Alveolar Attachment Research Articles

Comparison and analysis of alveolar bone structure characteristics in skeletal Class II and Class III malocclusion in the mandibular incisor region.

The aim of this study was to explore the differences in alveolar bone structure characteristics in skeletal class II and class III malocclusion in the mandibular incisor region. From January 2021 to November 2023, 100 cases of skeletal malocclusion patients were selected from our hospital, including 56 cases of skeletal Class II malocclusion and 44 cases of skeletal Class III malocclusion. The alveolar bone structure characteristics in the mandibular incisor region of skeletal class II and class III malocclusion patients are compared. The labial alveolar bone attachment height and lingual alveolar bone attachment height were compared between patients with skeletal Class II and Class III malocclusion (P < .05). The labial alveolar bone thickness at the root apex in patients with skeletal Class II malocclusion was (3.96 ± 0.63) mm, which was higher than that in Class III malocclusion patients (P < .05). In patients with skeletal Class II malocclusion, the cementoenamel junction was 2, 4, 6 mm below, and at the root apex, the alveolar bone thickness was (0.19 ± 0.05) mm, (0.93 ± 0.10) mm, (2.10 ± 0.10) mm, and (12.26 ± 2.10) mm, respectively, which was higher than that in Class III malocclusion patients (P < .05). In patients with skeletal Class II malocclusion, the labial side alveolar bone area at the root apex was (3.89 ± 0.72) mm2, which was higher than in Class III malocclusion patients (P < .05). On the lingual side, the alveolar bone thickness below cementoenamel junction at 6 mm and at the root apex was (1.95 ± 0.45) mm2 and (1.92 ± 0.51) mm2, respectively, which were higher than in Class III malocclusion patients (P < .05). Compared to skeletal Class II malocclusion, in skeletal Class III malocclusion, the alveolar bone thickness in the mandibular incisor area is thinner and narrower. This should be given special attention during orthodontic treatment.

Active targeting microemulsion-based thermosensitive hydrogel against periodontitis by reconstructing Th17/Treg homeostasis via regulating ROS-macrophages polarization cascade

Periodontitis is a multifactorial inflammatory disease characterized by severe alveolar bone damage and attachment loss. The imbalance of T help 17 (Th17) / regulatory T cells (Treg) induces excessive interleukin (IL)-17, which leads to alveolar bone damage and aggravates the development of periodontitis. Therefore, we proposed a therapeutic strategy to restore Th17/Treg homeostasis by interfering reactive oxygen species (ROS)-macrophage polarization cascade using active targeting microemulsions-based thermosensitive hydrogel. Folic acid-modified quercetin-loaded microemulsions (FA-Qu-MEs) were dispersed in poloxamer 407 and poly(N-isopropylacrylamide) matrix of hydrogel (FA-Qu-MEs@Gel). FA-Qu-MEs@Gel could be locally injected into the periodontal pocket and sustainedly release drugs. FA-Qu-MEs exhibited excellent ROS scavenging potency by targeting macrophages, resulting M1 phenotype macrophage from to M2 phenotype macrophage. Subsequently, the phenotypic changes of macrophages lead to decreased expression of IL-6 and tumor necrosis factor-α, which inhibited activated Th17, while IL-10 secreted by M2 macrophages promoted Treg differentiation. Finally, the restored Th17/Treg homeostasis reduced the level of IL-17 to accelerate alveolar bone regeneration. This study deigns a novel system that promote alveolar bone regeneration by remodeling Th17/Treg homeostasis via regulating ROS-macrophages polarization cascade for periodontitis treatment.

Effects of Coriander on the Repair Process of Experimentally-induced Periodontitis in Rats.

The aim of this study was to evaluate the effects of Coriandrum sativum L. (CSL) seed extract on gingival levels of antioxidant enzymes, pro-inflammatory cytokines and on alveolar bone and attachment levels after experimental periodontitis induction in rats and compare it with low-dose doxycycline (LDD). Forty adult male Wistar Albino rats were divided randomly into 5 groups as follows: 1 = periodontally healthy (control); 2 = periodontitis; 3 = periodontitis + CSL (32 mg/kg); 4 = periodontitis + CSL (200 mg/kg); and 5 = periodontitis + LDD (6 mg/kg). Gingival superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) levels were evaluated by enzyme-linked immunosorbent assay. The presence of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1βeta (IL-1β) immunoreactivity was detected immunohistochemically. Alveolar bone area in the furcation space (ABA), alveolar bone loss (ABL), and attachment loss (AL) were evaluated histomorphometrically. The SOD level was lower in group 5 than in groups 2, 3, and 4. The IL-1β level was highest in group 4. The TNF-α level was statistically higher in groups 2 and 4 than in groups 1, 3, and 5. The IL-6 level was highest in group 4. Its level was higher in groups 2 and 3 than in group 5. ABA was less in groups 2, 3, and 4 compared to groups 1 and 5. ABL was less in group 5 than in groups 2, 3, and 4. AL was greater in group 4 than in group 5. The use of 200 mg/kg CSL showed a pro-inflammatory effect and IL-1β and TNF-α levels decreased after 32 mg/kg CSL application in the treatment of periodontitis.

Assessment of Periodontal Health Status and Serum Level of Vascular Endothelial Growth Factor in Women with Breast Cancer

Periodontal diseases are inflammatory diseases that affect the periodontium which lead to alveolar bone and attachment loss. Breast cancer is the most common cancer in women worldwide. Expression of (VEG F) is elevated in both diseases and it is the marker of angiogenesis related to cancer development. 1. To determine the periodontal health status and the serum levels of (VEGF) in women with breast cancer in comparison to women without breast cancer. 2. To correlate between serum levels of VEGF with clinical periodontal parameters (PLI, GI, BOP, PPD, and CAL) in women with breast cancer in comparison to women without breast cancer. Eighty women with age ranged from (30-60) years old, 40 women with breast cancer and another 40 women without. Periodontal health status were taken for all participants and then they were subdivided into four groups: the (BC +CP) group which included participants with breast cancer and chronic periodontitis (n=20), the (BC+ G) group included participants with breast cancer and gingivitis (n=20), the (CP) group which included participants with chronic periodontitis only (n=20) and the (G) group which included participants with gingivitis only (n=20). Other than breast cancer, all subjects were systemically healthy females. Periodontal health status was determined by clinical periodontal examination of (PLI, GI, BOP, PPD and CAL). Blood samples were collected from each participant, serum levels of VEGF were determined by enzyme -linked immune-sorbent assay (ELISA). The results of this study showed that the median values of PLI and GI were slightly increased in BC+G group in comparison to other groups with non-significant differences, the percentages of BOP showed highly significant differences among the groups (P &lt;0.01). The median values of PPD showed slight increase in BC+CP group than CP group with non-significant differences. Median values of CAL were increased in CP group than BC+CP group with non-significant differences. VEGF serum levels were elevated in BC+CP group than other groups with non-significant differences. Also by using Spearman’s rank Correlation Coefficient, serum levels of VEGF were correlated positively with all clinical periodontal parameters. VEGF serum level could be associated with progression of both periodontal diseases and breast cancer.

The comparison of Mental Index based on dental status in women using panoramic radiographs

Background: Bones will experience a decrease in density due to an imbalance in the process of resorption and remodeling. Women are known to be at greater risk of bone density loss than men, due to aging and hormonal effects. Decreased bone density can also affect alveolar bone and attachment to teeth, leading to tooth loss and edentulous. Panoramic radiographs are one of the regular examinations at dental clinics. They observe changes in the thickness of the cortical bone of the mandible and detect abnormalities in bone density by measuring them using the Mental Index (MI).&#x0D; Objectives: This research is aimed to determine the differences in Mental Index (MI) between dentate and edentulous regions in women through panoramic radiographs. &#x0D; Materials and Methods: This research is using comparative analytic observational study with a cross-sectional approach, with 160 women panoramic radiograph samples available at the Dentistry Radiology Installation, RSGM-P, Trisakti University FKG, divided between 80 samples of the dentate region and 80 samples of the edentulous region. Calculations using MI with i-Dixel software version 2.2.0.3. (Morita, Japan) results in millimeters. &#x0D; Results: There is a significant difference of MI between dentate and edentulous region (p = 0.000). The mean of dentate MI (right region 3.7443 ± 0.47927 mm and left region 3.7373 ± 0.41075 mm) was greater than edentulous MI (right region 2.4725 ± 0.48391 mm and left region 2.4421 ± 0.43962 mm). &#x0D; Conclusion: The loss of teeth in women may lead to any change in the Mental Index (MI) &#x0D; Keywords: Bone Density; Dental Status; Mental Index; Panoramic Radiograph

Calotropis procera latex protein reduces inflammation and bone loss in ligature-induced period ontitis in male rats

ObjectiveCalotropis procera latex protein (CpLP) is a popular anti-inflammatory and therefore we aimed to study its effects on inflammatory bone loss. DesignMale Wistar rats were subjected to a ligature of molars. Groups of rats received intraperitoneally CpLP (0.3 mg/kg, 1 mg/kg, or 3 mg/kg) or saline (0.9% NaCl) one hour before ligature and then daily up to 11 days, compared to naïve. Gingiva was evaluated by myeloperoxidase activity and interleukin-1 beta (IL-1β) expression by ELISA. Bone resorption was evaluated in the region between the cement-enamel junction and the alveolar bone crest. The histology considered alveolar bone resorption and cementum integrity, leukocyte infiltration, and attachment level, followed by immunohistochemistry bone markers between 1st and 2nd molars. Systemically, the weight of the body and organs, and a leukogram were performed. ResultsThe periodontitis significantly increased myeloperoxidase activity and the IL-1β level. The increased bone resorption was histologically corroborated by periodontal destruction, leukocyte influx, and attachment loss, as well as the increasing receptor activator of the nuclear factor-kappa B ligand (RANKL)/osteoprotegerin (OPG) ratio, and Tartrate-resistant acid phosphatase (TRAP)+ cells when compared to naïve. CpLP significantly reduced myeloperoxidase activity, level of IL-1β, alveolar bone resorption, periodontal destruction, leukocyte influx, and attachment loss. The CpLp also reduced the RANKL/OPG ratio and TRAP+ cells, when compared with the saline group, and did not affect the systemic parameters. ConclusionsCpLP exhibited a periodontal protective effect by reducing inflammation and restricting osteoclastic alveolar bone resorption in this rat model.

Aggravating Effects of Psychological Stress on Ligature-Induced Periodontitis via the Involvement of Local Oxidative Damage and NF-κB Activation.

Periodontitis is the leading cause of tooth loss in adults, and psychological factors play an important role in the development of periodontitis. To elucidate the adverse effects of psychological stress on the inflammatory process and redox status of periodontitis tissue, fifty male Sprague-Dawley rats were divided into the control, experimental periodontitis, psychological stress, experimental periodontitis plus psychological stress, and experimental periodontitis plus psychological stress plus fluoxetine groups. Chronic unpredictable mild stress (CUMS) was used to establish psychological stress, and silk ligature was used to induce experimental periodontitis. Four weeks later, stressed rats showed altered behaviour, serum hormone levels, and sucrose preference. More obvious alveolar bone loss and attachment loss and higher protein expressions of inflammatory cytokines were observed in the experimental periodontitis plus psychological stress group. The combination of CUMS and periodontitis had synergistic effects on increasing hypoxia-inducible factor-1α (HIF-1α) protein expression and reactive oxygen species (ROS) and malondialdehyde (MDA) contents and decreasing antioxidant enzyme activities compared with those in the stress or periodontitis groups. Moreover, psychological stress further increased p-IκBα and p-NF-κB p65 protein levels and decreased IκBα protein levels in periodontitis rats. Fluoxetine administration alleviated the adverse effects of psychological stress on the progression of periodontitis in rats. These results hint us that psychological stress could aggravate inflammation in periodontitis tissues, which may be partly due to local worsening of oxidative damage and further activation of the nuclear factor kappa-B (NF-κB) signalling pathway.

The Potential Roles of Dec1 and Dec2 in Periodontal Inflammation.

Periodontal inflammation is a common inflammatory disease associated with chronic inflammation that can ultimately lead to alveolar attachment loss and bone destruction. Understanding autophagy and pyroptosis has suggested their significant roles in inflammation. In recent years, studies of differentiated embryo-chondrocyte expressed genes 1 and 2 (Dec1 and Dec2) have shown that they play important functions in autophagy and in pyroptosis, which contribute to the onset of periodontal inflammation. In this review, we summarize recent studies on the roles of clock genes, including Dec1 and Dec2, that are related to periodontal inflammation and other diseases.

Suppression of alveolar bone resorption by salubrinal in a mouse model of periodontal disease

AimsThe relationship between stress to endoplasmic reticulum (ER) and periodontitis has been known, and ER stress induced by Porphyromonas gingivalis results in the loss of alveolar bone. Salubrinal is a small synthetic compound and attenuates ER stress through inhibition of de-phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2α). In this study, we examined whether salubrinal attenuates periodontitis in a mouse model of experimental periodontal disease. Materials and methodsWe evaluated loss of alveolar bone and attachment levels in periodontium using micro-computed tomography (μCT) and hematoxylin-eosin (HE) staining, respectively. Furthermore, we measured osteoclast numbers using tartrate-resistant acid phosphatase (TRAP) staining and osteoblast numbers using HE staining for bone resorption and for bone formation, respectively. To examine the inhibitory effects of salubrinal against pro-inflammatory cytokines, we measured TNF-α and IL1-β score in periodontium using immunohistostaining. Key findingsThe results revealed that salubrinal suppressed loss of alveolar bone and attachment levels in periodontium induced by periodontitis. It decreased osteoclast numbers and increased osteoblasts. It also suppressed the expression levels of TNF-α in periodontium. SignificanceThese results show that salubrinal alleviates periodontitis through suppression of alveolar bone resorption and the pro-inflammatory cytokine, and promotion of the bone formation. Since salubrinal has been shown to have these beneficial effects for periodontal disease, it may provide a novel therapeutic possibility for the disease.

Guanabenz inhibits alveolar bone resorption in a rat model of periodontitis

Increase of sympathetic activity has been known to exacerbate osteoporosis through promotion of bone resorption. However, it is largely unknown about involvement of sympathetic activity in exacerbation of periodontitis. In this study, we investigated whether α2-adrenergic receptor (α2-AR) agonist guanabenz which decreases sympathetic activity, attenuates alveolar bone resorption in rats having high sympathetic activity with periodontitis. Volumes of residual alveolar bone and attachment levels in periodontium were examined using micro-computed tomography and hematoxylin-eosin staining, respectively. Furthermore, osteoclast numbers per bone surface and osteoclast surface per bone surface were measured using tartrate-resistant acid phosphatase staining. To examine the suppressive effects of guanabenz on pro-inflammatory cytokines, expression levels of tyrosine hydroxylase (TH), TNF-α, IL1-β, and IL-6 in periodontium were measured using immunohistostaining. Administration of guanabenz attenuated loss of alveolar bone and attachment levels in rats having high sympathetic activity. Furthermore, its administration suppressed osteoclast numbers in rats having high sympathetic activity. TH, TNF-α, IL-1β, and IL-6 positive cells in periodontium in rats treated with guanabenz for 12 weeks, were lower than those in control rats having high sympathetic activity. This study demonstrated administration of α2-AR agonist guanabenz attenuates alveolar bone resorption through decrease of sympathetic activity in rats.

Effects of a β2-adrenergic receptor blocker on experimental periodontitis in spontaneously hypertensive rats

AimsRecent studies have reported a relationship between periodontal disease and hypertension, and previous evidence suggests that the sympathetic nervous system plays an important role in the control of bone metabolism. This study sought to evaluate the effect of the beta-2 adrenergic receptor (β2-AR) blocker butoxamine on experimental periodontitis in a rat model. Materials and methodsWistar-Kyoto and spontaneously hypertensive rats (n = 6 per group) were orally administered butoxamine 1 mg/kg/day and experimental periodontitis was induced by applying an orthodontic ligature wire. The rats were sacrificed after 4 weeks and the residual alveolar bone was measured using micro-computed tomography (micro-CT) imaging analysis software for histological analysis. Key findingsMicro-CT imaging analysis showed a higher ratio of residual alveolar bone, BV/TV, and Tb.N in both Wistar-Kyoto and spontaneously hypertensive rats treated with butoxamine compared with the corresponding control rats. In histological analysis, compared with the Wistar-Kyoto and spontaneously hypertensive rat control groups, the corresponding butoxamine-treated groups showed a lower ratio of attachment level, lower values of osteoclast number and surface. Significanceβ2-AR blockers maintained the alveolar bone mass and attachment level by suppressing osteoclast activity. Thus, β2-AR blockers may be effective in preventing periodontitis.

Specific inhibition of IL-6 receptor attenuates inflammatory bone loss in experimental periodontitis.

Periodontal pathogenesis takes into consideration that disease results from a complex inflammatory immune response. Among the major cytokines related to periodontal damage, interleukin (IL)-6 enhances a cascade of tissue destruction. Tocilizumab (TCZ) is a humanized monoclonal anti-human IL-6 receptor that inhibits IL-6-mediated proinflammatory activity. This study aimed to elucidate whether TCZ inhibits the deleterious effect of ligature-induced periodontitis. Experimental ligature-induced periodontitis was treated with systemic administration of TCZ intraperitoneally in three different concentration dosages (2mg/kg, 4mg/kg, and 8mg/kg. Euthanasia occurred at 7 and 14 days after the initiation of the study. Local changes in the alveolar bone were measured by bone volume, the ratio of bone volume, and trabecular thickness using microcomputed tomography. Attachment loss and inflammatory infiltrate were evaluated by histology. Immune response was analyzed focusing on the Th17 pattern. TCZ inhibited alveolar bone resorption and attachment loss in 7 and 14 days for all dosage groups in comparison to controls (P < 0.05). Besides, TCZ induced lower expression of inflammatory infiltrate (P<0.05) and less production of Th17-related cytokines (P<0.05) and RANKL (P<0.05). The inhibition of IL-6-mediated proinflammatory activity by IL-6R blocking reduced alveolar bone resorption and attachment loss supported by the modulation of the Th17 periodontal response. Considering the inflammatory status, modulatory therapy may be a promising approach to periodontal disease.

The effect of ellagic acid on the repair process of periodontal defects related to experimental periodontitis in rats.

Objective This study aims to evaluate the effect of ellagic acid (EA) by measuring the levels of alveolar bone resorption and inflammatory and oxidative stress markers in the periodontal tissues and serum on the periodontal repair process related to experimental periodontitis in rats.Methodology Forty Wistar rats were divided into four study groups as follows: Group 1=healthy control (n=10); Group 2=EA control (15 mg/kg)(n=10); Group 3=periodontitis (n=10); Group 4=periodontitis+EA (15 mg/kg) (n=10). The periodontitis model was established by ligating bilateral mandibular first molars for 14 days. Then, rats were given normal saline or EA for another 14 days by gavage administration. Serum and gingiva myeloperoxidase (MPO) activity, 8-hydroxydeoxyguanosine(8-OHdG), and glutathione (GSH) levels were analyzed by ELISA. İmmunohistochemical analysis was used to detect Interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) immunoreactivities in the periodontal tissues. Alveolar bone loss (ABL) and attachment loss (AL) was evaluated by histomorphometry analysis.Results ABL and AL were statistically higher in group 3 than in groups 1, 2 and 4 and in group 4 than in groups 1 and 2 (p<0.05). MPO activities in gingival tissue and serum were significantly increased in group 3 compared to groups 1 and 2 (p<0.05). Significantly higher serum GSH levels, lower gingiva, and serum 8-OHdG levels, and MPO activity were observed in group 4 compared to group 3 (p<0.05). Rats with periodontitis (group 3) expressed significantly higher immunoreactivities of IL-6 and TNF-α and lower IL-10 immunoreactivity compared to those other groups (p<0.05). IL-6 and TNF-α immunoreactivities significantly decreased and IL-10 immunoreactivity increased in group 4 after the use of EA compared to group 3 (p<0.001).Conclusions Our findings showed that EA provides significant improvements on gingival oxidative stress and inflammatory markers and alveolar bone resorption in the repair process associated with experimental periodontitis. Therefore, EA may have a therapeutic potential on periodontitis.

Extracorporeal Shock Waves Increase Markers of Cellular Proliferation in Bronchial Epithelium and in Primary Bronchial Fibroblasts of COPD Patients.

Chronic obstructive pulmonary disease (COPD) is due to structural changes and narrowing of small airways and parenchymal destruction (loss of the alveolar attachment as a result of pulmonary emphysema), which all lead to airflow limitation. Extracorporeal shock waves (ESW) increase cell proliferation and differentiation of connective tissue fibroblasts. To date no studies are available on ESW treatment of human bronchial fibroblasts and epithelial cells from COPD and control subjects. We obtained primary bronchial fibroblasts from bronchial biopsies of 3 patients with mild/moderate COPD and 3 control smokers with normal lung function. 16HBE cells were also studied. Cells were treated with a piezoelectric shock wave generator at low energy (0.3 mJ/mm2, 500 pulses). After treatment, viability was evaluated and cells were recultured and followed up for 4, 24, 48, and 72 h. Cell growth (WST-1 test) was assessed, and proliferation markers were analyzed by qRT-PCR in cell lysates and by ELISA tests in cell supernatants and cell lysates. After ESW treatment, we observed a significant increase of cell proliferation in all cell types. C-Kit (CD117) mRNA was significantly increased in 16HBE cells at 4 h. Protein levels were significantly increased for c-Kit (CD117) at 4 h in 16HBE (p < 0.0001) and at 24 h in COPD-fibroblasts (p = 0.037); for PCNA at 4 h in 16HBE (p = 0.046); for Thy1 (CD90) at 24 and 72 h in CS-fibroblasts (p = 0.031 and p = 0.041); for TGFβ1 at 72 h in CS-fibroblasts (p = 0.038); for procollagen-1 at 4 h in COPD-fibroblasts (p = 0.020); and for NF-κB-p65 at 4 and 24 h in 16HBE (p = 0.015 and p = 0.0002). In the peripheral lung tissue of a representative COPD patient, alveolar type II epithelial cells (TTF‐1+) coexpressing c-Kit (CD117) and PCNA were occasionally observed. These data show an increase of cell proliferation induced by a low dosage of extracorporeal shock waves in 16HBE cells and primary bronchial fibroblasts of COPD and control smoking subjects.

Nonsurgical and surgical management of biologic complications around dental implants: peri-implant mucositis and peri-implantitis.

Biologic complications around dental implants may be categorized into peri-implant mucositis and peri-implantitis. Peri-implant mucositis is defined as reversible inflammation in the peri-implant mucosa without any apparent bone destruction. Peri-implantitis refers to inflammatory process that resulted in destruction of alveolar bone and attachment. Potential etiologic and contributing factors to both diseases are discussed in this review. By targeting and eliminating the etiologic factors nonsurgically as well as surgically, dental implants presenting with peri-implant diseases may be rescued, and then maintained with proper long-term peri-implant supportive therapy. Furthermore, clinical cases and their management are presented to demonstrate the available treatment options. Implant therapy should be carefully planned and executed with consideration of potential etiologic and contributing factors to developing biologic complications. During the initial consideration, patients should be informed of the potential biologic complications in dental implant therapy. Clinicians should monitor implants for any development or recurrence of peri-implant disease to ensure timely therapeutic intervention.

Immune modulatory and antioxidant effects of locally administrated vitamin C in experimental periodontitis in rats

Background: Vitamin C is an important water-soluble vitamin with antioxidant and immune-modulatory actions. The aim of this study was to investigate the effects of locally applied vitamin C on alveolar bone resorption in rats with experimental periodontitis.Methods: Twenty-one male Sprague-Dawley rats divided into three groups with seven animals in each group: (1) control, (2) experimental periodontitis and 3) experimental periodontitis-local vitamin C treatment group. After ligature was removed, 50 μL vitamin C was locally administered into the subperiosteum of the buccal gingiva of periodontitis vitamin C (PvitC) group rats for three times in intervals of 2 days. At the end of the study, the animals were scarified, and serum and gingival samples were collected for analysis of serum IL-1β, oxidative stress index (OSI), CTX and malondialdehyde (MDA) levels and gingival MMP-8 immunostaining. Alveolar bone loss and attachment loss were determined based on measurements on histological sections obtained from rat mandibles.Results: Serum MDA and OSI levels which are related to the oxidative stress were significantly lower in the PvitC group as compared with those in the P group (p < .05). Serum CTX levels which are related to the bone resorption were significantly lower in the PvitC group as compared with those in the P group (p < .05). The numeric density of MMP-8-positive cells was significantly lower in the PvitC group compared to P group (p < .05). Alveolar bone loss and attachment loss were significantly lower in the PvitC group compared to P group (p < .05)Conclusions: The local vitamin C administration provided protection against inflammation-induced alveolar bone resorption by decreasing oxidative stress and inflammation-induced tissue breakdown vitamin C may be a therapeutic agent that can be used in periodontitis treatment.

Histopathological and biochemical evaluation of the effect of Paeoniflorin on the periodontium during and after periodontitis formation in rats

ObjectivesAppraise the effect of systemic Paeoniflorin (Pae) application on the periodontium during and after induction of experimental periodontitis in the presence of ligature and after its removal. DesignSeventy male Wistar rats were separated into seven equal groups. The first group was reserved as healthy control group (Group 1: no periodontitis, no medication) and experimental periodontitis was induced with ligature in the remaining rats. In experimental periodontitis groups, Pae or saline was administered systemically in three differet periods; during the experimental periodontitis induction (period 1), after experimental periodontitis induction which ligature removed (period 2) or ligature kept in position (period 3). Only, one of the groups acted as the control periodontitis group and received no treatment. Experimental periodontitis groups were as follows; Group 2: medication in period 1, Group 3: periodontitis and no medication, Group 4: medication in period 2, Group 5: saline application in period 2, Group 6: medication in period 3, Group 7: saline application in period 3. Matrix metalloproteinases-9 (MMP-9) levels and interleukin-10 (IL-10) levels were detected biochemically and histomorphometric analyses were performed. These analyses included measurements of the area of alveolar bone, the level of alveolar bone, and attachment loss. ResultsArea of alveolar bone and IL-10 levels were higher in the Pae-administered groups; level of alveolar bone, attachment loss, and MMP-9 levels were correspondingly lower (P < 0.05). The beneficial effects at histomorphometrical and biochemical levels of Pae were the strongest in the rats that were administered Pae after the removal of ligature. ConclusionsSystemically administered Pae had a positive effect on the healing of periodontal tissues. Pae can be used as a new therapeutic agent for periodontal diseases, but microbiology-based studies and more extensive biochemistry-based experimental and clinical studies are needed to address this possibility.

Genetic susceptibility of common polymorphisms in NIN and SIGLEC5 to chronic periodontitis

Chronic periodontitis (CP) is a common oral disease characterized by the slow progression of alveolar attachment loss and bone destruction. Genetic components have been reported to play an important role in the onset and development of CP. In the present study, we aimed to replicate the association signals of NIN and SIGLEC5 identified in previous genome-wide association studies (GWASs) of samples from Chinese Han individuals. Association signals between clinical severity indicators of CP and relevant single nucleotide polymorphisms (SNPs) were also examined. A total of 3,160 study subjects, including 1,076 CP patients and 2,084 healthy controls, were recruited. A total of 32 SNPs, including 22 from NIN and 10 from SIGLEC5, were selected for genotyping. SNPs rs12883458 (OR = 1.45, P = 1.22 × 10−5, NIN) and rs4284742 (OR = 0.75, P = 1.69 × 10−5, SIGLEC5) were significantly associated with CP disease status. rs4284742 was significantly associated with all 3 clinical severity indicators, including bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (CAL). According to evidence from bioinformatics analyses, both significant SNPs, rs12883458 and rs4284742, are likely surrogates of underlying variants with true effects. In summary, our findings provide direct evidence for the association of NIN and SIGLEC5 with CP susceptibility.

Effects of &amp;lt;i&amp;gt;Streptococcus salivarius&amp;lt;/i&amp;gt; K12 on Experimental Periodontitis and Oral Microbiota in Mice

Background: Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth, and may lead to severe periodontal destruction and even tooth loss. Streptococcus salivarius K12 (S. salivarius K12), one of oral probiotics, has been reported to be able to inhibit various potentially deleterious bacteria. This study was the first time to investigate the effects of S. salivarius K12 on ligature-induced periodontitis in mice. Methods: A silk ligature was tied around the second left maxillary molar to establish the model of periodontitis, and then, mice in group S. salivarius K12 were administered with S. salivarius K12 (2 x 109 CFU) twice daily for 30 d, the others were treated with isopyknic water. Results: Administration with S. salivarius K12 markedly decreased the anaerobic bacteria accumulation on the teeth, and it also considerably alleviated periodontitis-induced alveolar bone resorption and attachment loss. Moreover, S. salivarius K12 administration increased the relative species abundance of Gram-positive bacterium in oral cavity while decreased Gram-negative bacterium, as well as the diversity of the bacterial community. Conclusion: Oral administration of the probiotic S. salivarius K12 may mitigate the alveolar bone resorption and attachment loss of periodontitis by modulating the oral microbiota.

Histopathological and biochemical evaluation of paeoniflorin administration in an experimental periodontitis model.

The purpose of this study was to evaluate the effects of administered Paeoniflorin (Pae) on periodontal tissues within an experimental periodontitis model. Forty male Wistar rats were used in this study and experimental periodontitis was created in all rats except in the control group (n = 10, first group). In the periodontitis group, experimental periodontitis was created but no other application was performed (n = 10, second group). In the other groups created experimental periodontitis, systemic Pae (n = 10, third group) or saline (n = 10, fourth group) was applied. A biochemical analysis of the gingival vascular endothelial growth factor (VEGF) levels and a histomorphometric analysis (measurements of the area of alveolar bone, alveolar bone resorption, and attachment loss) were performed. In the Pae group, the area of the alveolar bone was increased, while alveolar bone resorption and attachment loss decreased. Gingival VEGF levels increased in all groups that created experimental periodontitis and the greatest increase seen in the Pae group. Histomorphometric and biochemical analyses in this study suggest that Pae has a curative effect on periodontal tissues. However, additional studies are needed to confirm these results.