Translation of mouse model to human gives insights into periodontitis etiology.

To suggest candidate genes involved in periodontitis, we combined gene expression data of periodontal biopsies from Collaborative Cross (CC) mouse lines, with previous reported quantitative trait loci (QTL) in mouse and with human genome-wide association studies (GWAS) associated with periodontitis. Periodontal samples from two susceptible, two resistant and two lines that showed bone formation after periodontal infection were collected during infection and naïve status. Differential expressed genes (DEGs) were analyzed in a case-control and case-only design. After infection, eleven protein-coding genes were significantly stronger expressed in resistant CC lines compared to susceptible ones. Of these, the most upregulated genes were MMP20 (P = 0.001), RSPO4 (P = 0.032), CALB1 (P = 1.06×10-4), and AMTN (P = 0.05). In addition, human orthologous of candidate genes were tested for their association in a case-controls samples of aggressive (AgP) and chronic (CP) periodontitis (5,095 cases, 9,908 controls). In this analysis, variants at two loci, TTLL11/PTGS1 (rs9695213, P = 5.77×10-5) and RNASE2 (rs2771342, P = 2.84×10-5) suggested association with both AgP and CP. In the association analysis with AgP only, the most significant associations were located at the HLA loci HLA-DQH1 (rs9271850, P = 2.52×10-14) and HLA-DPA1 (rs17214512, P = 5.14×10-5). This study demonstrates the utility of the CC RIL populations as a suitable model to investigate the mechanism of periodontal disease.

Hidden noise in immunologic parameters might explain rapid progression in early-onset periodontitis.

To investigate in datasets of immunologic parameters from early-onset and late-onset periodontitis patients (EOP and LOP), the existence of hidden random fluctuations (anomalies or noise), which may be the source for increased frequencies and longer periods of exacerbation, resulting in rapid progression in EOP. Principal component analysis (PCA) was applied on a dataset of 28 immunologic parameters and serum IgG titers against periodontal pathogens derived from 68 EOP and 43 LOP patients. After excluding the PCA parameters that explain the majority of variance in the datasets, i.e. the overall aberrant immune function, the remaining parameters of the residual subspace were analyzed by computing their sample entropy to detect possible anomalies. The performance of entropy anomaly detection was tested by using unsupervised clustering based on a log-likelihood distance yielding parameters with anomalies. An aggregate local outlier factor score (LOF) was used for a supervised classification of EOP and LOP. Entropy values on data for neutrophil chemotaxis, CD4, CD8, CD20 counts and serum IgG titer against Aggregatibacter actinomycetemcomitans indicated the existence of possible anomalies. Unsupervised clustering confirmed that the above parameters are possible sources of anomalies. LOF presented 94% sensitivity and 83% specificity in identifying EOP (87% sensitivity and 83% specificity in 10-fold cross-validation). Any generalization of the result should be performed with caution due to a relatively high false positive rate (17%). Random fluctuations in immunologic parameters from a sample of EOP and LOP patients were detected, suggesting that their existence may cause more frequently periods of disease activity, where the aberrant immune response in EOP patients result in the phenotype "rapid progression".

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.

Aggregatibacter actinomycetemcomitans (Aa) Under the Radar: Myths and Misunderstandings of Aa and Its Role in Aggressive Periodontitis.

Aggregatibacter actinomycetemcomitans (Aa) is a low-abundance Gram-negative oral pathobiont that is highly associated with a silent but aggressive orphan disease that results in periodontitis and tooth loss in adolescents of African heritage. For the most part Aa conducts its business by utilizing strategies allowing it to conceal itself below the radar of the host mucosal immune defense system. A great deal of misinformation has been conveyed with respect to Aa biology in health and disease. The purpose of this review is to present misconceptions about Aa and the strategies that it uses to colonize, survive, and evade the host. In the process Aa manages to undermine host mucosal defenses and contribute to disease initiation. This review will present clinical observational, molecular, and interventional studies that illustrate genetic, phenotypic, and biogeographical tactics that have been recently clarified and demonstrate how Aa survives and suppresses host mucosal defenses to take part in disease pathogenesis. At one point in time Aa was considered to be the causative agent of Localized Aggressive Periodontitis. Currently, it is most accurate to look at Aa as a community activist and necessary partner of a pathogenic consortium that suppresses the initial host response so as to encourage overgrowth of its partners. The data for Aa's activist role stems from molecular genetic studies complemented by experimental animal investigations that demonstrate how Aa establishes a habitat (housing), nutritional sustenance in that habitat (food), and biogeographical mobilization and/or relocation from its initial habitat (transportation). In this manner Aa can transfer to a protected but vulnerable domain (pocket or sulcus) where its community activism is most useful. Aa's "strategy" includes obtaining housing, food, and transportation at no cost to its partners challenging the economic theory that "there ain't no such thing as a free lunch." This "strategy" illustrates how co-evolution can promote Aa's survival, on one hand, and overgrowth of community members, on the other, which can result in local host dysbiosis and susceptibility to infection.

Superoxide Dismutase, Uric Acid, Total Antioxidant Status, and Lipid Peroxidation Assay in Chronic and Aggressive Periodontitis Patients.

AIM: It has been suggested that periodontitis may be associated with increased oxidative stress. The objective of this study is to evaluate the possible differences in antioxidant status between chronic periodontitis (CP) and aggressive periodontitis (AP), by assessing the concentrations of antioxidants with total antioxi-dant status (TAS) and lipid peroxidation status in serum and gingival crevicular fluid (GCF) of these patients. MATERIALS AND METHODS: Forty-six patients with CP, 32 patients with AP, and 50 healthy controls were included in this study. The level of enzymatic antioxidant, superoxide dismutase (SOD), nonenzymatic antioxidant uric acid, and TAS with lipid peroxidation measured in serum and GCF of patients suffering from CP and AP were compared with the healthy controls. RESULTS: The TAS is decreased and malondialdehyde (MDA) level is increased in both serum and GCF in CP and AP compared with healthy controls (p < 0.001). Superoxide dismutase activities in GCF and serum are found to be low in both the groups of periodontitis (p < 0.001). The uric acid levels are found to be inconsistent in GCF and serum in both the groups of periodontitis. CONCLUSION: Lipid peroxidation and TAS were affected at systemic level in serum and in GCF of the periodontal pockets, in CP and AP. Similar comments may be made for the decrease in SOD activities and inconsistent uric acid levels. CLINICAL SIGNIFICANCE: Increased oxidative stress may have a role in the pathogenesis of periodontal disease activity.

Herpesviruses in etiopathogenesis of aggressive periodontitis: A meta-analysis based on case-control studies.

OBJECTIVE: Previous studies have found that herpesviruses are associated with aggressive periodontitis (AgP). However, these findings are controversial. This meta-analysis was aimed at clarifying the association between herpesviruses and AgP. METHODS: We identified eligible case-control studies evaluating the association between herpesviruses and AgP from PubMed and Embase databases in October 2015. Original data were extracted and quality assessment was done. Overall odds ratios (ORs) and 95% confidence intervals (CIs) were estimated. Random-effects model was determined. The stability was evaluated by sensitivity analysis. Finally, Egger's funnel plot was used to investigate the publication bias. RESULTS: Twelve case-control studies involving 322 patients and 342 controls were included in the present meta-analysis. The included case-control studies were assessed as high quality. The quantitative synthesis results for Epstein-Barr virus (EBV) showed significance (10 studies: p = 0.0008, OR = 6.11, 95% CI = 2.13-17.51); nevertheless, evidence of publication bias for EBV was considerable (EBV: Egger's test, p<0.001). Human cytomegalovirus (HCMV) and Herpes simplex virus type 1 (HSV-1) had significant association with AgP (12 studies for HCMV: p = 0.009, OR = 3.63, 95% CI = 2.15-6.13; 4 studies for HSV-1: p<0.001, OR = 19.19, 95% CI = 4.16-79.06). Sensitivity analyses showed the results yielded consistency, and no significant publication bias was observed for HCMV. The association between Herpes simplex virus type 2 (HSV-2) and AgP was inconclusive (2 studies: p = 0.20, OR = 3.46, 95% CI = 0.51-23.51). CONCLUSION: This meta-analysis suggests that HCMV and HSV-1 are significantly associated with AgP. However, due to the heterogeneity among studies these conclusions should be cautiously interpreted. There is insufficient evidence to draw any conclusion between EBV, HSV-2 and AgP based on the currently limited data.

Aggressive forms of periodontitis secondary to systemic disorders.

A number of systemic disorders increase a patient's susceptibility to destructive periodontitis and have impacts on periodontal disease progression and severity. The underlying factors are usually genetic and are mainly related to alterations in the immune response and in certain endocrine functions, leading to various syndromes in which periodontitis and/or early tooth loss are secondary manifestations. Neutrophils are important immune defense cells that play a significant role in controlling the spread of microbial plaque infections in the dentogingival region. This review focuses on a selected group of systemic disorders that are associated with alterations in either neutrophil counts (quantitative disorders) or function (qualitative disorders), and defects in the mineralization of bone and dental tissues. In most of these diseases controlling the periodontal disease progression is very challenging. Proper diagnosis is a prerequisite for proper management of the periodontal problem. Future advances in research, including gene targeting and the resolution of enzyme deficiencies, may bring about remedies of the underlying systemic disorders and may significantly improve the outcome of periodontal treatment in these patients.

Haplotype analysis of interleukin-8 gene polymorphisms in chronic and aggressive periodontitis.

OBJECTIVES: Periodontitis is an inflammatory disease characterized by connective tissue loss and alveolar bone destruction. Interleukin-8 (IL8) is important in the regulation of the immune response. The aim of this study was to analyze four polymorphisms in the IL8 gene in relation to chronic (CP) and aggressive (AgP) periodontitis. METHODS: A total of 492 unrelated subjects were included in this case-control association study. Genomic DNA of 278 patients with CP, 58 patients with AgP, and 156 controls were genotyped, using the 5' nuclease TaqMan assay, for IL8 (rs4073, rs2227307, rs2227306, and rs2227532) gene polymorphisms. Subgingival bacterial colonization was investigated by the DNA-microarray detection kit in a subgroup of subjects (N = 247). RESULTS: Allele and genotype frequencies of all investigated IL8 polymorphisms were not significantly different between the subjects with CP and/or AgP and controls (P > 0.05). Nevertheless, the A(-251)/T(+396)/T(+781) and T(-251)/G(+396)/C(+781) haplotypes were significantly less frequent in patients with CP (2.0% versus 5.1%, P < 0.02, OR = 0.34, 95% CI: 0.15-0.78, resp., 2.0% versus 4.5%, P < 0.05, OR = 0.41, 95% CI: 0.18-0.97) than in controls. CONCLUSIONS: Although none of the investigated SNPs in the IL8 gene was individually associated with periodontitis, some haplotypes can be protective against CP in the Czech population.

Potential effect of neutrophil functional disorders on pathogenesis of aggressive periodontitis.

INTRODUCTION: Leukocytes play a key role in maintaining the balance between an effective host defence response to microorganisms and periodontal tissue destruction. Neutrophil dysfunction has been associated with increased susceptibility to periodontal diseases. We undertook this study to determine to what extent neutrophil dysfunction constitutes to the pathogenesis of aggressive periodontitis (AgP) in tropical country like ours. MATERIALS AND METHODS: Age- and sex-matched groups consisting of 20 subjects each of generalized aggressive periodontitis (GAP)-cases and nonperiodontitis (NP)-controls. diabetes mellitus, HIV infection, prolonged antibiotic use and smoking were excluded. Each neutrophil function was assessed using the chemotactic assay using case in, phagocytosis assay, candidacidal assay (for intracellular killing) and NBT assay (for respiratory burst failure). STATISTICAL ANALYSIS USED: Student's t-test, Fisher's exact test and Chi-square test. RESULTS: In the study 17 out of 20 subjects (85%) had at least one abnormal neutrophil assay either hypofunctional or hyperfunctional of which 16 (80%) had hypofunctional assays and 8 (40%) had hyperfunctional assays. Defective phagocytosis was the commonest (50%) followed by chemotactic defect (45%), defective respiratory burst (40%) and defective intracellular killing (30%). Mean of chemotaxis assay was significantly less in AgP when compared to controls (103 vs 129 µm, p=0.002), similarly for phagocytic defect (3.45 vs 4.65, p≤0.001) and with candidacidal assay (26.80 vs 37.35, p<0.001). CONCLUSION: The prevalence of neutrophil dysfunction, predominantly hypofunctional, was significantly very high in GAP patients with few even having hyperactive respiratory burst function. Multiple level neutrophil defects could account for the aggressive nature of AgP even in apparently healthy subjects.

Integrated periodontal, orthodontic, and prosthodontic treatment in a case of severe generalized aggressive periodontitis.

OBJECTIVE: This article reports a case of severe generalized aggressive periodontitis and subsequent collapse of the occlusion in a psychiatric patient, treated by an extremely conservative orthodontic-periodontal-prosthodontic treatment. SUMMARY: A woman presented with severe anterior proclination caused by severe periodontal disease and Angle's class II molar malocclusion. The patient wanted to preserve her teeth and rejected the idea of implant treatment. This case report demonstrates that combining periodontal therapy, orthodontic treatment, and prosthodontics (through a decision-making system with a proper interdisciplinary coordination) can greatly improve function and the esthetic result. Comprehensive periodontal treatment took place before other intervention, and periodontal maintenance and follow-up throughout the treatment and after played a crucial role.

Adolescents with high periodontal risk in Public Dental Service.

The purpose of the present study was to investigate the prevalence of adolescents with high periodontal risk and to identify factors with influence on the decision to refer a patient to a specialist clinic of Periodontology, on compliance rate and on treatment outcome. The investigation was conducted as a retrospective study on adolescents at age 13-17. In total, clinical examinations and risk evaluations according to caries- and periodontal risk were performed on 50347 adolescents in general dentistry at ages 13, 15 and 17 in 2007. Individuals with a high periodontal risk were included in the present investigation. A high periodontal risk was defined as presence of sites with periodontal pocket depths >6mm and loss of periodontal tissue support. Multiple logistic regression analyses were adopted to calculate the influence of the potential predictors on the investigated dependent variables. In total, 0.5% of the adolescents were found to have high periodontal risk. The diagnosis local periodontitis and the number of periodontal pockets with probing depths >6 mm were positively and significantly correlated to referral to a periodontist. Eighteen percent dropped out before the treatment was completed. Smokers had a significantly lower compliance than non-smokers. The success rate was significantly lower for individuals with many periodontal pockets and for those with the diagnosis local periodontitis. The prevalence of adolescents classified as having high periodontal risk was low. A large frequency of subjects dropped out before the periodontal treatment was completed, especially at the specialist clinics.

Periodontal diseases in children and adolescents: a clinician's perspective part.

UNLABELLED: Contrasting forms of periodontal disease can affect children and adolescents with varying prevalence, severity and extent, leading to a diverse prognosis in these age groups. For an early diagnosis and treatment of periodontal conditions in young patients, it is essential for the dental practitioner to be able to identify and classify the disease correctly at the earliest opportunity, applying basic principles along with understanding of aetiology and risk factors. The first part of this article discusses the classification, plaque-induced and non-plaque-induced gingival diseases, localized and generalized forms of chronic, as well as aggressive, periodontitis. CLINICAL RELEVANCE: Knowledge of different forms of periodontal diseases affecting children and adolescents may help to distinguish between different forms of diseases and have value in screening and early diagnosis of the disease.

Leukocyte adhesion deficiency: a case report and review.

Leukocyte adhesion deficiency (LAD) is a rare inherited primary immunodeficiency disorder characterized by the presence of a defect of phagocytic function resulting from a lack of leukocyte cell surface expression of ß2 integrin molecules (CD11 and CD18) that are essential for leukocyte adhesion to endothelial cells and chemotaxis. A small number of patients with LAD-1 have a milder defect, with residual expression of CD18. These patients tend to survive beyond infancy; they manifest progressive severe periodontitis, leading to partial or total premature loss of the primary and permanent dentitions. Close cooperation with pediatricians and immunologists is often the key to successful management of pediatric patients with LAD. The purpose of this report was to present the case of a 5-year-old boy with moderate leukocyte adhesion deficiency-1 and severe periodontitis, cellulitis and illustrate the need for periodic oral checkups to avoid the progression of oral diseases and prevent premature tooth loss.

Infection of human gingival fibroblasts with Aggregatibacter actinomycetemcomitans: An in vitro study.

OBJECTIVE: Aggregatibacter actinomycetemcomitans is known to be a major cause of localized aggressive periodontitis. Previous research has suggested that A. actinomycetemcomitans can damage many types of host cells. There is evidence for the ability of this organism to invade endothelial and epithelial cells, but information pertaining to its potential for invading gingival fibroblasts is very limited. Internalization of bacteria is not only responsible for damaging host tissue but also a means to evade the host immune response. It was hypothesized that A. actinomycetemcomitans can invade and reside in human gingival fibroblasts (HGF). METHODS: Primary cultures of HGF were infected with A. actinomycetemcomitans at a ratio of 1:100. Bacterial internalization was determined by an antibiotic protection assay. Bacterial-fibroblast interaction was examined using phase-contrast, scanning and transmission electron microscopy. RESULTS: It was demonstrated that A. actinomycetemcomitans was internalized into HGF at an efficiency of 0.084%. Transmission electron microscopic study showed the presence of A. actinomycetemcomitans in the cytoplasm of HGF without the surrounding membrane. Scanning electron micrographs revealed the sloughing of HGF surfaces on which A. actinomycetemcomitans adhered. Rounded cells, attachment loss and damaged cells were also observed. CONCLUSIONS: It is concluded that the attachment and invasion of A. actinomycetemcomitans into human gingival fibroblasts play a role in periodontal tissue damage and may also be a means of immune evasion.

Prevalence and risk indicators of gingivitis and periodontitis in a multi-centre study in North Jordan: a cross sectional study.

BACKGROUND: There are limited data about the epidemiology and risk factors/indicators of gingivitis, aggressive periodontitis (AgP) and chronic periodontitis (CP) in Jordan. The aim of this study was to assess the prevalence and risk indicators of gingivitis, AgP and CP. METHODS: A sample of 595 subjects was randomly selected from subjects escorting out-patients attending a Medical Center, a Dental Teaching Hospital, and 2 private dental clinics. The socio-demographic variables, oral hygiene habits, income, smoking and Body Mass Index (BMI) were recorded. Full mouth periodontal examination was performed, and radiographs were taken for sites with probing depth > 3 mm. RESULTS: About 76% had gingivitis, 2.2% had AgP and 5.5% had CP. Periodontitis was more frequent among males than females with a M: F ratio of 1.6:1 and the prevalence increased with age. Subjects who reported not using a tooth brush, smokers and subjects with BMI > 30 kg/m2 had significantly higher prevalence of periodontitis. The risk for periodontitis was greater among subjects who reported positive family history and subjects with ≤ 12 years of education. CONCLUSIONS: This is the first study to report on the prevalence of gingivitis, CP and AgP in North Jordanian. Age, low education, low frequency of tooth brushing and family history were significantly associated with increased risk of periodontitis.

Neutrophils in periodontal inflammation.

Neutrophils (also called polymorphonuclear leukocytes) are the most abundant leukocytes whose primary purpose as anti-microbial professional phagocytes is to kill extracellular pathogens. Neutrophils and macrophages are phagocytic cell types that along with other cells effectively link the innate and adaptive arms of the immune response, and help promote inflammatory resolution and tissue healing. Found extensively within the gingival crevice and epithelium, neutrophils are considered the key protective cell type in the periodontal tissues. Histopathology of periodontal lesions indicates that neutrophils form a 'wall' between the junctional epithelium and the pathogen-rich dental plaque which functions as a robust anti-microbial secretory structure and as a unified phagocytic apparatus. However, neutrophil protection is not without cost and is always considered a two-edged sword in that overactivity of neutrophils can cause tissue damage and prolong the extent and severity of inflammatory periodontal diseases. This review will cover the innate and inflammatory functions of neutrophils, and describe the importance and utility of neutrophils to the host response and the integrity of the periodontium in health and disease.

Single nucleotide polymorphisms in interleukin-1gene cluster and subgingival colonization with Aggregatibacter actinomycetemcomitans in patients with aggressive periodontitis.

Periodontitis is initiated by the subgingival occurrence of periodontopathogens. It is triggered by a specific host-dependent immune response that is influenced by genetic predisposition. Polymorphisms in the interleukin-1 (IL-1) gene cluster have been suggested to influence the pathogenesis of periodontitis. A total of 159 periodontitis patients (chronic disease: n = 73, aggressive disease: n = 86) and 89 periodontitis-free controls were included in the study. Polymorphisms IL-1α (rs1800587), IL-1ß (rs16944, rs1143634), IL-1 receptor (rs2234650), and IL-1 receptor antagonist (rs315952) were determined by polymerase chain reaction with sequence-specific primers (PCR-SSP). Subgingival bacterial colonization was assessed using a polymerase chain reaction/DNA probe test (micro-Ident). Haplotype block structure was determined using Haploview 4.2. Statistical analyses were performed applying SPSS 17.0 considering dominant, recessive, and codominant genetic models. In this case-control study, no association between genomic variants of the IL-1 gene cluster and the incidence of severe periodontitis could be shown. Carriers of the rare genotypes of rs1800587 (p(corr) = 0.009), rs1143634 (p(corr) = 0.009) and composite genotype (rs1800587+rs1143634) (p(corr) = 0.031) had a twofold higher risk for subgingival occurrence of Aggregatibacter actinomycetemcomitans. In forward stepwise binary logistic regression analyses considering age, gender, smoking, and approximal plaque index as potential confounders these significant associations were demonstrated. Despite the genetic background of IL-1 gene cluster could be shown to be associated with subgingival colonization of A actinomycetemcomitans, there is no evidence that it is an independent risk indicator for periodontitis.

Severe presentation of necrotizing ulcerative periodontitis in a Nigerian HIV-positive patient: a case report.

OBJECTIVE: To report a case of severe necrotizing ulcerative periodontitis (NUP) with a rarely associated sequestrum formation in a Nigerian HIV-positive patient. CLINICAL PRESENTATION AND INTERVENTION: A 47-year-old HIV-positive male patient with no history of previous dental visits presented with a severe toothache in his lower jaw of 4 weeks' duration, which had affected his ability to chew properly. Clinical examination revealed marked gingival inflammation, moderate gingival recession and mobility of some of his lower anterior teeth: 31, 32, and 33. There was also a sequestrum present associated with the affected teeth. His CD4 cell count was 226 cells/mm(3). His viral load was very high (360,082 copies/ml). The intervention included thorough debridement of the necrotic lesion and sequestrectomy. The patient responded well to treatment after 1 week of follow-up. Unfortunately, the CD4 count was not assessed further because the patient was lost to follow-up. CONCLUSION: This case showed that a high CD4 cell count does not necessarily prevent the occurrence of NUP in HIV-positive patients. Intervention might have enhanced a rapid positive response to the treatment within a short time.

Sequelae of iatrogenic periodontal destruction associated with elastics and permanent incisors: literature review and report of 3 cases.

The purpose of this paper was to report 3 cases of localized aggressive periodontal bone destruction related to improper use of orthodontic elastic bands to close diastemas in permanent anterior teeth and to compare the results to previous studies. Some common signs and symptoms of this particular destruction were observed with these patients that had been previously reported when the comparisons of these cases were made. The patients usually experienced a painful sensation, and an isolated pyogenic-like granuloma appeared at the interdental area. Radiographs revealed localized periodontal destruction, with tooth extrusion and clinical crown divergence and radiographic root convergence; the two involved teeth moved simultaneously during mobility testing. Surgical intervention and treatment of the cases was described. The prognosis is usually decided by the severity of the condition, and many factors may influence the healing of treated cases.