periodontium disese
49338687
Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri Implant Diseases and Conditions.
Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non dental plaque biofilm induced gingival diseases and dental plaque induced gingivitis. Non dental plaque biofilm induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced) A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1) and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.
Journal of clinical periodontology
Iain L C Chapple Brian L Mealey Thomas E Van Dyke P Mark Bartold Henrik Dommisch Peter Eickholz Maria L Geisinger Robert J Genco Michael Glogauer Moshe Goldstein Terrence J Griffin P Holmstrup Georgia K Johnson Yvonne L Kapila Niklaus P Lang Joerg Meyle Shinya Murakami Jacqueline M Plemons Giuseppe Alexandre Romito Lior Shapira Dimitris N Tatakis Wim Teughels Leonardo Trombelli Clemens Walter Gernot Wimmer Pinelopi Xenoudi Hiromasa Yoshie
49337078
Periodontal health and gingival diseases and conditions on an intact and a reduced periodontium: Consensus report of workgroup 1 of the 2017 World Workshop on the Classification of Periodontal and Peri Implant Diseases and Conditions.
Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non dental plaque biofilm induced gingival diseases and dental plaque induced gingivitis. Non dental plaque biofilm induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non periodontitis patient or in a currently stable "periodontitis patient" i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced) A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1) and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient centered approach to care, and therefore, creates differences in the way in which a "case" of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.
Journal of periodontology
Iain L C Chapple Brian L Mealey Thomas E Van Dyke P Mark Bartold Henrik Dommisch Peter Eickholz Maria L Geisinger Robert J Genco Michael Glogauer Moshe Goldstein Terrence J Griffin P Holmstrup Georgia K Johnson Yvonne L Kapila Niklaus P Lang Joerg Meyle Shinya Murakami Jacqueline M Plemons Giuseppe Alexandre Romito Lior Shapira Dimitris N Tatakis Wim Teughels Leonardo Trombelli Clemens Walter Gernot Wimmer Pinelopi Xenoudi Hiromasa Yoshie
58573460
BILATERAL INTERRELATIONSHIP OF DIABETES AND PERIODONTIUM.
Periodontitis is a chronic inflammatory disease characterised by destruction of the supporting structures of the teeth which is a common cause of tooth mortality in all individuals throughout the world. Diabetes is a group of metabolic dysregulation, primarily of carbohydrate metabolism, characterized by hyperglycemia that results from defects in insulin secretion, impaired insulin action, or both. Systematic reviews and meta analysis have shown that the prevalance of periodontitis is increased in diabetic patients. Based on the evidence, degree of hyperglycemia and severity of periodontitis are inter related. Diabetic patients with severe periodontitis are six times to have poor glycemic control than patients with healthy periodontium. However, improved glycemic control has been postulated to reduce the severity of periodontal disease In this mini review, we have presented the previous reviewed studies from the literature and focused on two way relationship of diabetes and periodontitis, various pathways involved in it such as RANK/RANKL/OPG axis, AGE RAGE pathway, Oxidative stress mechanism, obesity that influence the possibility of periodontitis Diabetes Mellitus (DM)
Current diabetes reviews
Apoorva B Badiger Triveni M Gowda Khyati Chandra Dhoom Singh Mehta
195066228
Periodontal Ligament Stem Cells: Regenerative Potency in Periodontium.
Periodontium is consisted of root cementum, bone lining the tooth socket, gingiva facing the tooth, and periodontal ligament (PDL) Its primary functions are support of the tooth and protection of tooth, nerve, and blood vessels from injury by mechanical loading. Severe periodontitis induces the destruction of periodontium and results in a significant cause of tooth loss among adults. Unfortunately, conventional therapies such as scaling and root planning are often only palliative. Therefore, the ultimate goal of the treatment for periodontitis is to restore disrupted periodontium to its original shape and function. Tissue engineering refers to the process of combining cells, scaffolds, and signaling molecules for the production of functional tissues to restore, maintain, and improve damaged organs. The discovery of PDL stem cells (PDLSCs) highlighted the possibility for development of tissue engineering technology based therapeutics for disrupted periodontium. PDLSCs are a kind of somatic stem cells that show a potential to differentiate into multiple cell types and undergo robust clonal self renewal. Therefore, PDLSCs are considered as a highly promising stem cell population for regenerative therapy in periodontium, however their rarity prevents the progression of basic and clinical researches. In this review, we summarize recent research advancement and accumulated information regarding the self renewal capacity, multipotency, and immunomoduratory effect of PDLSCs, as well as their contribution to repair and regeneration of periodontium and other tissues. We also discuss the possibility of PDLSCs for clinical application of regenerative medicine and provide an outline of the genetic approaches to overcome the issue about the rarity of PDLSCs.
Stem cells and development
Atsushi Tomokiyo Naohisa Wada Hidefumi Maeda
51970378
ACVR1 is essential for periodontium development and promotes alveolar bone formation.
OBJECTIVE To explore the role of a BMP type I receptor (ACVR1) in regulating periodontium development, Acvr1 was conditionally disrupted in Osterix expressing cells. METHODS Mandibles from both control (Acvr1 fx/ Osterix Cre and cKO (Acvr1 fx/ Osterix Cre mice at postnatal day 21 (PN21) were scanned by micro CT, followed by decalcification and histological observations. Distributions and levels of differentiation markers of fibroblasts, osteoblasts and cementocytes in the periodontium were detected by immunohistochemical (IHC) staining. RESULTS Micro CT results showed that bone mass and bone mineral density of the alveolar bones in the cKO mice were lower than those in the controls. Histomorphometry within the alveolar bones revealed that the lower bone mass observed in the cKO mice was caused by increased numbers and resorption activities of osteoclasts. The markers for osteoblast differentiation, Col I and DMP1, were reduced and the signals of the RANKL/OPG ratio were increased in the alveolar bones of the cKO mice compared to those of the control mice. The periodontal ligament in the cKO mice exhibited disorganized collagen fibers with weaker signals of Col I and periostin. However, there was no difference in terms of the cellular cementum between the two groups. CONCLUSION ACVR1 is essential for normal periodontium development. ACVR1 in the osteoblasts negatively regulates osteoclast differentiation in association with the RANKL/OPG axis and thus promotes alveolar bone formation.
Archives of oral biology
Xue Zhang Qi-lin Liu Huan Zhao Yue Hu Cangwei Liu Guangxing Yan Daowei Li Yuji Mishina Ce Shi Hongchen Sun
51969390
Epigallocatechin 3 gallate prevents disruption of connective tissue in periodontium and salivary glands of rats during systemic inflammation.
OBJECTIVE Introduction: The connective tissue remodeling is essential for periodontal and salivary glands (SG) pathology. Recently there has been demonstrated the number of pharmacological effects of green tea (Camellia sinensis) such as antioxidant, anti inflammatory, anti aging, antibacterial, antiviral and DNA protective effects, associated with the presence of epigallocatechin 3 gallate (EGCG) as an inducer of the Keap1 Nrf2 antioxidant response element signaling pathway. However, the EGCG effects on the components of soft connective tissues of periodontium and SG are still unclear. The aim: To investigate the effect of EGCG on markers of disruption of periodontal and submandibular SG connective tissues in rats during the conditions of experimental systemic inflammation (SI) PATIENTS AND METHODS Materials and methods: The studies were conducted on 30 white rats of the Wistar line, divided into 3 groups: the 1st included intact animals, the 2nd was made up of animals after induced SI (by intraperitoneal administration of lipopolysaccharide Salmonella typhi) and the 3rd included animals, which were injected EGCG (production of Sigma Aldrich, Inc. USA) intraperitoneally in a dose of 21.1 mg kg 3 times a week, starting on the 30th day of SI induction. The level of collagenolysis was assessed by the content of free hydroxyproline (FHP) The process of depolymerization of proteoglycans and sialoglycoproteins was evaluated by determining their monomers, glycosaminoglycans (GAGs) and N acetylneuraminic acid (NANA) respectively. The molar roots exposure index (MREI) was calculated. RESULTS Results: Administering EGCG reduced the content of FHP by 33.3 (p<0.01) the content of GAGs by 39.4% (p<0.02) and content of NANA by 34.3% (p<0.001) in the soft periodontal tissues compared with the relevant findings in the second group of the animals. In this condition the concentration of these compounds in the calcified components of periodontium (alveolar bone) lowered as well: FHP by 41.9% (p<0.001) GAGs by 41.0% (p<0.001) NANA by 53.3% (p<0.001) MREI reduced to 27.1+1.6, i.e. by 27.7% (p<0.01) compared with the relevant findings in the second group of the animals. The administration of EGCG also reduced the content of FHP by 37.8% (p<0.001) the content of GAGs by 39.8% (p<0.001) and the content of NANA by 37.6% (p<0.001) in SG tissues compared with the relevant results of the second group of the animals. CONCLUSION Conclusions: The administration of EGCG under modeled systemic inflammation is an effective means of preventing and correcting the disruption of connective tissue of periodontium and submandibular salivary glands in rats: it reduces collagenolysis and depolymerization of proteoglycans and glycoproteins.
Wiadomosci lekarskie
A M Yelins'ka Olena O Shvaykovs'ka Vitalii O Kostenko
3787616
Tissue specific composite cell aggregates drive periodontium tissue regeneration by reconstructing a regenerative microenvironment
Periodontitis is the most common cause of periodontium destruction. Regeneration of damaged tissue is the expected treatment goal. However, the regeneration of a functional periodontal ligament (PDL) insertion remains a difficulty, due to complicated factors. Recently, periodontal ligament stem cells (PDLSCs) and bone marrow derived mesenchymal stem cells (BMMSCs) have been shown to participate in PDL regeneration, both pathologically and physiologically. Besides, interactions affect the biofunctions of different derived cells during the regenerative process. Therefore, the purpose of this study was to discuss the different derived composite cell aggregate (CA) systems of PDLSCs and BMMSCs (iliac derived or jaw derived) for periodontium regeneration under regenerative microenvironment reconstruction. Our results showed although all three mono MSC CAs were compacted and the cells arranged regularly in them, jaw derived BMMSC (JBMMSC) CAs secreted more extracellular matrix than the others. Furthermore, PDLSC/JBMMSC compound CAs highly expressed ALP, Col I, fibronectin, integrin b1 and periostin, suggesting that their biofunction is more appropriate for periodontal structure regeneration. Inspiringly, PDLSC/JBMMSC compound CAs regenerated more functional PDL like tissue insertions in both nude mice ectopic and minipig orthotopic transplantation. The results indicated that the different derived CAs of PDLSCs/JBMMSCs provided an appropriate regenerative microenvironment facilitating a more stable and regular regeneration of functional periodontium tissue. This method may provide a possible strategy to solve periodontium defects in periodontitis and powerful experimental evidence for clinical applications in the future. Copyright (c) 2015 John Wiley Sons, Ltd.
Journal of tissue engineering and regenerative medicine
Bin Zhu Wenjia Liu Hao Zhang Xicong Zhao Yan Duan Dehua Li Yan Jin
6392634
Jawbone microenvironment promotes periodontium regeneration by regulating the function of periodontal ligament stem cells
During tooth development, the jawbone interacts with dental germ and provides the development microenvironment. Jawbone derived mesenchymal stem cells (JBMSCs) maintain this microenvironment for root and periodontium development. However, the effect of the jawbone microenvironment on periodontium tissue regeneration is largely elusive. Our previous study showed that cell aggregates (CAs) of bone marrow mesenchymal stem cells promoted periodontium regeneration on the treated dentin scaffold. Here, we found that JBMSCs enhanced not only the osteogenic differentiation of periodontal ligament stem cells (PDLSCs) but also their adhesion to titanium (Ti) material surface. Importantly, the compound CAs of PDLSCs and JBMSCs regenerated periodontal ligament like fibers and mineralized matrix on the Ti scaffold surface, both in nude mice ectopic and minipig orthotopic transplantations. Our data revealed that an effective regenerative microenvironment, reconstructed by JBMSCs, promoted periodontium regeneration by regulating PDLSCs function on the Ti material.
Scientific Reports
Bin Zhu Wenjia Liu Yi-han Liu Xicong Zhao H Zhang Zhuojing Luo Yan Jin
23382881
Impaired periodontium and temporomandibular joints in tumour necrosis factor &agr; transgenic mice
AIM Tumour necrosis factor (TNF) a is a pathological factor causing the characteristic symptoms of periodontal disease and rheumatoid arthritis. In this study, we describe the phenotypes of human TNF a transgenic mice (hTNFtg) with respect to their periodontium and the temporomandibular joint (TMJ) MATERIAL AND METHODS Periodontal structures, TMJ and skull shape of hTNFtg mice and wild type (WT) littermates were assessed by microcomputed tomography, automated segmentation, geometric morphometrics and histologic ground sections. RESULTS We show that hTNFtg mice have an eroded lamina dura and reduced periodontal ligament space compared to (WT) littermates. Transgenic mice further exhibit severe destruction of the TMJ. Geometric morphometrics revealed that hTNFtg mice have a more laterally positioned TMJ with a concomitantly enlarged zygomatic process. Mandibular and maxillary teeth occluded properly. CONCLUSIONS Our findings suggest that chronic inflammation in hTNFtg mice causes destructive changes of the periodontium and the TMJ.
Journal of clinical periodontology
Toni Dobsak Patrick Heimel Stefan Tangl Uwe Yacine Schwarze Georg Schett Reinhard Gruber
24638670
Chronic treatment with zoledronic acid increases inflammatory markers in periodontium of rats
BACKGROUND Bisphosphonates (BF) rise proinflammatory markers and irreversibly bind to bone. Chronically, BF can lead to an inflammatory status and can increase the local oxidative stress in periodontium. Therefore, the objective of this study was to evaluate whether the chronic infusion of Zoledronic Acid (ZA) increases inflammatory markers in periodontium of rats. METHODS AND RESULTS Chronically, infusion therapy was performed with ZA (0.04, 0.2 or 1 mg/kg or saline) by four doses in over a 70 day period to analyze periodontium of the first right inferior molar using histologic, histochemical (toluidine blue) and immunohistochemical (CD68, tumor necrosis factor a (TNF a) interleukin 1beta (IL 1b) inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF kB) tests. The experiment was replicated (ZA 0.2 mg/kg versus saline) for myeloperoxidase (MPO) assay and dose TNF a, IL 1b, malondialdehyde (MDA) and glutathione (GSH) in gingiva of the same tooth. Despite there is no alteration in mast cells (P .608) and CD68 mononuclear positive cells (P .351) in the periodontium of the ZA treated group, was observed an increase in the presence of inflammatory cells (P .001) and cytoplasmic immunostaining for TNF a (P .003) IL 1b (P .004) iNOS (P .008) and NF kB (P .025) Levels of MPO (P .001) TNF a (P .002) IL 1b (P .001) and GSH (P .005) were augmented in gingiva of ZA treated group but MDA (P .993) levels and NF kB nuclear staining (P .923) were not altered. CONCLUSIONS Chronic treatment with ZA increase proinflammatory cytokines and the number of inflammatory cells in periodontium of rats and GSH are expressed probably in a compensatory manner.
Journal of oral pathology medicine official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
Paulo Goberlanio de Barros Silva Antonio Ernando Carlos Ferreira Junior Camila Carvalho de Oliveira Luiz Andre Cavalcante Brizeno Deysi Viviana Tenazoa Wong Roberto Cesar Pereira Lima Junior Fabricio Bitu Sousa Mario Rogerio Lima Mota Ana Paula Negreiros Nunes Alves