Gingival Inflammatory Response Research Articles

Application of Concentrated Growth Factors in Combination with Bio-Oss for Extraction of Mandibular Proximal Impacted Wisdom Teeth

In this study, we investigate the combined application of concentrated growth factor (CGF) and Bio-Oss (BO) for the treatment of periodontal bone defect (BD) after extraction of impacted wisdom teeth. Firstly, we assess the osteogenic properties of CGF in periodontal ligament stem cells (PDLSCs). The concentration-dependent effect of CGF on enhancing the activity of PDLSCs has been demonstrated. Furthermore, CGF effectively promotes differentiation and enhances the osteogenic function of PDLSCs, leading to improved expression of related osteogenic proteins. Subsequently, a total of 64 patients with loss of alveolar bone in the second molar, who received treatment at our hospital between July 2020 and July 2023, are included. They are randomly divided into a BO group (treated with BO) and a CGF/BO group (treated with CGF+BO). We observe that the combined application of CGF and BO demonstrated superior efficacy in alleviating pain, reducing swelling, and preventing dry socket incidence. In addition, it exhibited enhanced effectiveness in restoring periodontal tissue, including reducing probing depth, gingival depth, and clinical attachment loss. It also displayed better inhibition of gingival inflammatory response and gingival bleeding. Furthermore, it could enhance the restoration of periodontal BD, such as increasing the width of the alveolar bone and root depth, reducing the vertical distance from the apex of the alveolar ridge, as well as improving dental function. Therefore, the combined application of CGF and BO holds great potential in periodontal BD therapy for promoting the regeneration of periodontal bone, thus restoring dental function.

Gingival Health and Periodontal Diseases during Puberty in Females Students in Maal High School in Omdurman, Sudan (2021 – 2022)

Background: Periodontal health and diseases are influenced by sex hormones, puberty, menses, pregnancy and menopause. Gingival diseases modified by systemic factors that contribute to gingivitis such as the endocrine changes associated with puberty, the menstrual cycle, pregnancy and diabetes that may exacerbate the gingival inflammatory response to plaque. Aim: To assess the effect of puberty on gingival health and periodontal diseases. Material and Methods: descriptive cross sectional study, among 85 students, in Maal high school in Omdurman, Sudan .Data collected via self administer questionnaire completed for each students. Collected data was entered into the SPSS software (version 26). Data was analyzed and results presented as proportions in table and figures Results: The results of this study showed that 95% of females students had a menstrual cycle, 60% had a good oral hygiene and 52.50% brush their teeth twice a day, majority of students86.25% brushed their teeth, gum and tongue, 62.50% used a medium tooth brush, and 50% of females students had an oral feeling during menstrual cycle, however about 50% of females did not observe any symptoms in oral cavity. Conclusion: This study indicated that hormonal changes occurring during the menstrual cycle influence the periodontium and induce inflammatory symptoms and signs.

TUMOR NECROSIS FACTOR-ALPHA A POTENTIAL THERAPEUTIC TARGET FOR PERIODONTITIS AND DIABETES MELLITUS

Introduction: Diabetes mellitus (DM) is a systemic disease that affects many human populations in the world. One of DM’s oral complications is periodontitis. The pro-inflammatory cytokine that plays a major role in the relationship between these two diseases is TNF-α. Review: Diabetes mellitus is a systemic disease characterized by high blood glucose levels (hyperglycemia) due to inadequate insulin secretion, insulin resistance or both. Metabolic disorders caused by hyperglycemia can cause endothelial dysfunction in blood vessels. Endothelial dysfunction that occurs due to hyperglycemia can trigger an inflammatory response that can increase the progression of periodontitis. Periodontitis is a chronic inflammatory response in periodontal tissue to pathological microorganisms in dental biofilm. The periodontitis process begins with gingival inflammatory response. The initial phase of gingival inflammation is characterized by redness and bleeding on probing. Worsening inflammation will cause loss of periodontal tissue attachment and alveolar bone resorption which can lead to tooth loss. The inflammatory process that occurs in periodontitis involves pro-inflammatory cytokines that can influence insulin resistance, such as Tumor necrosis factor-alpha (TNF-α). Tumor necrosis factor-alpha is also a cytokine that plays a major role in the pathogenesis of diabetes mellitus, so that periodontitis and diabetes mellitus are interrelated diseases Conclusion: The TNF-α cytokine is a potential therapy target for periodontitis and diabetes mellitus.

Obesity Is Associated with a Weakened Gingival Inflammatory Cytokine Response.

Background and Objectives: An obesity-related elevated body mass index (BMI) across life is associated with chronic low-grade inflammation and increased levels of C-reactive protein (CRP) in blood. CRP is a marker and promoter of inflammation. The objectives of this study were to examine the effect of obesity on the relationship between peripheral and gingival CRP levels and to examine the effects of gingival CRP levels on gingival fluid inflammatory cytokines in periodontitis-resistant obese individuals. Materials and Methods: Thirty-nine participants in good periodontal health were recruited. Twenty patients were classified as lean and nineteen as obese based on their BMI levels. A thorough periodontal assessment was carried out. Gingival crevicular fluid (GCF) and blood samples were collected. Both GCF and blood samples were analyzed for interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-17A (IL-17A), and CRP. Results: GCF CRP levels were significantly higher in the obese than in the lean individuals. No statistically significant differences were noted between the two groups in either GCF or blood in terms of any of the inflammatory cytokine levels. IL-17A was not detected in the GCF of most subjects in both groups. GCF CRP levels were positively associated with blood CRP levels, and the association tended to be stronger in the obese individuals. GCF CRP showed no associations with GCF IL-10 in both groups. Although GCF CRP levels were positively associated with multiple GCF inflammatory cytokines (e.g., IL-1β, IL-6, IL-8, and TNF-α) in all subjects, the associations tended to be weaker in the obese individuals (e.g., IL-1β, IL-6, and TNF-α). Furthermore, the levels of the GCF inflammatory cytokines IL-6 and TNF-α were decreased in the obese individuals. Conclusions: Obesity unfavorably influences the relationship between blood and GCF CRP levels and promotes increased CRP levels in GCF. Collectively, the findings suggest a weakened inflammatory cytokine response in the gingival tissues of obese individuals.

MiRNAs from Inflamed Gingiva Link Gene Signaling to Increased MET Expression

Several array-based microRNA (miRNA) expression studies independently showed increased expression of miRNAs hsa-miR-130a-3p, -142-3p, -144-3p, -144-5p, -223-3p, -17-5p, and -30e-5p in gingiva affected by periodontal inflammation. We aimed to determine direct target genes and signaling pathways regulated by these miRNAs to identify processes relevant to gingival inflammatory responses and tissue homeostasis. We transfected miRNA mimics (mirVana) for each of the 7 miRNAs separately into human primary gingival fibroblasts cultured from 3 different donors. Following RNA sequencing, differential gene expression and second-generation gene set enrichment analyses were performed. miRNA inhibition and upregulation was validated at the transcript and protein levels using quantitative reverse transcriptase polymerase chain reaction, Western blotting, and reporter gene assays. All 7 miRNAs significantly increased expression of the gene MET proto-oncogene, receptor tyrosine kinase (MET). Expression of known periodontitis risk genes CPEB1, ABCA1, and ATP6V1C1 was significantly repressed by hsa-miR-130a-3p, -144-3p, and -144-5p, respectively. The genes WASL, ENPP5, ARL6IP1, and IDH1 showed the most significant and strongest downregulation after hsa-miR-142-3p, -17-5p, -223-3p, and -30e-5p transfection, respectively. The most significantly regulated gene set of each miRNA related to cell cycle (hsa-miRNA-144-3p and -5p [Padj = 4 × 10−40 and Padj = 4 × 10−6], -miR-17-5p [Padj = 9.5 × 10−23], -miR-30e-5p [Padj = 8.2 × 10−18], -miR-130a-3p [Padj = 5 × 10−15]), integrin cell surface interaction (-miR-223-3p [Padj = 2.4 × 10−7]), and interferon signaling (-miR-142-3p [Padj = 5 × 10−11]). At the end of acute inflammation, gingival miRNAs bring together complex regulatory networks that lead to increased expression of the gene MET. This underscores the importance of mesenchymal cell migration and invasion during gingival tissue remodeling and proliferation in restoring periodontal tissue homeostasis after active inflammation. MET, a receptor of the mitogenic hepatocyte growth factor fibroblast secreted, is a core gene of this process.

Assessment of knowledge, awareness and practice of dental practitioners on the relationship between poly cystic ovarian syndrome (PCOS) in periodontally compromised women-A questionnaire based survey

Polycystic Ovary Syndrome (PCOS) is a common endocrinal disorder of uncertain etiology characterized by hyperandrogenism, anovulatory infertility, menstrual dysfunction, hirsutism, alopecia and acne. Periodontitis is a common chronic infection characterized by an exaggerated gingival inflammatory response against pathogenic bacterial microflora, resulting in alveolar bone and eventually tooth loss. The relationship of PCOS in periodontally compromised women are very distinctly studied.A cross-sectional survey study design was conducted with closed it's close ended questions. The question were self-prepared, validated and made reliable. Data collection done and analyzed using the SPSS software. Descriptive and inferential statistical analyses were determined.95 percent of the participants were aware of a condition called PCOS. A total of 71 percent of participants have expressed that they carry out routine screening in their clinical practice. However, only a total of 57% of the total participants were able to diagnose PCOS in their clinical practice. A total of 64% of the participants have expressed that intrigue knowledge on the oral manifestations of PCOS have helped diagnose PCOS in their patients. 63 percent of the total participants were aware of the medical specialty of choice to consult for patients diagnosed with PCOS of which only 28 percent of the total participants were aware of the clinical grading of PCOS.This survey helps conclude that even though knowledge of PCOS, clinical manifestations and oral manifestations of PCOS are aware for majority, only 10% achieve to diagnose it in daily practice. This study hopes to shed light on the relationship between Poly Cystic Ovarian Syndrome (PCOS) in periodontally compromised women to better enhance the diagnosis, treatment planning and the systemic corelation of the oral manifestations of the condition.

Anti-bacterial Efficacy of Probiotics used in Provisional Polymethyl Methacrylate Crowns against Porphyromonos gingivalis – an In vitro Study

Aim: To evaluate the effect of Probiotic used in PMMA Temporary restorations on gingival inflammatory response by its action on the marginal gingival epithelial cells.
 Materials and Methods: This is an in vitro Interventional pilot study using discs of PMMA ( Group A ) and PMMA incorporated with Probiotics (Group B . The effect of probiotics incorporated PMMA on strains of Porphyromonos gingivalis grown on culture plates will be assessed using zone of inhibition test and minimum inhibitory concentration was assessed . Data was recorded, tabulated and statistically evaluated using SPSS software.
 Results: The zone of Inhibition in the Group B was (Mean = 16.30mm) is comparatively higher than that of Group A with mean value 12.92mm. Results states that among the various concentration of Probiotic Lozenges (2.5, 5, 10, 15 and 20 µg/ml) used to determine the antibacterial activity , Highest mean zone of inhibition was observed with 20 µg/ml with 16 mm, followed by 15 µg/ml with 14mm , 10 µg/ml with 9mm, 5 µg/ml with 11 mm & with the lowest inhibition observed in 2.5 µg/ml with 8mm. There is significant correlation between concentration of probiotics and its antibacterial efficacy. The increase in concentration of probiotics in the PMMA discs is directly proportional to its antibacterial efficacy against P. gingivalis.
 Conclusion: Thus the study proved a significant correlation between Probiotic used in PMMA Temporary crowns and reduction in gingival Inflammation at the margins of the restoration which will be beneficial when used in crowns used in patients undergoing Orthodontic treatment or Immediate Implant Loading with acrylic crowns.

Salivary levels of MPO, MMP-8 and TIMP-1 are associated with gingival inflammation response patterns during experimental gingivitis

AimThis study aimed to investigate the association between salivary levels of myeloperoxidase (MPO), neutrophil elastase (NE), soluble urokinase-type plasminogen activator receptor (suPAR), matrix metalloproteinase (MMP)-8 and tissue inhibitor of matrix metalloproteinases (TIMP)-1 and gingival inflammation development during an experimental gingivitis study. MethodsA three-week experimental gingivitis study was conducted. Clinical recordings of dental plaque biofilm (Modified Quigley Hein Plaque Index, TQHPI) and gingival inflammation (Modified Gingival Index, MGI) were made at specific time points for each of the 42 participants. Salivary levels of MPO, NE, suPAR, MMP-8 and TIMP-1 at the same time points were measured using distinct immunoassays. For data analysis growth curve modelling was employed to account for the time-varying outcome (MGI score) and the time-varying covariates (salivary marker levels, and TQHPI score). Analyses were stratified according to the MGI-score trajectory groups previously identified as ‘fast’, respectively ‘slow’ responders. ResultsOverall, higher MGI scores were statistically significantly positively associated with higher levels of MPO, MMP-8 and TIMP-1. Stratified analysis according to inflammation development trajectory group revealed higher levels of salivary MPO, MMP-8 and MMP-8/TIMP-1 ratio among the ‘fast’ responders than among ‘slow’ responders. None of the investigated salivary protein markers was associated with a ‘slow’ inflammation development response. ConclusionsSalivary levels of MPO, MMP-8 and TIMP-1 were associated with the extent and severity of gingival inflammation. While the ‘fast’ gingival inflammation response was associated with increased levels of MPO, MMP-8 and MMP-8/TIMP-1 ratio, the ‘slow’ response was not associated with any of the salivary protein markers investigated in this study. Neutrophil activity seems to orchestrate a ‘fast’ gingival inflammatory response among participants previously primed to gingival inflammation.

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.

Antibacterial activity and effect on gingival cells of microwave-pulsed non-thermal atmospheric pressure plasma in artificial saliva

Although various oral pathogens are inactivated by non-thermal atmospheric pressure plasma (NTAPP), the in vivo effects of NTAPP are poorly understood. The first aim of this study was to examine the antibacterial activity of microwave-pulsed NTAPP against Staphylococcus aureus in artificial saliva to mimic oral environmental conditions. The second aim was to determine the influence of microwave-pulsed NTAPP on human gingival fibroblasts (HGFs). The microwave-pulsed NTAPP reduced bacterial viability (as measured by colony forming units [CFU]) to a greater extent in artificial saliva than in saline. Extending the post-treatment incubation time increased bacterial inactivation in artificial saliva compared to saline. HGFs viability was unaffected by microwave-pulsed NTAPP for bacterial inactivation. Rather, HGFs proliferation increased after a 5-min microwave-pulsed NTAPP. Less tumor necrosis factor alpha was released by microwave-pulsed NTAPP-treated HGFs stimulated with lipopolysaccharide (LPS) than by untreated, LPS-stimulated HGFs; thus, plasma appeared to suppress the inflammatory response. Our study suggests that microwave-pulsed NTAPP may have stronger in vivo antibacterial activity than in vitro activity, and that microwave-pulsed NTAPP may have the additional advantage of suppressing gingival inflammatory responses.

Immune system transcriptome in gingival tissues of young nonhuman primates.

Young/adolescent humans harbor many microorganisms associated with periodontal disease in adults and show substantial gingival inflammatory responses. However, younger individuals do not demonstrate the soft- and hard-tissue destruction that hallmark periodontitis. This study evaluated responses to the oral microbial ecology in gingival tissues from clinically healthy young Macaca mulatta (<3years of age) compared with older animals (5-23 years of age). RNA was isolated from the tissues and analyzed for the transcriptome using the Rhesus Macaque GeneChip (Affymetrix). Global transcriptional profiling of four age groups revealed a subset of 159 genes that were differentially expressed across at least one of the age comparisons. Correlation metrics generated a relevance network abstraction of these genes. Partitioning of the relevance network revealed seven distinct communities comprising functionally related genes associated with host inflammatory and immune responses. A group of genes was identified that were selectively increased/decreased or positively/negatively correlated with gingival profiles in the animals. A principal components analysis created metagenes of expression profiles for classifying the 23 animals. The results provide novel system-level insights into gene-expression differences in gingival tissues from healthy young animals, weighted toward host responses associated with anti-inflammatory biomolecules or those linked with T-cell regulation of responses. The combination of the regulated microenvironment may help to explain the apparent 'resistance' of younger individuals to developing periodontal disease.

Evaluation of Subgingival Dental Plaque Microbiota Changes In Fixed Orthodontic Patients with Syber Green Real Time PCR

Introduction: One of the most common problems we confront in orthodontic therapy is periodontal diseases. Initial factor which causes these diseases is colonization of anaerobic microorganisms in subgingival plaque. Technically, local environmental changes related to orthodontic band and brackets may influence the bacterial species in periodontal plaque. However, it seems necessary to assess variations in subgingival plaque caused by orthodontic appliances. The aim of this study was to investigate changes in subgingival microbiota and clinical parameters before and after bracket placement. Methods: Clinical parameters including probing depth (PD), plaque index (PI), clinical attachment level (CAL), bleeding on probing (BOP) and gingival index (GI) were recorded and subgingival microbial samples were collected in 30 people aged between 13 and 25. As a control group, 15 persons getting matched as to their age and sex with no need to orthodontic treatment were opted using specific primers, SYBER Green Real-Time PCR was carried out in order to determine bacterial flora in stored samples. All mentioned procedures were reassessed in experimental group and in control group three months after band and bracket bonding. A descriptive analysis was conducted, and paired t test and Wilcoxon test were used for differences between groups (P<0.05). Results: No changes in clinical attachment level were observed, but scores for bleeding on probing, plaque index, and gingival index increased 3 months after bracket placement in experimental group (P<0.05). Prevotella intermedia rose in experimental group after brackets placement compared with control group but Actinobacillus actinomycetem comitans and Tanerella forsythia proportions did increase. Conclusions: treatment with fixed appliances may transitionally raise the growth of periodontopathogenic bacteria and consequently result in gingival inflammatory response but without destructive effect on deep periodontal tissues.

Fracture toughness of zirconia ceramic crowns made by feather-edge tooth preparation design

Fracture toughness determines functional crown strenght and prevents damages on ceramics during mastication. There is a lack of relevant literature data about fracture toughness of crowns made by feather-edge preparation. Mechanical testing of ceramic samples is supposed to show if feather-edge tooth preparation is a successful method for making ceramic crowns without any risk of reduction of their mechanical properties. This research was done to establish effects of feather-edge tooth preparation on fracture toughness of single zirconia ceramic crowns. The research was performed as an experimental study. Sixty (60) ceramic crowns were made on non-carious extracted human premolars. Thirty (30) crowns were made on the basis of feather-edge preparation (experimental group I). The group II included 30 crowns made on 1 mm rounded shoulder. Crowns fabrication was executed on a copy mill production system "Zirkonzahn" (Zirkonzahn GMBH, Gais, Germany). The spherical compression test was used to determine fracture toughness, using 6 mmn diameter ceramic ball. Fracture load for damaging ceramic crown was recorded on a universal testing machine--Zwick, type 1464, with the speed of 0.05 mm/min. The results of this research introduced significant differences between fracture toughness of ceramic samples in every examined group. However, fracture toughness of crowns from both group was above 2000 N, what was double beyond a recommended value. The mean value of fracture toughness in the feather-edge group was 2090 N, and in shoulder group it was 2214 N. This research showed a high fracture toughness of zirconia crowns made on feather-edge preparation. The examined crowns showed a fracture resistance at a sufficient distance in relation to the minimum values of functional loads. Further research of functional loads of these crown is necessary, as well as research of marginal adaptation of cemented crowns and gingival inflammatory response.

Periodontal Disease for the Primary Care Physician

Genetic discoveries in arthritis and their associated biological pathways spanning the innate and adaptive immune system demonstrate the strong association between susceptibility to arthritis and control of exogenous organisms. The canonical theory of the aetiology of immune-mediated arthritis and other immune-mediated diseases is that the introduction of exogenous antigenic stimuli to a genetically susceptible host sets up the environment for an abnormal immune response manifesting as disease. A disruption in host-microbe homeostasis driven by disease-associated genetic variants could ultimately provide the source of exogenous antigen triggering disease development. We discuss genetic variants impacting the innate and adaptive arms of the immune system and their relationship to microbial control and arthritic disease. We go on to consider the evidence for a relationship between HLA-B27, infection and arthritis, and then emerging evidence for an interaction between microbiota and rheumatoid arthritis.

Periodontal disease in polycystic ovary syndrome

Polycystic ovary syndrome (PCOS) and periodontal disease (inflammatory diseases of the tissues around teeth) are common disorders associated with diabetes and cardiometabolic risk. Comprehensively examining the periodontal status in PCOS, this study suggests that the susceptibility for periodontal disease may significantly increase in patients with PCOS compared with healthy young women, and that local/periodontal oxidant status appears to be affected in PCOS.

Experimental gingivitis: reproducibility of plaque accumulation and gingival inflammation parameters in selected populations during a repeat trial

This study aimed to assess whether and to what extent the experimental gingivitis clinical parameters are reproducible within selected populations with different gingival inflammatory response (high or low) to plaque accumulation. In addition, the consistency in developing a high or low gingival inflammatory response within the selected populations was evaluated. Thirty-seven subjects previously identified as high (HR, n=20) or low responders (LR, n=17) during an experimental gingivitis trial (first trial) were enrolled in a "repeat" experimental gingivitis trial. No significant differences in plaque accumulation parameters and bleeding index values were detected between first and repeat trial for the 37 participants. Gingival index was higher during the repeat trial but behaved consistently in terms of the temporal changes in the course of both trials in both populations. Of the 17 LR participants, 10 manifested low susceptibility to inflammation after repeat trial. Among the 20 HR, 10 manifested high susceptibility to inflammation after repeat trial. These results indicate that our experimental gingivitis model is reproducible to some extent in selected populations. The high reproducibility of plaque and, to a lesser extent, of inflammation parameters under the employed controlled conditions could be a valuable tool in gingivitis research.

Effects of fixed orthodontic appliances on subgingival microflora

Fixed orthodontic appliances cause plaque accumulation around bands and brackets. Since the microbiological composition of dental plaque is closely connected to periodontal tissue health, the aim of this study was to determine the effects of fixed orthodontic appliances on subgingival microflora and periodontal status. This prospective study was carried out on 32 adolescents scheduled for fixed orthodontic treatment. Subgingival dental plaque samples and periodontal records (pocket probing depth and clinical attachment level) were obtained in four recording times: before bonding of fixed appliances (T0), 1 (T1), 3 (T2) and 6 (T3) months after the beginning of orthodontic therapy, in order to detect the changes in periodontopathic anaerobe microbial flora and its effects on periodontal status. The values of pocket probing depth, total number of microorganisms and number of patients with positive findings of Prevotella intermedia and other periodontopathic anaerobes increased from T0 to the maximum obtained in T2 recording time. Both clinical and microbiological values decreased 6 months after the beginning of orthodontic therapy. The therapy with fixed appliances may transitionally increase the growth of periodontopathogenic bacteria and consequently result in gingival inflammatory response but without destructive effect on deep periodontal tissues.

Dental biofilm, gingivitis and interleukin‐1 adjacent to approximal sites of a bonded ceramic

The aim of this study was to investigate in vivo the influence of aged, resin-bonded, ceramic restorations on approximal dental biofilm formation and gingival inflammatory response, associated with and without customary oral hygiene. In a cross-sectional and in a 10-day experimental gingivitis study, Quigley-Hein plaque index, gingival index (GI), crevicular fluid and its levels of interleukin (IL)-1alpha, -1beta and receptor antagonist were measured at appoximal surfaces of leucite-reinforced bonded ceramic coverages, resin composite restorations and enamel and compared intra-individually in 17 participants. No differences were found between the ceramic, composite and enamel regarding plaque index, GI, levels of IL-1alpha, -1beta and the receptor antagonist. Throughout, higher crevicular fluid amounts were observed at ceramic sites compared with the enamel (p<0.05). In the experimental gingivitis, plaque index, GI, crevicular fluid and its IL-1alpha levels increased significantly. The need for optimal oral hygiene and professional preventive oral health care does not seem to be reduced with regard to approximal surfaces of aged, resin-bonded, leucite-reinforced ceramic restorations in comparison with those of a hybrid, resin composite and enamel.

Modulation of clinical expression of plaque‐induced gingivitis: response in aggressive periodontitis subjects

The aim of this study was to characterize the gingival inflammatory response to de novo plaque accumulation in subjects treated for aggressive periodontitis (AP). The gingival inflammatory response of the AP subjects was retrospectively compared with that of periodontally healthy individuals (PH) matched for exposure to plaque and of periodontally healthy subjects previously identified as "high responders" (HR) and "low responders" (LR). 13 AP subjects and 26 matched PH subjects participated in a 21-day experimental gingivitis trial. Plaque index (PlI), Gingival index (GI), gingival crevicular fluid volume (GCF) and angulated bleeding score (AngBS) were recorded at days 0, 7, 14 and 21. Cumulative plaque exposure (CPE), i.e. PlI over time, was also calculated. GCF was significantly higher in AP compared with PH group at each observation interval (p< or =0.001). In addition, GCF was significantly higher in AP group compared with either LR or HR groups at each observation interval (p<0.001). These results suggest that susceptibility to gingival inflammation in response to de novo plaque accumulation may be related to susceptibility to periodontitis.

Modulation of clinical expression of plaque-induced gingivitis. I. Background review and rationale.

The purpose of this article is to provide the necessary background and rationale for the accompanying studies, which are ultimately aimed at identifying genetic and environmental factors determining gingivitis susceptibility. The literature on factors reported to modify the clinical expression of gingivitis, i.e., factors that determine individual variability in gingival inflammatory response to plaque, is presented. Clinical evidence suggests that the gingival inflammatory response to plaque accumulation may differ substantially among individuals. However, most of the available studies are of small scale and not purposely designed to address the issue. Systemic factors implicated in modulation of the clinical expression of gingivitis include metabolic, genetic, environmental and other factors. The significance of such factors in designing and conducting a large-scale experimental gingivitis trial and means to account for them are discussed. Although several factors have been implicated, genetic or environmental factors underlying differences in gingivitis expression are not fully elucidated. The accompanying studies aim to identify and characterize, among participants in a specifically designed large-scale experimental gingivitis trial, subjects that differ significantly in their gingival inflammatory response to plaque. This is the first step in an effort to determine genetic or environmental factors underlying such differences.