Cytokine levels in serum from the different groups were determined by Luminex assay. We found no significant differences in the frequencies of major immune cell populations [CD4+ T cells, CD8+ T cells, γδ T cells, CD4+ CD45RO+ CD25+ CD127low regulatory T cells (Tregs ), CD19+ B cells, CD14+ monocytes] or of cytokine-producing T cells, or in the phenotype of CD14+ monocytes in peripheral blood from these patient cohorts. Additionally, no significant differences were observed in serum levels of prototypical inflammatory cytokines. These results suggest that the local gingival inflammatory response is not reflected by obvious changes in major blood immune cell subset frequencies.

Nonincised Papillae Surgical Approach (NIPSA) in Periodontal Regeneration: Preliminary Results of a Case Series.

A new surgical approach has been developed to optimize the preservation of the gingival margin and papillae when treating periodontal defects. The flap is raised by one mucosal incision far away from the marginal tissues. This case series reports on the effectiveness of a nonincised surgical approach (NIPSA) in conjunction with a hydroxyapatite-based graft biomaterial and enamel matrix derivative in treating intrabony defects. Ten defects in 10 patients were treated. The follow-up period ranged from 6 to 18 months (mean: 10.8 ± 4.7 months). Probing pocket depth was 9.6 ± 2.3 mm before surgery and 2.3 ± 0.5 mm postsurgery. Clinical attachment level (CAL) decreased from 10.4 ± 2.7 mm to 3.1 ± 0.87 mm postsurgery. The gingival papilla height, keratinized tissue width, and buccal gingival margin remained stable over time. No wound dehiscence was recorded. Mean Early Healing Index was 1.5 ± 0.7. Results show a substantial CAL gain, limited postsurgical shrinkage, minimal morbidity, and early healing.

Meta-Analysis of the Use of 8-OHdG in Saliva as a Marker of Periodontal Disease.

The objective was to collect the available evidence on oxidative stress marker measurements in periodontal patients, focusing specifically on 8-hydroxy-2'-deoxyguanosine (8-OHdG) as a salivary marker of periodontal disease, and to perform meta-analyses to calculate differences in concentration compared to healthy persons. A systematic search in PubMed, Cochrane Library, Embase, and Scopus identified 81 articles. Of these, 38 were duplicates. After reading the abstracts of the remaining 43, 42 were selected for full-text assessment. Finally, 17 articles were included in the qualitative synthesis. Those excluded were of low quality, did not answer the research question, or did not meet the inclusion and exclusion criteria. Of the 17 in the qualitative synthesis, 9 were included in the meta-analysis. The 9 studies in the meta-analysis were combined in a random effects model. Their heterogeneity was high (Q = 3982.02, p < 0.001, I2 = 99.8%). The difference in mean 8-OHdG concentration in saliva between periodontal and healthy subjects was estimated at 2.11 ng/ml (95% CI 1.23-2.98). The different saliva collection methods (stimulated/unstimulated) did not explain the heterogeneity. The 8-OHdG levels in saliva of periodontal patients were almost double to those of healthy patients: 8-OHdG is clearly a powerful periodontal disease marker.

Localization and density of Porphyromonas gingivalis and Tannerella forsythia in gingival and subgingival granulation tissues affected by chronic or aggressive periodontitis.

Porphyromonas gingivalis and Tannerella forsythia have been thought to be associated with periodontitis; however comprehensive histopathological localization of bacteria in affected human periodontal tissues is not well documented. In the present study, we examined formalin-fixed paraffin-embedded gingival and subgingival granulation tissues from 71 patients with chronic periodontitis and 11 patients with aggressive periodontitis, using immunohistochemistry with novel monoclonal antibodies specific to P. gingivalis or T. forsythia, together with quantitative real-time polymerase chain reaction for each bacterial DNA. Immunohistochemisty revealed both bacterial species extracellularly, as aggregates or within bacterial plaque, and intracellularly in stromal inflammatory cells, squamous epithelium, and capillary endothelium of granulation tissue. Combined analysis with the results from polymerase chain reaction suggested that localization and density of T. forsythia is closely associated with those of P. gingivalis, and that bacterial density is a factor responsible for the cell-invasiveness and tissue-invasiveness of these periodontal bacteria. Detection of these bacteria in the capillary endothelium in some samples suggested possible bacterial translocation into the systemic circulation from inflamed gingival and subgingival granulation tissues. Immunohistochemistry with the novel antibodies showed high specificity and sensitivity, and can be used to locate these periodontal bacteria in routinely-used formalin-fixed paraffin-embedded human tissue sections from systemic locations.

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.

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.

Aggressive periodontitis presents a higher degree of bilateral symmetry in comparison with chronic periodontitis.

The purpose of this cross-sectional study was to evaluate the occurrence of bilateral symmetry in the distribution of clinical parameters in subjects with generalized aggressive periodontitis (GAP) and severe chronic periodontitis (SCP). The sample comprised 53 subjects with GAP and 33 with SCP. Probing depth (PD) and clinical attachment loss (CAL) were recorded from both buccal and lingual interproximal sites of incisors and molars. The symmetry of periodontal destruction was analyzed in terms of intraclass coefficient correlations (ICC) for pairs of contralateral sites at which PD and/or CAL was ≥5 mm at one of the sites of the subjects in each group. GAP patients had a higher proportion of both PD and CAL ≥ 5 mm and also a higher mean proportion of subjects having PD and/or CAL ≥ 5 mm at one or both sites. The GAP group had 20 pairs of contralateral sites with PD (ICC = 0.22-0.63) and 26 pairs with CAL (ICC = 0.20-0.63), the correlation being statistically significant, while the SCP group had only 2 pairs (ICC = 0.36-0.48) with PD and 5 pairs with CAL (ICC = 0.33-0.58) showing a significant correlation. It can be concluded that GAP shows more symmetric periodontal destruction than SCP.

Effects of paraoxonase 1 on the cytodifferentiation and mineralization of periodontal ligament cells.

BACKGROUND AND OBJECTIVE: Single nucleotide polymorphisms (SNPs) of paraoxonase 1 (PON1) are known to be associated with the pathogenesis of osteoporosis and periodontitis. However, the effects of PON1 on the osteoblastic differentiation of periodontal ligament (PDL) cells are unclear. In this study, we examined the effects of PON1 on the osteoblastic differentiation of PDL cells, and analysed the role of PON1 SNPs on the pathogenesis of aggressive periodontitis (AgP) in the Japanese population. MATERIAL AND METHODS: Human PDL (HPDL) cells were exposed to the PON1 plasmid and PON1 inhibitor, 2-hydroxyquinoline, and cultured in mineralization medium. Expression of calcification-related genes and calcified nodule formation were assessed by real-time PCR, an alkaline phosphatase (ALPase) activity assay and Alizarin red staining. Sanger sequencing was performed to evaluate whether PON1 SNPs are associated with the pathogenesis of AgP in Japanese people. RESULTS: During osteoblastic differentiation of HPDL cells, expression of PON1 mRNA increased in a time-dependent manner. PON1 stimulated an increase in expression of mRNA for calcification-related genes, as well as ALPase activity. In contrast, 2-hydroxyquinoline clearly inhibited the expression of calcification-related genes, ALPase activity and calcified nodule formation in HPDL cells. Moreover, there was a statistically significant difference in the minor allele frequency of PON1 SNP rs854560 between the Japanese control database and patients with AgP in the Japanese population (P = .0190). CONCLUSION: PON1 induced cytodifferentiation and mineralization of HPDL cells, and PON1 SNP rs854560 may be associated with the pathogenesis of AgP in the Japanese population.

Polymorphism IL-1RN rs419598 reduces the susceptibility to generalized periodontitis in a population of European descent.

Interleukin (IL) 1-ra is a potent endogenous competitive inhibitor of IL-α and ß and has an anti-inflammatory role. Study objectives were: 1) to assess the associations of IL-1RN genetic single nucleotide polymorphism (SNP) (rs419598) with generalized chronic periodontitis (GCP), generalized aggressive periodontitis (GAgP), and absence of periodontitis and 2) to assess its association with the load of five periodontopathogenic bacteria and periodontal clinical variables. A cross-sectional analytic study was conducted in 123 patients with GCP, 60 patients with GAgP, and 20 controls. Reverse hybridization PCR was used for genotyping analysis to detect SNPs in IL-1A (rs1800587), IL-1B (rs1143634), and IL-1RN (rs419598) genes and for determination of the load of five periodontopathogenic bacteria. The severity and extension of periodontitis were assessed. Multinomial logistic regression and mediated regression analyses were performed. Considering results for GCP and GAgP patients together, the presence of polymorphism in IL-1A and/or IL-1B gene was associated with a higher likelihood of periodontitis, (OR = 8.11; 95%CI [1.85-35.48]), but this likelihood was reduced when IL-1RN polymorphism was also present, (OR = 5.91; 95%CI [1.08-32.27]). IL-1RN polymorphism was significantly associated with lower counts of red complex bacteria, specifically Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia, which were associated with improved clinical outcomes. The polymorphic expression of IL-1RN (rs419598) gene may be associated with a reduced susceptibility to GAgP and GCP in populations of European descent. This effect may be mediated by a decreased load of Porphyromona gingivalis, Tannerella forsythia, and Prevotella intermedia.

[CAUSES AND WAYS OF THE NECK PHLEGMON SPREADING ON MEDIASTINUM WITH A DESCENDING PURULENT MEDIASTINITIS OCCURRENCE].

Results of treatment in 2000-2016 yrs of 183 patients for the neck phlegmon were analyzed. In 60 (32.8%) of them a descending purulent mediastinitis (DPM) was diagnosed. The main causes of the DPM occurrence were tonsilogenic and odontogenous factors. Postoperative lethality in DPM have constituted 25%.

Lack of association between the TNF-α-1031genotypes and generalized aggressive periodontitis disease.

Periodontal disease is one of the most prevalent inflammatory illnesses and is a main cause of tooth loss in human population. Tumor necrosis factor-α (TNF-α) gene is one of pro-inflammatory cytokines which has important role in pathogenesis of periodontal disease. The main purpose of this study is to determine genotype abundance of TNF-α-1031 gene in both groups of patients and controls, and also investigation of relation of single nucleotide polymorphism (SNP) these genotypes with periodontal disease risk. DNA was extracted from blood tissue of 31 patients and 54 controls. The TNF-α-1031 polymorphism was evaluated by polymerase chain reaction- confronting two-pair primer (PCR-CTPP) method. In the GAP group, the frequencies of TT, TC and CC genotypes were 35.48%, 61.29 and 3.23%, respectively. In controls the frequencies of TT, TC and CC genotypes were 22.22%, 72.22%, and 5.56%, respectively. Results of this study showed that there was no significant association between TNF-α (-1031 T/C promoter) gene polymorphisms and the risk of generalized aggressive periodontitis disease.

Immature, but Not Mature, Dendritic Cells Are More Often Present in Aggressive Periodontitis Than Chronic Periodontitis: An Immunohistochemical Study.

BACKGROUND: Dendritic cells (DCs) form a key link between innate and adaptive immune responses. The aim of this study is to analyze presence and distribution of immature (im) and mature (m) DCs in gingival tissue samples obtained from patients diagnosed with aggressive periodontitis (AgP), chronic periodontitis (CP), and clinically healthy periodontium (control group). METHODS: Gingival tissue samples obtained from patients with: 1) AgP (aged <35 years); 2) CP (aged ≥35 years); and 3) control group (aged >18 years) (n = 10 per group) were collected. Two-way analysis of variance and posterior Fisher least significant difference test were used to observe differences between the means of cells positively marked for imDC (S100, CD1a, and CD207) and mDC (CD208) immunomarkers. RESULTS: imDCs were more numerous in AgP than CP and control groups, being statistically significant only for S100+ cells. Conversely, mDCs were visualized in higher numbers in CP than AgP and control groups (both P <0.05). Considering frequency of immunostained cells, the number of S100+ cells was greater than CD207+ and CD1a+ cells, followed by a lesser number of CD208+ cells, in all groups. CONCLUSIONS: Considering that the ability of DCs to regulate immunity is dependent on DC maturation, results suggest that predominance of imDCs appears to be involved in AgP pathogenesis, probably due to lack of ability to induce immune cell activation. Further studies are necessary to elucidate the role of DC maturation in regulating immune responses in periodontal disease.

Platelet activation and platelet-leukocyte interaction in generalized aggressive periodontitis.

Generalized aggressive periodontitis (GAgP) is an inflammatory disease of host response to bacterial challenge. To explore the role of platelets in host-microbial interactions in patients with periodontitis, 124 patients with GAgP and 57 healthy subjects were enrolled. Reliable indicators of subclinical platelet functional status, platelet count (PLT), platelet large cell ratio (PLCR), and mean platelet volume (MPV), were significantly lower in the GAgP group than in the control group and were negatively correlated with clinical periodontal parameters. The levels of important cytosolic protein in neutrophils, calprotectin (S100A8/A9) in plasma, and gingival crevicular fluid (GCF) were significantly higher in patients with GAgP compared with healthy subjects. Moreover, the GCF calprotectin level was negatively correlated with PLCR and MPV values. To explore the possible mechanisms of changes in platelet indices in periodontitis, flow cytometry analysis was performed, and patients with GAgP were found to have a higher status of platelet activation compared with healthy controls. Porphyromonas gingivalis (P. gingivalis) and recombinant human S100A8/A9 (rhS100A8/A9) induced platelet activation and facilitated platelet-leukocyte aggregate formation in whole blood of healthy subjects. In response to P. gingivalis and rhS100A8/A9, platelets from patients with GAgP increased activation and increased formation of platelet-leukocyte aggregates compared with those from healthy subjects. Platelet aggregates and platelets attached to leukocytes were found on gingival tissues from patients with GAgP, suggesting that decreased platelet size and count in the circulation might be related to consumption of large, activated platelets at inflamed gingiva. Platelets may have a previously unrecognized role in host response to periodontal infection.

Width of Keratinized Mucosa at Implant Sites in Patients Treated for Generalized Aggressive Periodontitis: A Cohort Study.

PURPOSE: The aim of this cohort study was to evaluate the width of keratinized mucosa at implant sites of partially edentulous patients who were treated for generalized aggressive periodontitis. MATERIALS AND METHODS: Dental implants were placed in 35 patients who were treated for generalized aggressive periodontitis and 18 periodontally healthy individuals (controls). At baseline, the keratinized mucosa of all implants was ≥ 2 mm. Follow-up examinations were conducted every 3 months over a 4-year period. RESULTS: The implant survival rate was 97.3% in patients with generalized aggressive periodontitis and 100% in the control group. Four years after implant insertion, patients with generalized aggressive periodontitis had significantly higher clinical attachment levels at the teeth and implants compared with the controls. At all time points, in both groups the mean probing depth at the implants was significantly larger than at the teeth. The mean widths of keratinized mucosa and keratinized gingiva were not significantly different between the two groups. In both groups, the widths of keratinized mucosa and keratinized gingiva were significantly higher at the maxilla than at the mandible. Four years after baseline, the implants in the mandible showed the smallest keratinized mucosa (mean: ≤ 1 mm). CONCLUSION: During the first 4 years after implant placement, no significant changes in the keratinized mucosa at implants could be shown, either in periodontally healthy patients or in patients treated for generalized aggressive periodontitis. The keratinized gingiva at the teeth was generally significantly wider than the keratinized mucosa at the implants.

Clinical and histological characterization of an aggressive periodontitis case associated with unusual root canal curvatures.

The article presents the histological and clinical characteristics in a severe generalized aggressive periodontitis case associated with multiple root curvatures and the complex therapeutic approach of the severe periodontal destructions. The patient received a complex therapy, including periodontal non-surgical, regenerative and reconstructive approaches, and also endodontic and prosthetic treatments. Recall appointments were fixed at 3-month intervals. One year after the finalization of the active therapy, a hyperplasic, inflamed interdental papilla associated with a recurrent clinical attachment loss was diagnosed at the mesial aspect of the right maxillary second premolar. A biopsy was harvested for histological examination and the recurrent site was treated. The histological study revealed important modifications of the epithelial layer and of the connective tissue of the gingiva. An extremely accentuated pattern of the gingival rete ridges at the epithelial-connective tissue junction, the presence of inflammatory cells infiltrating the epithelial layer and lamina propria and the disorganization of the fascicules of collagen fibers were observed. The inflammatory infiltrate was dominated by plasma and monocytic-like cells as immunohistochemical analyses highlighted. The complex therapeutic approach led to a satisfactory aesthetic and functional outcome. The severe root curvatures may be an unusual trait in this generalized aggressive periodontitis case substantially increasing the amount and the costs of non-periodontal procedures. In this case, the cell make-up of the inflammatory infiltrate and the paucity of collagen in the infiltrated tissue portions are considered to correspond to a fully developed recurrent lesion.