scholarly journals Periodontal disease in smokers

2005 ◽  
Vol 52 (2) ◽  
pp. 103-110 ◽  
Author(s):  
Olivera Cerovic ◽  
Vera Bundalo
Keyword(s):  
Periodontal Disease ◽  
Defense Mechanisms ◽  
Alveolar Bone ◽  
Negative Impact ◽  
Periodontal Therapy ◽  
Human Organism ◽  
Toxic Substances ◽  
Periodontal Tissues ◽  
Therapy Success ◽  
Antiseptic Solutions

Tobacco contains about 4000 different toxic substances from which almost 40 are proven to be cancerogenic. Nicotine, toxic alkaloid, is the most active substance in tobacco causing major number of harmful consequences for human organism as a whole, and for periodontal tissues as well. The aim of the paper was to show harmful effects of smoking on periodontal disease development, and to point out the problems caused by smoking during and after the periodontal treatment. Periodontal disease occurs in smokers more frequently as opposed to non-smokers. Typically, smokers have lower level of gingival inflammation, more excessive and accelerated loss of alveolar bone and epithelial insertion, deeper periodontal pockets and numerous gingival recessions. Along with that, smokers are carrying a decreased immune response that is expressed through various defense mechanisms. Smoking has negative impact on the outcome of conservative and surgical periodontal therapy. Effects of smoking on periodontal therapy success rate are requiring administration of antiseptic solutions and antibiotics throughout the treatment course. Every periodontologist must influence patients to stop smoking and thus act preventively on occurrence and progress of periodontal disease.

scholarly journals Management of Chronic Gingivitis with localized periodontitis by Nonsurgical (Phase I) Periodontal Therapy- A Case Report

2018 ◽  
Vol 7 (2) ◽  
pp. 33-37
Author(s):  
Md Huzzatul Islam Khan ◽  
Sultana Akter Eka ◽  
Md Ashif Iqbal
Keyword(s):  
Phase I ◽  
Oral Hygiene ◽  
Alveolar Bone ◽  
Bone Destruction ◽  
Chronic Inflammatory Disease ◽  
Periodontal Therapy ◽  
Periodontal Treatment ◽  
Periodontal Tissues ◽  
Hygiene Measures ◽  
Tissue Flap

Periodontitis is a chronic inflammatory disease of the periodontal tissues (periodontium) which surround and support the teeth, that results in attachment loss and alveolar bone destruction leads to ultimate tooth loss. It is caused by the bacteria present in dental plaque, which is a tenacious substance that forms on teeth and gingiva just after teeth are brushed. Periodontal treatment is aimed at controlling the infection in order to stop the progression of the disease and to be able to maintain a healthy periodontium. Mechanical debridement of supragingival and subgingival biofilms, together with adequate oral hygiene measures is the standard periodontal therapy. This mechanical subgingi- val biofilm debridement consists of an initial (nonsurgical /phase I) phase involving scaling and root planing (SRP) and the elimination of plaque retentive factors, followed by a surgical phase (if needed) including the elevation of a tissue flap and bone remodeling in further stages. The adjunct use of antibiotics has proven to additionally improve the outcome of periodontal treatment. A clinical case of a 40-years-old male patient with generalized severe chronic periodontitis with localized gingival swell- ing was treated with nonsurgical (phase I) periodontal therapy that was confined to oral hygiene instruction (OHI), SRP with an adjunct antimicrobial regimen.Update Dent. Coll. j: 2017; 7 (2): 33-37

scholarly journals THE EFFECTS OF NICOTINE ON THE PERIODONTAL TISSUE

2010 ◽  
Vol 1 (3) ◽  
pp. 151
Author(s):  
Herawati Herawati ◽  
Jenny Sunariani
Keyword(s):  
Significant Role ◽  
Host Response ◽  
Detrimental Effect ◽  
Periodontal Therapy ◽  
The Other ◽  
Toxic Substances ◽  
Periodontal Tissue ◽  
Chemical Substances ◽  
Periodontal Tissues ◽  
Periodontal Destruction

Tobacco contains thousands of chemical substances which known to be harmful to periodontal tissues. Nicotine was considered as the most toxic substances to periodontal tissues. The datas in this review indicate that smoking may have a significant role in the initiation and progression of periodontal destruction. The conclusion of this and the other studies indicate that smokers have a less favorable response to periodontal therapy than non smoker. Nicotine is potentially toxic substances that have a detrimental effect on periodontal tissue, by altering the host response or directly damage the cells of normal periodontium.

scholarly journals Role of Calprotectin as a Biomarker in Periodontal Disease

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Lili Wei ◽  
Mingwen Liu ◽  
Haofei Xiong
Keyword(s):  
Periodontal Disease ◽  
Calcium Binding ◽  
Alveolar Bone ◽  
Inflammatory Diseases ◽  
Periodontal Tissues ◽  
Adaptive Immune ◽  
S 100 ◽  
And Function ◽  
Plaque Biofilm

Periodontal disease (PD) is a common infectious and inflammatory disease characterised by inflammation of tissues surrounding and supporting the teeth and destruction of the associated alveolar bone, eventually resulting in tooth loss. This disease is caused by periodontopathic bacteria in plaque biofilm and resultant innate and adaptive immune responses in periodontal tissues. Calprotectin (CLP) is a calcium-binding protein of the S-100 protein family and is found to be induced by activated granulocytes, monocytes, and epithelial cells. CLP has been shown to play an important role in numerous inflammatory diseases and disorders. Increasing evidence indicates that CLP is involved in the progression of PD, and its levels may be associated with disease severity and outcome of periodontal treatments. This review will summarise recent studies regarding the presence, regulation, and function of CLP in PD. The findings indicate that CLP may be an effective biomarker for diagnosis and treatment for the PD.

scholarly journals Bone metabolism and RANKL/RANK/OPG trail in periodontal disease

2016 ◽  
Vol 29 (4) ◽  
pp. 171-175
Author(s):  
Lukasz Czupkallo ◽  
Mansur Rahnama ◽  
Dominik Kielbowicz ◽  
Michal Lobacz ◽  
Maryla Kozicka-Czupkallo
Keyword(s):  
Bone Resorption ◽  
Periodontal Disease ◽  
Defense Mechanisms ◽  
Gingival Crevicular Fluid ◽  
Nf Kappa B ◽  
Periodontal Tissues ◽  
Non Invasive ◽  
Receptor Activator ◽  
Crevicular Fluid ◽  
Necrosis Factor

Abstract Periodontal disease is an inflammatory disease of multifactorial etiology. In order for it to appear there must come to an imbalance between the effects of pathogens and host defense mechanisms. As a result of its course the destruction of structures supporting the teeth appears (periodontium, cement, bone), and consequently leads to teeth loosening and loss. In recent years, the participation of RANKL/RANK/OPG in bone remodeling process was highligted. At the molecular level the bone resorption is regulated through the interaction of the ligand receptor activator of nuclear NF-kappa B (RANKL) and osteoprotegerin (OPG), which is a system of two proteins belonging to the protein tumor necrosis factor (TNF). Recent findings about the RANKL protein and OPG have shed new light on the previously unexplained phenomenon of the basis of bone resorption. Research has shown that both protein OPG and RANKL can be detected in gingival crevicular fluid, which has become a window of opportunity in the analysis of non-invasive markers of periodontal tissues, confirming elevated levels of RANKL protein in periodontal disease, and decreased levels of OPG protein. Bone resorption is initiated by the binding of the RANKL protein to receptors RANK present on the surface of mature osteoclasts, and their precursors, which leads to the differentiation and activation of osteoclasts. OPG, being RANKL’s inhibitor, has, in turn, opposite characteristics to RANKL, resulting in the reduction of osteoclastogenesis process. Despite all this, the exact mechanism of bone resorption has not yet been elucidated.

scholarly journals Treatment of periodontal disease with guided tissue regeneration technique using a hydroxyapatite and polycaprolactone membrane

2016 ◽  
Vol 68 (6) ◽  
pp. 1413-1421 ◽  
Author(s):  
L.M.A. Martins ◽  
F.L. Valente ◽  
E.C.C. Reis ◽  
R.V. Sepúlveda ◽  
A.P.L. Perdigão ◽  
...  
Keyword(s):  
Periodontal Disease ◽  
Tissue Regeneration ◽  
Alveolar Bone ◽  
Experimental Period ◽  
Treated Group ◽  
Purulent Discharge ◽  
Control Group ◽  
Clinical Attachment Level ◽  
Periodontal Tissues ◽  
Attachment Level

ABSTRACT The aim of this study was to evaluate the use of a malleable membrane composed of hydroxyapatite (60%) and polycaprolactone (40%) as treatment of periodontal disease experimentally induced in dogs. A bone defect of standardized dimensions was created between the roots of the third and fourth premolar of 12 dogs for periodontal disease induction. Six dogs had the defect covered by the membrane and six dogs received only standard treatment for periodontal disease, also applied to dogs in the treated group. The animals were clinically monitored during the experiment. Radiographs were taken after surgery and at 60 days after treatment initiation. Clinical attachment level was also assessed in those moments. On the 60th day, dental sample of all animals, containing tooth, defect and periodontal tissues, were harvested, fixed in formalin and analyzed by microtomography and histology. During the experimental period, the animals showed no pain and purulent discharge, however, there was dehiscence in 50% of animals and membrane exposure in five out of six animals in the treated group. Clinical attachment level showed no difference between groups. Radiographs showed radiopacity equal to the alveolar bone in both groups. The microtomography revealed that the control group had higher bone volume in the defect compared to the treated group; however, the furcation was not filled by new alveolar bone in any animal. Histological analysis revealed that junctional epithelium invasion was lighter in the control group. New bone was only observed in the apical edge of the defect in both groups. Although the composite is biocompatible and able to keep the space of the defect, it did not promote periodontal tissue regeneration within 60 days of observation.

scholarly journals Inflammatory Response Mechanisms of the Dentine–Pulp Complex and the Periapical Tissues

2021 ◽  
Vol 22 (3) ◽  
pp. 1480
Author(s):  
Kerstin M. Galler ◽  
Manuel Weber ◽  
Yüksel Korkmaz ◽  
Matthias Widbiller ◽  
Markus Feuerer
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Oral Cavity ◽  
Root Canal ◽  
Dental Pulp ◽  
Defense Mechanisms ◽  
Alveolar Bone ◽  
Cell Types ◽  
Root Tip ◽  
Periodontal Tissues

The macroscopic and microscopic anatomy of the oral cavity is complex and unique in the human body. Soft-tissue structures are in close interaction with mineralized bone, but also dentine, cementum and enamel of our teeth. These are exposed to intense mechanical and chemical stress as well as to dense microbiologic colonization. Teeth are susceptible to damage, most commonly to caries, where microorganisms from the oral cavity degrade the mineralized tissues of enamel and dentine and invade the soft connective tissue at the core, the dental pulp. However, the pulp is well-equipped to sense and fend off bacteria and their products and mounts various and intricate defense mechanisms. The front rank is formed by a layer of odontoblasts, which line the pulp chamber towards the dentine. These highly specialized cells not only form mineralized tissue but exert important functions as barrier cells. They recognize pathogens early in the process, secrete antibacterial compounds and neutralize bacterial toxins, initiate the immune response and alert other key players of the host defense. As bacteria get closer to the pulp, additional cell types of the pulp, including fibroblasts, stem and immune cells, but also vascular and neuronal networks, contribute with a variety of distinct defense mechanisms, and inflammatory response mechanisms are critical for tissue homeostasis. Still, without therapeutic intervention, a deep carious lesion may lead to tissue necrosis, which allows bacteria to populate the root canal system and invade the periradicular bone via the apical foramen at the root tip. The periodontal tissues and alveolar bone react to the insult with an inflammatory response, most commonly by the formation of an apical granuloma. Healing can occur after pathogen removal, which is achieved by disinfection and obturation of the pulp space by root canal treatment. This review highlights the various mechanisms of pathogen recognition and defense of dental pulp cells and periradicular tissues, explains the different cell types involved in the immune response and discusses the mechanisms of healing and repair, pointing out the close links between inflammation and regeneration as well as between inflammation and potential malignant transformation.

scholarly journals Effect of smoking on alveolar bone resorption

2008 ◽  
Vol 55 (2) ◽  
pp. 107-114
Author(s):  
Jelena Racunica ◽  
Vesna Ivetic ◽  
Nada Naumovic ◽  
Milanko Djuric
Keyword(s):  
Bone Resorption ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Mean Value ◽  
Radiographic Examination ◽  
Control Group ◽  
X Rays ◽  
Periodontal Tissues ◽  
Bone Level ◽  
The Mean

Introduction: Periodontal disease is one of the most common diseases in adults. Although the cause of periodontal disease is bacterial infection from the dental plaque, the level of destruction of periodontal tissues depends on risk factors, and smoking is one of the most important ones. Aim: The aim of the present study was to determine the level of alveolar bone resorption in smokers. Materials and Methods: Radiographic examination of all present teeth was conducted in 30 smokers (12 men and 18 women) and 30 non-smokers (13 men and 17 women, control group), 20-60 years of age. Data on smoking habits, smoking period and the number of cigarettes a day were obtained using a questionnaire. The level of alveolar bone resorption was determined on retroalveolar X-rays, by measuring the distance from the amelo-cemental junction to the bone level on mesial and distal sides of each present tooth. Results: In smokers, significantly higher (p=0.00002) values of alveolar bone resorption (3.16 ? 2.07 mm) were found compared to the control group (1.72 ? 1.02 mm). In people who had been smoking for more than 15 years, significantly greater bone resorption was observed compared to those smoking for 15 years or less (p=0.00028). The interceptive relationship showed that smokers were at 2.98x greater risk (95% CI 1.04- 8.52) for the mean value of alveolar bone resorption of > 2 mm compared to non-smokers. Conclusion: The present results have shown that smoking increases alveolar bone resorption and that the period of smoking affects the level of resorption.

scholarly journals Platelet-Activating Factor Receptor Blockade Ameliorates Aggregatibacter actinomycetemcomitans-Induced Periodontal Disease in Mice

2013 ◽  
Vol 81 (11) ◽  
pp. 4244-4251 ◽  
Author(s):  
Mila Fernandes Moreira Madeira ◽  
Celso Martins Queiroz-Junior ◽  
Graciela Mitre Costa ◽  
Silvia Maria Cordeiro Werneck ◽  
Daniel Cisalpino ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Platelet Activating Factor ◽  
Aggregatibacter Actinomycetemcomitans ◽  
Content Type ◽  
Periodontal Tissues ◽  
Oral Inoculation ◽  
Paf Receptor

ABSTRACTPeriodontal disease (PD) is a chronic inflammatory and alveolar bone destructive disease triggered by oral biofilm-producing microorganisms, such asAggregatibacter actinomycetemcomitans. The levels of the phospholipid platelet-activating factor (PAF) in the saliva, gingival crevicular fluid, and periodontal tissues are significantly increased during inflammatory conditions, such as PD, but the exact mechanism that links PAF to alveolar bone resorption is not well understood. In the current study, alveolar bone resorption was induced by experimental PD through the oral inoculation ofA. actinomycetemcomitansin wild-type (WT) and PAF receptor knockout (Pafr−/−) mice.In vitroexperiments usingA. actinomycetemcomitanslipopolysaccharide (LPS)-stimulated RAW 264.7 cells treated with a PAF receptor antagonist (UK74505) were also performed. The expression of lyso-PAF acetyltransferase in periodontal tissues was significantly increased 3 h afterA. actinomycetemcomitansLPS injection in mice. WT andPafr−/−mice that were subjected to oral inoculation ofA. actinomycetemcomitanspresented neutrophil accumulation and increased levels of CXCL-1 and tumor necrosis factor alpha (TNF-α) in periodontal tissues. However,Pafr−/−mice presented less alveolar bone loss than WT mice. Thein vitroblockade of the PAF receptor impaired the resorptive activity ofA. actinomycetemcomitansLPS-activated osteoclasts. In conclusion, this study shows for the first time that the blockade of PAF receptor may contribute to the progression of PD triggered byA. actinomycetemcomitansby directly affecting the differentiation and activity of osteoclasts.

A Review of Tissue Engineering for Periodontal Tissue Regeneration

2021 ◽  
pp. 089875642110651
Author(s):  
Emily Ward
Keyword(s):  
Tissue Engineering ◽  
Veterinary Medicine ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Experimental Studies ◽  
Small Animal ◽  
Periodontal Tissues ◽  
The Cost ◽  
Open Flap Debridement ◽  
Repair Techniques

Periodontal disease is one of the most common diagnoses in small animal veterinary medicine. This infectious disease of the periodontium is characterized by the inflammation and destruction of the supporting structures of teeth, including periodontal ligament, cementum, and alveolar bone. Traditional periodontal repair techniques make use of open flap debridement, application of graft materials, and membranes to prevent epithelial downgrowth and formation of a long junctional epithelium, which inhibits regeneration and true healing. These techniques have variable efficacy and are made more challenging in veterinary patients due to the cost of treatment for clients, need for anesthesia for surgery and reevaluation, and difficulty in performing necessary diligent home care to maintain oral health. Tissue engineering focuses on methods to regenerate the periodontal apparatus and not simply to repair the tissue, with the possibility of restoring normal physiological functions and health to a previously diseased site. This paper examines tissue engineering applications in periodontal disease by discussing experimental studies that focus on dogs and other animal species where it could potentially be applied in veterinary medicine. The main areas of focus of tissue engineering are discussed, including scaffolds, signaling molecules, stem cells, and gene therapy. To date, although outcomes can still be unpredictable, tissue engineering has been proven to successfully regenerate lost periodontal tissues and this new possibility for treating veterinary patients is discussed.

Effects of periodontal therapy with topical antibiotics in the glycemic control of diabetic patients: systematic review.

2019 ◽  
Vol 27 (1) ◽  
pp. 31-42
Author(s):  
Gloria Cristina Aranzazu-Moya
Keyword(s):  
Periodontal Disease ◽  
Periodontal Therapy ◽  
Periodontal Treatment ◽  
Diabetic Patients ◽  
Inclusion Criteria ◽  
Topical Antibiotics ◽  
Bias Risk ◽  
Black Scale ◽  
Glycated Hemoglobin A ◽  
Modest Reduction

Background: Periodontal disease is considered as a diabetes complication and has been suggested that periodontal treatment plus antibiotics should reduce glycated hemoglobin A, by reducing local production of pro inflammatory substances. Objective: To evaluate diabetic patients with periodontal disease under periodontal treatment plus topical antibiotics and reduction of  HbA1c, compared to diabetic patients under periodontal treatment without antibiotics. Materials and Methods: Using PUBMED, SCOPUS, WEB OF SCIENCE, EMBASE and Google Scholar data bases, were screened documents from 2008 to 2018. The documents included were the clinical studies, which included non-surgical periodontal treatment plus topical antibiotics, whose outcomes included the HbA1c report. Two independent researchers evaluate title; abstract and bias risk with Downs Black scale and Cochrane tool. Documents with a score higher than 15 on average by the two evaluators were included. Results: Five articles, which find inclusion criteria, were identified. Two documents failed to demonstrate statistically significant effect when compared to non-surgical periodontal therapy alone. Conclusion: In general a modest reduction of HbA1c was identified when using antibiotic therapy.

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