Periodontal diseases.

American Academy of Periodontology Task Force Report on the Update to the 1999 Classification of Periodontal Diseases and Conditions.

Comprehensive Periodontal Therapy: A Statement by the American Academy of Periodontology

Periodontitis is defined as an inflammatory disease of the supporting tissues of teeth caused by microorganisms or groups of specific microorganisms, which result in progressive destruction of the periodontal ligament and alveolar bone, caused by multiple infectious agents and is interconnected with the humoral and cellular immune responses of the host. This study aimed to determine the prevalence of herpes simplex virus type 1 and 2 and cytomegalovirus in patients with chronic and aggressive periodontits and healthy subjects. Biopsies samples were taken from patients presenting to the clinic of the Universidad Autonoma de Nuevo Leon diagnosed with chronic periodontitis o aggressive periodontitis and control patients. The samples taken were submitted to polymerase chain reaction (PCR) to detect the presence of the virus. The presence of the different kinds of virus was negative in the evaluated subjects.

Diabetes mellitus is a much-studied disorder, characterized by hyperglycemia and numerous oral and medical complications. The latter includes (above all) decreased life-span - and these are widely discussed in the dental and medical literature. The oral complications include impaired wound healing; increased severity of periodontal disease and peri-implantitis; dry mouth (xerostomia); and dental caries. The relationship between diabetes and oral health is bi-directional: Optimal management of local oral disease can profoundly affect the systemic metabolic control of the diabetic patient, and strict management of the patient's hyperglycemia can reduce its impact on oral disease. The only host modulation therapy (HMT), approved by the U.S. Food and Drug Administration (FDA) to treat periodontal disease, is a novel NON-antimicrobial (low-dose) formulation of doxycycline (Periostat®; 20 mg b.i.d). A publication in Scientific Reports (2017), which supported the clinical rationale of efficacy and safety of low-dose doxycycline in diabetics, stated: "doxycycline not only ameliorated insulin resistance, fasting blood glucose, and insulin levels, and lipid profiles in the circulation and liver, but also improved islet morphology and increased glucose-stimulated insulin secretion." Additional developments include the biphenolic chemically-modified curcumins, as HMT for managing oral diseases. A lead compound, chemically-modified curcumin 2.24 (CMC2.24), has demonstrated safety and efficacy in vitro, in cell culture, and in vivo using mouse, rat, rabbit, and dog models of disease. In conclusion, novel host-modulation compounds have shown significant promise as adjuncts to traditional local therapy in the clinical management of periodontal and other oral diseases.

Human leukocyte antigens (HLA)/alleles have been considered as risk factors for periodontal disease. However, data from HLA associations is not consistent. Diversity of HLA antigen combinations and en bloc inherited HLA alleles (haplotypes), as known in systemic diseases, can be variable factors in disease association. Therefore, the aim of this study was to investigate the incidence of HLA homozygosities, heterozygosities and estimated haplotypes in German Caucasian groups with generalized aggressive (N = 50) and chronic (N = 102) periodontitis in comparison to control probands without periodontitis (N = 102). HLA-A, -B, -Cw, -DRB1, -DRB3/4/5, -DQB1 typing was carried out using both serologic (microlymphocytotoxicity test) and genomic (PCR-SSP: PCR with sequence specific primers) techniques. Frequencies of all homozygosities, heterozygosities and haplotypes were determined in all patients and controls. In both patient groups, associations to HLA homozygosities and heterozygosities were found. Most striking was the significantly lower frequency of HLA-DRBblank* homozygosity (non-DRB3*/DRB4*/DRB5*) in chronic periodontitis (p < 0.05), whereas HLA-DRB1*15 : DRB5*(DR51) : DQB1*06 showed a slightly higher homozygosity rate in all patients. As the combination HLA-A*02,A*03 was significantly decreased in aggressive periodontitis (p < 0.05), HLA-A*01,A*03 heterozygosity was significantly lowered in chronic periodontitis (p < 0.05). Among others, the known positive associations for HLA-A*68/69 (A28) and HLA-DRB1*04 were confirmed by the haplotypes HLA-A*68/69 : Cw*07 : B*18 in aggressive periodontitis (p < 0.05) and HLA-Cw*08 : B*14 : DRB1*04 in chronic periodontitis (p < 0.05). The present study elucidates the variety of HLA associations and therefore the difficulty to assign single HLA markers to periodontal disease. Susceptibility/resistance of both aggressive and chronic periodontitis may rather be influenced by particular HLA marker combinations. Associated HLA haplotypes may be of further importance for unknown gene loci representing a part of the genetic background for periodontitis. The different associations in aggressive and chronic periodontitis indicate different susceptibility/resistance factors for both diseases.

The aim of the present study was to investigate the association of single nucleotide polymorphism (SNP) with aggressive periodontitis (AgP) in Taiwanese. All subjects were Taiwanese ethnicity. The design of study was a case-control study, including the test groups of aggressive periodontitis (AgP) and chronic periodontitis (CP) volunteers, and the control group of periodontitis-free healthy participants. SNPs of interleukin-17A (IL-17A), cluster of differentiation (CD14), matrix metalloproteinase-1 (MMP-1) and toll-like receptor 4 (TLR4) were chosen. According to the principle of polymerase chain reaction (PCR), real-time polymerase chain reaction (RT-PCR) was utilized to amplify the small quantity of DNA from the peripheral blood sample. The effect of Real-time was achieved to determine the expression of the four SNPs quantitatively by using fluorescence signal detection system. We used the chi-square test or Fisher’s exact test to compare the means and proportions in allele/genotype frequencies of the three groups. Logistic regression analysis was performed to measure the relationship between the genotypes and periodontitis. Analysis of the polymorphisms showed patients with periodontitis (AgP and CP) had a higher distribution of G allele (AgP:39.3%, CP:38%, H:6.8%) for CD14 SNPs, patients with AgP had higher 1G/1G genotype and 1G allele (AgP:66.1%, CP:40%, H:34.1%) for MMP-1 SNPs (p<0.05). As for IL-17A and TLR4 SNPs, we found no correlation with periodontitis. The subjects with the combined allele associated with AgP had a higher percentage than the subjects with the single allele in AgP group. These data suggest that patients with CD14 polymorphism were associated with the occurrence of AgP and CP in Taiwanese ethnicity population. The MMP-1 polymorphism (1G allele) is genetically associated with vulnerability of patients with AgP. In addition, combined occurrence of the CD14 and MMP-1 SNPs allele may raise the susceptibility of one individual to AgP.

Periodontal diseases consists of a wide range of inflammatory conditions which causes degeneration of Periodontium and affects all supporting structures of teeth such as gingiva, periodontal ligament, cementum and alveolar bone etc. followed by teeth loss. WHO had reported about 10-15% of the world population is suffering from severe periodontal condition. It is complex infectious disease caused by aggressive microbial growth on teeth. The main aim of this study is to provide systemic update on periodontal disease regarding its stages, occurrence, pathophysiology, diagnosis, treatment and management. The pathophysiology of periodontal disease is associated with dental plaque, microbial biofilm formation and immunogenicity of the host cell. The severity of this disease depends upon risk factors and chronological stages. Prevention is attained by daily maintenance of oral hygiene. Various surgical and non-surgical treatments are available to control the formation of microbial biofilm. Daily maintenance and periodic management of this disease control worsening of condition and shows definite improvement in oral health.

ABSTRACTIn periodontal diseases, bacteria and microbes serve as the primary pathogens that initiate the condition, while the host refers to the body that hosts these microorganisms. Host modulation therapy is a drug-based treatment that can be used along with systematic periodontal therapy to help the disease get better and stop tissue damage. There is a new way to treat periodontitis called “Host-Modulation Therapy” (HMT). It involves reducing the bacteria biofilm through daily good oral hygiene and regular scaling and root planing (SRP). Using host modulation therapies to lower inflammation, restore microbiome balance, and change the immune response of the host holds a lot of promise for better periodontal disease treatment. This review examines host modulation in treating and preventing periodontal diseases. The review encompasses a variety of studies that evaluate pharmaceutical agents, probiotics, and immunomodulatory methods.

Objective:Based on the evidence regarding the relationship between inflammatory processes and stress responses, the present study investigated the association between psychological stress and elevation of inflammatory mediators related to periodontal disease in adult patients.Materials and Methods:The study consisted of 50 patients including 25 patients with chronic periodontitis and 25 cases with aggressive periodontitis. Twenty-five healthy subjects without any evidence of periodontal disorder were also randomly selected as the control group. The clinical parameters including plaque index (PI), bleeding on probing (BOP), probing depth (PPD) and clinical attachment loss (CAL) were recorded and GCF samples were collected for analysis of GCF contents of IL-6 and IL-1β levels. The Kettle stress questionnaire was also used to determine stress severity.Results:IL-1β was significantly higher, but IL-6 was only slightly higher(marginal p-value=0.058)The median score of stress was higher in aggressive periodontitis than the chronic disorder and also in the two periodontal disease groups than the healthy subjects. Among studied clinical parameters, CAL and PPD were positively correlated with the GCF IL-1β level. No significant correlations were found between clinical parameters and GCF IL-6 level. There were strong positive relationships between stress severity and in both aggressive and chronic periodontitis; however stress did not influence GCF contents of IL-6.Conclusion:Psychological stress has a pivotal role in the stimulation of inflammatory processes via IL-1β increase in aggressive and chronic periodontitis.

Developmental endothelial locus-1 (Del-1), lymphocyte function-associated antigen-1 (LFA-1), and interleukin 17 (IL-17) play critical roles in transendothelial migration of neutrophils in periodontal diseases. The aim of this study was to evaluate salivary Del-1, IL-17, and LFA-1 protein levels in patients with gingivitis (G), chronic periodontitis (CP), and generalized aggressive periodontitis (GAP). A total of 180 systemically healthy, non-smoking patients (45 periodontally healthy (H) and 45 G, 50 CP, and 40 GAP) individuals (between March 2014 and February 2016) were included in this study according to Armitage's (1999) classification. Clinical periodontal parameters, including clinical attachment level, probing depth, plaque index, and gingival index, were recorded. Del-1, IL-17, and LFA-1 protein expression levels were measured in unstimulated saliva samples collected from patients by using enzyme-linked immunosorbent assays. Kruskal-Wallis and Mann-Whitney U tests were used for multiple comparisons and post hoc statistical analyses, respectively. ROC curve analysis was used to evaluate the sensitivity and specificity of Del-1, IL-17, and LFA-1 in distinguishing periodontal disease from health and gingivitis. It was found a high level of IL-17 and a low level of Del-1 in the CP and GAP, as compared to the G and H groups (P<.001). Nevertheless, we found LFA-1 levels were higher in the GAP than in the CP or G groups (P=.00). Consistently, LFA-1 levels were lower in the H and G groups than in the CP and GAP groups (P=.00). The combination of three biomarkers was found as the best predictor yielded exhibited the highest AUC [0.893, 0.845-0.94 (%95 CI) P<.001] in discriminating periodontal disease from health and gingivitis. Salivary Del-1, LFA-1, and IL-17 levels might be useful markers for determining the clinical health and disease status of patients with periodontitis. However, further studies that evaluate the level of salivary Del-1, LFA-1, and IL-17 before and after periodontal therapy are required to understand the exact roles of these cytokines during the periodontal healing period.

Periodontal disease (PD) is one of the most prevalent oral inflammatory diseases in dogs. PD onset begins with the formation of a polymicrobial biofilm (dental plaque) on the surface of the teeth, followed by a local host inflammatory response. To manage this disease, several procedures focusing on the prevention and control of dental plaque establishment, as well as on the prevention of local and systemic PD-related consequences, are essential. The removal of dental plaque and the inhibition of its formation can be achieved by a combination of dental hygiene homecare procedures including tooth brushing, the application of different oral products and the use of specific diet and chew toys, and regular professional periodontal procedures. Additionally, in some cases, periodontal surgery may be required to reduce PD progression. Associated with these measures, host modulation therapy, antimicrobial therapy, and other innovative therapeutic options may be useful in PD management. Moreover, PD high prevalence and its relation with potential local and systemic consequences reinforce the need for investment in the development of new preventive measures, treatments, and oral procedures to improve the control of this disease in dogs. Knowledge on the specific guidelines and diversity of the available products and procedures are fundamental to apply the most adequate treatment to each dog with PD.

Periodontitis is an inflammatory condition of supporting tissues of teeth, for which several risk and susceptibility factors are proposed. Periodontal disease results when balance between host factors and etiologic agents is disrupted. Bacteria have a primary role in the initiation of periodontal disease, and a range of host related factors influence the clinical presentation and rate of progression of disease. Genetic variations that modify immunological reactions identify the disease susceptibility in various individuals. Many studies have proved the effect of various single or composite nucleotide polymorphisms to susceptibility, progression or severity of periodontal diseases. Despite these studies, association between periodontal disease and candidate genes is still not clear. The reports of familial nature of chronic periodontitis are less frequent as compared to aggressive periodontitis. The striking familial aggregation of trait in aggressive periodontitis is consistent with significant genetic etiology. In this paper, an attempt has been made to summarize recent views on various genes involved in the pathogenesis and progression of aggressive periodontal disease. Data were identified by searches of the Medline, and Pubmed. Articles published in English were selected, and most up-to-date or relevant references were chosen.

The control of bacterial dental plaque through daily oral hygiene is essential to prevent oral diseases such as caries or periodontal disease, especially in at-risk populations, including the elderly with mild cognitive impairment and dementia. The aim of this study was to determine the association between different levels of cognitive impairment and dementia in an elderly population and their capacity to maintain adequate oral hygiene. A case-control study (elderly with versus without mild cognitive impairment or dementia) was performed in Granada, Spain. Outcome variables were tooth/prosthesis-brushing frequency/day, bacterial plaque index, and gingival bleeding index. Statistical models were adjusted by age, sex, educational level, and tobacco and alcohol habits. The study included 240 cases and 324 controls. The final model, adjusted by age, sex, educational level, and tobacco and alcohol consumption, showed a significant association between degree of cognitive impairment and daily oral hygiene, accumulation of bacterial plaque, and gingival bleeding. In summary, deficient daily oral hygiene, evidenced by greater bacterial dental plaque accumulation and gingival inflammation, is independently associated with cognitive impairment, even at its earliest stage.

Periodontal diseases, including chronic gingivitis, chronic periodontitis, and aggressive periodontitis, are driven by complex immune responses, with mast cells (MCs) playing a pivotal role through the release of mediators during degranulation. Although MC involvement in chronic periodontal conditions has been documented, its role in aggressive periodontitis and the relationship between MC degranulation and inflammation intensity remain poorly understood. This study aimed to quantify MCs and assess their degranulation in gingival tissues across healthy gingiva, chronic gingivitis, chronic periodontitis, and aggressive periodontitis using histochemical staining to elucidate their role in periodontal inflammation and disease progression. This cross-sectional study included 120 systemically healthy subjects recruited from the Periodontology Outpatient Department. The groups included healthy periodontium (n = 30), chronic gingivitis (n = 30), chronic periodontitis (n = 30), and aggressive periodontitis (n = 30) groups. Gingival biopsies were obtained, fixed, sectioned, and stained with toluidine blue to identify intact and degranulated MCs in juxta-epithelial (Z1) and deep connective tissue (Z2) zones. MC counts were performed under 40x magnification, with examiner calibration to ensure reliability (intraclass correlation(ICC) ≥ 0.85). Nonparametric tests (Kruskal-Wallis with Dunn's test) were used to analyze MC density and degranulation, with a significance level of p < 0.05. MC counts were highest in chronic periodontitis (7.10 ± 2.50 in Z1, 6.70 ± 2.10 in Z2) and aggressive periodontitis (6.10 ± 1.70 in Z1, 6.50 ± 2.00 in Z2), followed by chronic gingivitis and healthy gingiva (p < 0.00001). Degranulated MCs were significantly elevated in diseased groups, particularly chronic periodontitis (4.69 ± 2.09 in Z1, 4.51 ± 1.89 in Z2) compared to healthy controls (p = 0.0001). Intact MCs showed less variation, with significant differences between the healthy and aggressive periodontitis groups (p = 0.045). Increased MC degranulation was associated with periodontal disease severity, particularly in chronic and aggressive periodontitis, suggesting a key role of MC degranulation in inflammatory progression. These findings highlight the potential of MCs as therapeutic targets in periodontal management.

To investigate the long-term effects of non-surgical treatment on clinical and hematologic states of patients with generalized aggressive periodontitis (GAgP). Patients with GAgP (n = 25) and healthy controls (n = 28) were recruited. The clinical parameters, including probing depth (PD), bleeding index (BI), attachment loss (AL) were examined and recorded. Blood cell variables, including white blood cells (WBC), leukocyte, neutrophil, and lymphocyte counts, as well as serum triglycerides, fasting glucose and protein parameters, including total protein, albumin, globulin, and albumin/globulin ratio (A/G), were analyzed. Twenty-five GAgP patients received non-surgical treatment and the clinical and blood parameters 3 to 7 years after treatment were re-evaluated. Clinical and hematological parameters of the two groups were compared. Comparisons of clinical and hematologic parameters pre- and post-treatment in GAgP group were performed through one-way ANOVA and paired-t test. Elevated white blood cells, neutrophil numbers and serum total protein, globulin levels were observed in patients with GAgP compared to controls[(6.3 ± 2.0)×10(9)cell/L vs.(5.4 ± 1.0)×10(9)cell/L, (4.1 ± 1.8)×10(9) cell/L vs.(3.0 ± 0.9)×10(9) cell/L, (78.2 ± 4.4) g/L vs. (75.6 ± 4.6) g/L and (29.3 ± 3.8) g/L vs.(26.5 ± 3.9) g/L respectively, P < 0.05]. A/G ratio was lower in the GAgP group than in the control group (1.7 ± 0.2 vs.1.9 ± 0.3, P < 0.01). Three to seven years after periodontal treatment, the reduction of PD and BI was observed in GAgP group(P < 0.05). There were significant decreases of WBC count, neutrophil count, serum total protein and globulin level, and significant increases of albumin level and A/G at 3 to 7 years after treatment(P < 0.05). Non-surgical treatment may have long-term beneficial effect on the periodontal clinical status and hematologic parameters of generalized aggressive periodontitis.