Alveolar Bone Loss, Plaque Index, and Gingival Index among Non-Diabetics Treated with Class II Amalgam Restorations for Different Service Lives

In this study, hydroxyapatite coated vs uncoated implants were used to evaluate the type and dimensions of bone defects after progressive peri-implantitis in dogs. Thirty-two dental implants with 4 different surfaces—machined (M), sandblasted acid-etched (SA), 1-μm thin sputter hydroxyapatite (HA)-coated (S), and plasma-sprayed HA-coated (P)—were inserted into the mandibles of 4 beagle dogs after extracting all mandibular premolars. Experimental peri-implantitis was induced after 3 months using ligature to allow for plaque accumulation. After 4 months, ligatures were removed and plaque accumulation continued for 5 months (progression period). The open flap surgery demonstrated 3 patterns of peri-implantitis bone defect: (1) Class I defect: represented as circumferential intra-alveolar bone loss; (2) Class II defect: circumferential intra-alveolar defect with supra-alveolar bone loss exposing the implant surface; and (3) Class III defect: represented as circumferential intra-alveolar defect with supra-alveolar bone loss and buccal dehiscence. Class I was the most frequent (62.5%) defect pattern around implant types M, SA, and S; while implant type-P showed a recurring majority of Class II (62.5%). Comparison among the 4 implant groups revealed a significant defect width (DW) in implant type-P relative to other types (P < 0.01). However, no statistically significant differences were noted for defect depth (DD) (P > 0.05). We concluded that the shape and size of peri-implantitis bone defects were influenced by the type and thickness of the HA coat together with the quantity of the available peri-implant bone. Plasma-sprayed HA-coated implants showed larger peri-implant defects than did thin sputter HA-coated implants.

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Inter-Relationship Between Rheumatoid Arthritis and Periodontitis

Kathmandu University Medical Journal ◽

10.3126/kumj.v11i1.11018 ◽

2014 ◽

Vol 11 (1) ◽

pp. 22-26 ◽

Cited By ~ 4

Author(s):

J Rajkarnikar ◽

BS Thomas ◽

SK Rao

Keyword(s):

Rheumatoid Arthritis ◽

Bone Loss ◽

Inflammatory Response ◽

Sedimentation Rate ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Gingival Index ◽

C Reactive Protein ◽

Reactive Protein ◽

Erythrocyte Sedimentation

Background Periodontal medicine defines a rapidly emerging branch of Periodontology focusing on establishing a strong relationship between periodontal health and systemic health. It is speculated that the major common dysregulation which links Periodontitis with Rheumatoid arthritis (RA) is being played by the mediators of immune inflammatory response. Objectives To determine whether there is any relationship between periodontal disease and Rheumatoid arthritis. Methods A total of 100 patients were included for the present study which was divided into two groups: one group (cases) included 50 patients attending the Department of Orthopedics, Kasturba Medical College, Manipal who were diagnosed of Rheumatoid arthritis. Another subject population included 50 patients as controls attending the Department of Oral Medicine, Manipal College of Dental Sciences, Manipal with age and gender matched with those of rheumatoid arthritis group. Specific measures for periodontitis included plaque index, gingival index, number of missing teeth, and radiographic alveolar bone loss scores. Measures of rheumatoid arthritis included health assessment questionaires, levels of C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Various periodontal parameters were compared between the cases and controls. Results The average alveolar bone loss was statistically more severe in Rheumatoid arthritis (RA) group than in the controls although there were similar plaque index in both the groups. The gingival index was statistically higher in the RA group. The Erythrocyte Sedimentation Rate (ESR) and C- Reactive Protein (CRP) levels of RA patients were also significantly associated with the severity of periodontal disease. Conclusion There was a significant association between Rheumatoid arthritis and Periodontitis which may be due to a common underlying deregulation of the inflammatory response in these individuals. DOI: http://dx.doi.org/10.3126/kumj.v11i1.11018 Kathmandu University Medical Journal Vol.11(1) 2013: 22-26

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Alveolar bone loss around mandibular anterior teeth in Class I, II, and III malocclusions: a CBCT evaluation study

10.21203/rs.3.rs-34913/v1 ◽

2020 ◽

Author(s):

Zixiao Wang ◽

Zhigui Ma ◽

Chi Yang

Keyword(s):

Bone Loss ◽

Alveolar Bone ◽

Class Ii ◽

Alveolar Bone Loss ◽

Class I ◽

Class Ii Malocclusion ◽

Class Iii ◽

Bone Thickness ◽

Anterior Teeth ◽

Significant Difference

Abstract Background: To quantitatively and qualitatively evaluate alveolar defects of mandibular anterior alveolar bone in three different types of malocclusion with cone-beam computed tomography (CBCT).Methods: A total of 542 teeth from 30 skeletal class I malocclusion (mean age: 19.26±5.63), 33 class II malocclusion (mean age: 19.36±4.17), and 28 class III malocclusion (mean age: 21.47±4.53) patients were evaluated with CBCT. Sagittal sectional views were evaluated with regard to labial and lingual alveolar bone thickness and vertical alveolar bone level. Analysis of variance and Tukey’s test were used for statistical comparisons at P<.05 Results: Qualitative analysis: Class II (64.47%) and Class III malocclusions (58.43%) had higher prevalence of dehiscence than Class I malocclusions (32.96%),P<0.05. No significant difference was found in the prevalence of fenestration among the three groups. Quantitative analysis: In general, Class II and III groups had lesser alveolar bone volume than the Class I group. Furthermore, the vertical alveolar height and coronal alveolar bone thickness in Class II malocclusion was significantly lesser than that in the Class III group. Conclusions: The Class II group, followed by the class III group, showed the most severe alveolar bone deficiency For these patients undergoing orthodontic treatment, special care should be taken to avoid aggravated preexisting alveolar bone loss in the mandibular anterior teeth.

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EFFECTS OF ALENDRONATE THERAPY ON CYCLOSPORINE INDUCED ALVEOLAR BONE LOSS : A MORPHO-METRIC AND BIO-CHEMICAL STUDY IN RATS

International Journal of Advanced Research ◽

10.21474/ijar01/193 ◽

2016 ◽

Vol 4 (4) ◽

pp. 947-955

Author(s):

Sneha R Bhat ◽

◽

Aravind R Kudva ◽

Dhoom S Mehta ◽

◽

...

Keyword(s):

Bone Loss ◽

Alveolar Bone ◽

Chemical Study ◽

Alveolar Bone Loss

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3,4,5-Trihydroxybenzoic acid attenuates ligature-induced periodontal disease in Wistar rats.

Anti-Inflammatory & Anti-Allergy Agents in Medicinal Chemistry ◽

10.2174/1871523019666200206094335 ◽

2020 ◽

Vol 19 ◽

Author(s):

Ozkan Karatas ◽

Fikret Gevrek

Keyword(s):

Bone Loss ◽

Gallic Acid ◽

Wistar Rats ◽

Alveolar Bone ◽

Alveolar Bone Loss ◽

Collagenase Activity ◽

Osteoblastic Activity ◽

Cell Counts ◽

Experimental Periodontitis ◽

Anti Inflammatory

Background: 3,4,5-Trihydroxybenzoic acid, which is also known as gallic acid, is an anti-inflammatory agent who could provide beneficial effects in preventing periodontal inflammation. The present study aimed to evaluate the anti-inflammatory effects of gallic acid on experimental periodontitis in Wistar rats. Alveolar bone loss, osteoclastic activity, osteoblastic activity, and collagenase activity were also determined. Methods: 32 Wistar rats were used in the present study. Study groups were created as following: Healthy control (C,n=8) group; periodontitis (P,n=8) group; periodontitis and 30 mg/kg gallic acid administered group (G30,n=8); periodontitis and 60 mg/kg gallic acid administered group (G60,n=8). Experimental periodontitis was created by placing 4-0 silk sutures around the mandibular right first molar tooth. Morphological changes in alveolar bone were determined by stereomicroscopic evaluation. Mandibles were undergone histological evaluation. Matrix metalloproteinase (MMP)-8, tissue inhibitor of MMPs (TIMP)-1, bone morphogenetic protein (BMP)-2 expressions, tartrate-resistant acid phosphatase (TRAP) positive osteoclast cells, osteoblast, and inflammatory cell counts were determined. Results: Highest alveolar bone loss was observed in the periodontitis group. Both doses of gallic acid decreased alveolar bone loss compared to the P group. TRAP-positive osteoclast cell counts were higher in the P group, and gallic acid successfully lowered these counts. Osteoblast cells also increased in gallic acid administered groups. Inflammation in the P group was also higher than those of C, G30, and G60 groups supporting the role of gallic acid in preventing inflammation. 30 and 60 mg/kg doses of gallic acid decreased MMP-8 levels and increased TIMP-1 levels. BMP levels increased in gallic acid administered groups, similar to several osteoblasts. Conclusion: Present results revealed an anti-inflammatory effect of gallic acid, which was indicated by decreased alveolar bone loss and collagenase activity and increased osteoblastic activity.

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Gram-positive bacteria cell wall-derived lipoteichoic acid induces inflammatory alveolar bone loss through prostaglandin E production in osteoblasts

Scientific Reports ◽

10.1038/s41598-021-92744-5 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Tsukasa Tominari ◽

Ayumi Sanada ◽

Ryota Ichimaru ◽

Chiho Matsumoto ◽

Michiko Hirata ◽

...

Keyword(s):

Cell Wall ◽

Bone Loss ◽

Alveolar Bone ◽

Osteoclast Differentiation ◽

Lipoteichoic Acid ◽

Alveolar Bone Loss ◽

Gram Negative Bacteria ◽

Gram Positive ◽

Gram Negative ◽

Gram Positive Bacteria

AbstractPeriodontitis is an inflammatory disease associated with severe alveolar bone loss and is dominantly induced by lipopolysaccharide from Gram-negative bacteria; however, the role of Gram-positive bacteria in periodontal bone resorption remains unclear. In this study, we examined the effects of lipoteichoic acid (LTA), a major cell-wall factor of Gram-positive bacteria, on the progression of inflammatory alveolar bone loss in a model of periodontitis. In coculture of mouse primary osteoblasts and bone marrow cells, LTA induced osteoclast differentiation in a dose-dependent manner. LTA enhanced the production of PGE2 accompanying the upregulation of the mRNA expression of mPGES-1, COX-2 and RANKL in osteoblasts. The addition of indomethacin effectively blocked the LTA-induced osteoclast differentiation by suppressing the production of PGE2. Using ex vivo organ cultures of mouse alveolar bone, we found that LTA induced alveolar bone resorption and that this was suppressed by indomethacin. In an experimental model of periodontitis, LTA was locally injected into the mouse lower gingiva, and we clearly detected alveolar bone destruction using 3D-μCT. We herein demonstrate a new concept indicating that Gram-positive bacteria in addition to Gram-negative bacteria are associated with the progression of periodontal bone loss.

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