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

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.

2021 ◽  
Vol 2 ◽  
Author(s):  
Thais de Cássia Negrini ◽  
Iracilda Zeppone Carlos ◽  
Cristiane Duque ◽  
Karina Sampaio Caiaffa ◽  
Rodrigo Alex Arthur

This comprehensive review of the literature aimed to investigate the interplay between the oral microbiome, oral cavity conditions, and host immune response in Diabetes mellitus (DM). Moreover, this review also aimed to investigate how DM related risk factors, such as advanced age, hyperglycemia, hyperlipidemia, obesity, hypertension and polycystic ovary syndrome (PCOS), act in promoting or modifying specific mechanisms that could potentially perpetuate both altered systemic and oral conditions. We found that poorly controlled glycemic index may exert a negative effect on the immune system of affected individuals, leading to a deficient immune response or to an exacerbation of the inflammatory response exacerbating DM-related complications. Hyperglycemia induces alterations in the oral microbiome since poor glycemic control is associated with increased levels and frequencies of periodontal pathogens in the subgingival biofilm of individuals with DM. A bidirectional relationship between periodontal diseases and DM has been suggested: DM patients may have an exaggerated inflammatory response, poor repair and bone resorption that aggravates periodontal disease whereas the increased levels of systemic pro-inflammatory mediators found in individuals affected with periodontal disease exacerbates insulin resistance. SARS-CoV-2 infection may represent an aggravating factor for individuals with DM. Individuals with DM tend to have low salivary flow and a high prevalence of xerostomia, but the association between prevalence/experience of dental caries and DM is still unclear. DM has also been associated to the development of lesions in the oral mucosa, especially potentially malignant ones and those associated with fungal infections. Obesity plays an important role in the induction and progression of DM. Co-affected obese and DM individuals tend to present worse oral health conditions. A decrease in HDL and, an increase in triglycerides bloodstream levels seem to be associated with an increase on the load of periodontopathogens on oral cavity. Moreover, DM may increase the likelihood of halitosis. Prevalence of impaired taste perception and impaired smell recognition tend to be greater in DM patients. An important interplay among oral cavity microbiome, DM, obesity and hypertension has been proposed as the reduction of nitrate into nitrite, in addition to contribute to lowering of blood pressure, reduces oxidative stress and increases insulin secretion, being these effects desirable for the control of obesity and DM. Women with PCOS tend to present a distinct oral microbial composition and an elevated systemic response to selective members of this microbial community, but the association between oral microbiome, PCOS are DM is still unknown. The results of the studies presented in this review suggest the interplay among the oral microbiome, oral cavity conditions, host immune response and DM and some of the DM associated risk factors exist. DM individuals need to be encouraged and motivated for an adequate oral health care. In addition, these results show the importance of adopting multidisciplinary management of DM and of strengthening physicians-dentists relationship focusing on both systemic and on oral cavity conditions of DM patients.


2005 ◽  
Vol 6 (2) ◽  
pp. 118-129 ◽  
Author(s):  
Pradeep S. Anand ◽  
K. Nandakumar

Abstract The pulp and the periodontal attachment are the two components that enable a tooth to function in the oral cavity. Lesions of the periodontal ligament and adjacent alveolar bone may originate from infections of the periodontium or tissues of the dental pulp. The simultaneous existence of pulpal problems and inflammatory periodontal disease can complicate diagnosis and treatment planning. The function of the tooth is severely compromised when either one of these is involved in the disease process. Treatment of disease conditions involving both of these structures can be challenging and frequently requires combining both endodontic and periodontal treatment procedures. This article presents cases of periodontitis associated with endodontic lesions managed by both endodontic and periodontal therapy. Citation Anand PS, Nandakumar K. Management of Periodontitis Associated with Endodontically Involved Teeth: A Case Series. J Contemp Dent Pract 2005 May;(6)2:118-129.


2005 ◽  
Vol 52 (2) ◽  
pp. 103-110 ◽  
Author(s):  
Olivera Cerovic ◽  
Vera Bundalo

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.


2021 ◽  
Vol 2 (1) ◽  
pp. 17-24
Author(s):  
M.V. Khaitovich

A search was conducted in the databases Scopus, Web of Science, MedLine, The Cochrane Library. Periodontal disease is the main cause of tooth loss. Periodontitis is an inflammatory dise-ase caused by a specific microflora and leads to the progressive destruction of the ligaments of the tooth and alveolar bone. This is accompanied by the formation of the gums recession, the formation of periodontal pockets, both separately and mutually. Periodontitis is observed in 9–85 % of children, 70–90 % of adolescents, more than half of adults. Activation of inflammation in the periodontium is inextricably linked with systemic processes in the body, which are accompanied by an inflammatory response, and therefore perio-dontitis is a concomitant factor in coronary heart disease and cerebrovascular disease/ischemic stroke, adversely affects the digestive, cardiovascular, endocrine and other systems. Uncontrolled inflammatory response of the body in the conditions of microbial biofilm, which is tightly adjacent to the tooth surface, leads to the destruction of periodontal tissues, bone loss. If the acute inflammation subsides in time, preventing destruction without the complete return of tissues to homeostasis, it leads to damage caused by neutrophils and chronic inflammation. Systemic anti-inflammatory therapy with the use of non-selective nonsteroidal anti-inflammatory drugs is an important direction of periodontitis therapy, which reduces the intensity of inflammation, minimizes the destruction of periodontal tissues, limits the resource of nutrients for pathogenic microorganisms, prevents resorption of alveolar bone. For the prevention of gastropathy, it is advisable to use a synthetic analogue of prostaglandin E2 misoprostol in the complex therapy. The mana-gement of drug interaction should be used when prescribing nonsteroidal anti-inflammatory drugs to a patient taking sulfonylureas, warfarin, antihypertensive drugs, and the like.


2013 ◽  
Vol 12 (1) ◽  
pp. 49
Author(s):  
Rifi Aranti ◽  
Yulianti Kemal

Cyclosporine is an immunosuppressant drug that suppresses effectively the immune response, and main drug used toprevent rejection in organ transplantation. Negative impact in the oral cavity of cyclosporine therapy is characterizedby the occurrence of gingival enlargement in 8-70% of cases, which occurred in the first 3-6 months of use, as well asthe loss of alveolar bone. The effect of the drug on gingival enlargement is a serious problem in patients receivingcyclosporine therapy. Pathogenesis of gingival enlargement on cyclosporine therapy is not known at all, but theinfluence of fibroblast proliferation and extracellular matrix were estimated reduction capabilities play a role in thisaspect. Dental plaque does not have a significant relationship to the occurrence of gingival enlargement oncyclosporine therapy, but support the occurrence of chronic inflammation that contributes to gingival enlargement.Adequate oral hygiene with initial periodontal treatment can reduce inflammation and gingival enlargement due tocyclosporine therapy. Patients who will undergo organ transplantation, previously had to undergo dental and oralhealth care comprehensively.


2019 ◽  
Vol 1 (7) ◽  
pp. 29-32 ◽  
Author(s):  
L. S. Kruglova ◽  
E. M. Gensler

Over the past decades, the first breakthrough milestone in the treatment of severe forms of atopic dermatitis (AD) has been targeted therapy aimed at inhibiting IL-4 and IL-13. This was made possible thanks to advances in the understanding of the pathogenesis of AD, the driver of which is the Th2-type immune response, which also underlies such manifestations of atopy as bronchial asthma, allergic rhinitis, and polynosis. In the case of the Th2-type immune response, cytokines IL-4 and IL-13 are secreted, which are the main promoters of the inflammatory response in AD. Inhibition of IL-4 and IL-13 leads to the prevention of inflammation and is an effective approach to therapy. The use of therapy aimed at inhibition of cytokines allows you to effectively cope with the manifestations of severe and moderately severe blood pressure.


Author(s):  
O. L. Zolotukhina ◽  
◽  
Ju. G. Romanova ◽  
O. V. Maslov ◽  
◽  
...  

Diseases of periodontal tissues occupy one of the leading positions among modern dental problems, namely the multifactorial nature of these diseases. In modern dental science, the issue of the development of periodontal pathology against the background of somatic pathology and risk factors remains relevant. Pathology of periodontal tissues in 68–90 % of cases is accompanied by chronic diseases of the gastrointestinal tract. Today, there is no doubt that Helicobacter pylori infection can be present in the biotopes of the oral cavity and can affect the course of periodontal pathology. As you know, smoking is one of the important risk factors for the development of inflammatory-dystrophic diseases of periodontal tissues, which can aggravate the course of the latter. The purpose of the work is to determine the prevalence of oral Helicobacter pylori infection in tobacco-dependent patients with chronic generalized periodontitis on the background of chronic hyperacid gastritis during treatment. Patients who received the proposed therapeutic and prophylactic complex (ultraphonophoresis procedures with the created gel «Apisan», and probiotic drug BioGaia ProDentis and angioprotective drug of natural origin — Detralex) showed a gradual decrease in the level of total urease activity and, as a consequence, a decrease the prevalence of Helicobacter pylori infection in the oral cavity according to the results of a urease rapid test with material from the oral cavity, both in the presence of a risk factor — smoking, and in its absence. The use of the proposed therapeutic and prophylactic complex proved to be effective in reducing the prevalence of oral Helicobacter pylori infection in smoking patients and patients who do not smoke, with chronic generalized periodontitis against the background of chronic hyperacidal gastritis associated with Helicobacter pylori.


2021 ◽  
pp. 002203452110199
Author(s):  
Y. Xie ◽  
Q. Tang ◽  
S. Yu ◽  
W. Zheng ◽  
G. Chen ◽  
...  

Orthodontic tooth movement (OTM) depends on periodontal ligament cells (PDLCs) sensing biomechanical stimuli and subsequently releasing signals to initiate alveolar bone remodeling. However, the mechanisms by which PDLCs sense biomechanical stimuli and affect osteoclastic activities are still unclear. This study demonstrates that the core circadian protein aryl hydrocarbon receptor nuclear translocator–like protein 1 (BMAL1) in PDLCs is highly involved in sensing and delivering biomechanical signals. Orthodontic force upregulates BMAL1 expression in periodontal tissues and cultured PDLCs in manners dependent on ERK (extracellular signal–regulated kinase) and AP1 (activator protein 1). Increased BMAL1 expression can enhance secretion of CCL2 (C-C motif chemokine 2) and RANKL (receptor activator of nuclear factor–κB ligand) in PDLCs, which subsequently promotes the recruitment of monocytes that differentiate into osteoclasts. The mechanistic delineation clarifies that AP1 induced by orthodontic force can directly interact with the BMAL1 promoter and activate gene transcription in PDLCs. Localized administration of the ERK phosphorylation inhibitor U0126 or the BMAL1 inhibitor GSK4112 suppressed ERK/AP1/BMAL1 signaling. These treatments dramatically reduced osteoclastic activity in the compression side of a rat orthodontic model, and the OTM rate was almost nonexistent. In summary, our results suggest that force-induced expression of BMAL1 in PDLCs is closely involved in controlling osteoclastic activities during OTM and plays a vital role in alveolar bone remodeling. It could be a useful therapeutic target for accelerating the OTM rate and controlling pathologic bone-remodeling activities.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hui Yu ◽  
Tianyi Zhang ◽  
Haibin Lu ◽  
Qi Ma ◽  
Dong Zhao ◽  
...  

Abstract Background Granulocyte colony-stimulating factor (G-CSF) is an important immune factor that mediates bone metabolism by regulating the functions of osteoclasts and osteoblasts. Bone loss is a serious and progressive result of periodontitis. However, the mechanisms underlying the effects of G-CSF on periodontal inflammation have yet not been completely elucidated. Here, we examined whether an anti-G-CSF antibody could inhibit bone resorption in a model of experimental periodontitis and investigated the local expression of G-CSF in periodontal tissues. Methods Experimental periodontitis was induced in mice using ligatures. The levels of G-CSF in serum and bone marrow were measured; immunofluorescence was then performed to analyze the localization and expression of G-CSF in periodontal tissues. Mice with periodontitis were administered anti-G-CSF antibody by tail vein injection to assess the inhibition of bone resorption. Three-dimensional reconstruction was performed to measure bone destruction‐related parameters via micro-computed tomography analysis. Immunofluorescence staining was used to investigate the presence of osteocalcin-positive osteoblasts; tartrate-resistant acid phosphatase (TRAP) staining was used to observe osteoclast activity in alveolar bone. Results The level of G-CSF in serum was significantly elevated in mice with periodontitis. Immunofluorescence analyses showed that G-CSF was mostly expressed in the cell membrane of gingival epithelial cells; this expression was enhanced in the periodontitis group. Additionally, systemic administration of anti-G-CSF antibody significantly inhibited alveolar bone resorption, as evidenced by improvements in bone volume/total volume, bone surface area/bone volume, trabecular thickness, trabecular spacing, and trabecular pattern factor values. Immunofluorescence analysis revealed an enhanced number of osteocalcin-positive osteoblasts, while TRAP staining revealed reduction of osteoclast activity. Conclusions G-CSF expression levels were significantly up-regulated in the serum and gingival epithelial cells. Together, anti-G-CSF antibody administration could alleviates alveolar bone resorption, suggesting that G-CSF may be one of the essential immune factors that mediate the bone loss in periodontitis.


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