Relationship between periapical and periodontal status

What Is The Difference Between A Periapical And Periodontal Abscess? | Dentist in Couer d'Alene, ID

relationship between periapical and periodontal status

Given the close relation between inflammation periodontal and apical disease . Request PDF on ResearchGate | Periodontal healing in teeth with periapical was to explore possible relationships between clinical periodontal status in. possible relationship between periodontal disease and CVD. Apical periodontitis, on the other hand, is the late consequence of an endodontic infection, which is.

Regarding systemic inflammatory markers, Cintra et al. The results showed that the presence of one AP focus did not alter the expression of proinflammatory cytokines systemically. These results suggest that the inflammatory changes reflect the amount of local inflammation. In addition, Samuel et al. Moreover, Zhang et al. The authors concluded that AP may trigger a systemic immune response, impair remote organs, and affect the general health of patients.

Frontiers | Oxidative Stress in the Local and Systemic Events of Apical Periodontitis | Physiology

The tests were conducted before endodontic treatment and 30 and 90 days after the treatment. The results showed that, on recruitment, patients with chronic AP exhibited significantly higher levels of oxidative stress than controls, as determined by the d-ROM and BAP tests. The levels of oxidative stress in these patients tended to reduce and return to normal by 90 days following treatment.

Bidirectional relationship between systemic disorders and endodontic infection a. Diabetes and endodontic infection Many clinicians and researchers have studied the interrelationship between oral infections and systemic disorders. The bidirectional relationship between endodontic infection and the systemic metabolic disease diabetes has been one of the targets of studies to better understand the connections between local and systemic inflammatory processes.

It is well established that diabetes can influence the pathogenesis of AP, especially its severity and development. The first paper describing the influence of diabetes on the pathogenesis of AP was published in by Kohsaka et al.

Consequently, lesions in the periapical area were larger in diabetic rats compared to those in the control group. In humans, several studies have been performed in order to study the correlation between the prevalence of AP and diabetes.

Their study showed AP in at least one tooth in The authors concluded that type 2 diabetes mellitus is significantly associated with an increased prevalence of AP.

After adjusting for teeth number, multivariate logistic regression analysis showed that periapical status and the number of root-filled teeth were significantly associated with diabetic status. In addition, Marotta et al.

According to the authors, diabetes may serve as a disease modifier of AP in the sense that individuals with diabetes can be more prone to develop primary disease. In agreement with the previous studies, Smadi 35 found that there is a higher prevalence of AP in diabetes mellitus patients compared with that in the nondiabetic group, with an increased prevalence of persistent chronic AP.

In comparison with well-controlled diabetes, poor glycemic control may be associated with a higher prevalence of AP and an increased rate of endodontic failures. However, the published results trend to converge on a positive association between diabetes and a larger number of periapical lesions. In order to obtain a more precise prognosis of endodontic treatment in diabetic patients, many studies have been performed to compare the healing outcomes after conventional endodontic treatment between diabetic and normoglycemic patients.

Fouad and Burleson 38 performed conventional endodontic treatment in diabetic patients and followed up 73 of them for two years postoperatively. Patients with diabetes showed increased periodontal disease of teeth with endodontic involvement compared with normoglycemic patients. There was a trend toward increased symptomatic periradicular disease in patients with diabetes who received insulin, as well as flare-ups in all diabetic patients.

In addition, the presence of diabetes was associated with significantly reduced successful outcomes. In accordance with these previous studies, Segura-Egea et al. Thus, diabetes is an important putative pre-operative prognostic factor in root canal treatment. However, Marotta et al.

In fact, TOS was reported to be significantly higher in ALs than in healthy periodontal ligament controls. Analysis of oral gingival crevicular fluid showed reduced TAS levels in asymptomatic AP teeth and were restored to normal levels after endodontic treatment Dezerega et al.

Bone homeostasis results from the balance between bone formation by osteoblasts and bone resorption by osteoclasts Hofbauer and Heufelder, ; Crotti et al. ROS suppress alveolar bone formation, by inhibiting osteoblastic differentiation and stimulate osteoclastogenesis Mody et al.

What Is The Difference Between A Periapical And Periodontal Abscess?

Direct exposure of periodontal ligament fibroblasts to hydrogen peroxide arrests cell viability, proliferation, and osteoblast differentiation. In contrast, osteoblastic differentiation accompanied by the induction of the transcription factors osterix and Runx2, was stimulated by continuous and low concentrations of hydrogen peroxide, whereas these effects were inhibited by CAT Choe et al. These results suggest a dose-dependent dual role of ROS, and particularly of hydrogen peroxide, in bone formation.

Receptor activator of nuclear factor-kappa B ligand RANKL stimulates the differentiation, maturation, and survival of cells into osteoclasts from their monocyte-macrophage precursors, leading to bone loss. Superoxide and hydrogen peroxide-induced RANKL over expression with the participation of extracellular signal-regulated kinases ERK and nuclear factor erythroid-derived 2-related factor Erf-2among others, have been demonstrated in different human and mouse osteoblastic cell lines Bai et al.

Experimentally-induced ALs in phagocyte oxidase PHOX —null mice resulted in the lack of identifiable tartrate resistant acid phosphatase TRAP —positive osteoclasts in ALs and healthy periodontal tissues, in contrast to wild type controls.

Oxidative non-proteolytic MMP activation seems to be pivotal in periodontal inflammation. Ex vivo studies suggest that oxidative activation of MMP-8 and MMP-9 represents the dominant mechanism in destructive periodontal lesions Hernandez et al.

Additionally, our group demonstrated increased oxidative stress along with higher MMP-9 levels and activity in ALs Dezerega et al.

Similarly, peroxide was also able to induce MAPK-mediated secretion of IL-8 in periodontal ligament fibroblasts, which was abolished in presence of high concentrations that associated to cell cytotoxicity Lee et al. These results support that non-lethal concentrations of ROS enhance pro-inflammatory mediators and extracellular matrix enzymes contributing to destructive amplification loops in the apical tissues, leading to the development of an AL.

Periodontal ligament fibroblasts are key cells for periodontal soft and hard tissue homeostasis. Concomitantly, low concentrations of ROS can modify signal transduction pathways through the presence of redox-sensitive cysteines. Overall, ROS can induce a plethora of signaling pathways and effects, depending on the cell target, concentration, and exposure patterns Choe et al.

  • Relationship between periapical and periodontal status. A clinical retrospective study.
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The ROS-mediated mechanisms in apical tissue breakdown are summarized in Figure 1. ROS-mediated mechanisms in apical tissue breakdown. ROS induce apical tissue breakdown by causing molecular damage or disrupted cell signaling. Oxidative Stress in AP-associated Atherogenesis The association between apical periodontitis and systemic diseases has regained the attention of researchers during the last years.

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Although most mechanistic evidence still comes from chronic marginal periodontitis, few studies already support a role of ROS in systemic complications associated with AP. Figure 2 shows an schematic representation linking oxidative stress, and oral infections and cardiovascular diseases. In fact, a hyper-reactive phagocyte phenotype characterized by higher ROS production was found in PMN from peripheral blood in chronic AP patients, in comparison to healthy controls, whereas superoxide levels significantly decreased after surgical removal of ALs Minczykowski et al.

A later study reported that chronic AP patients had higher levels of oxidants, measured as increased plasmatic reactive oxygen metabolites, and lower antioxidant potential compared to healthy individuals; while endodontic treatment tended to restore the systemic oxidative balance Inchingolo et al. Accordingly, early endothelial dysfunction and overproduction of asymmetrical dimethylarginine, the endogenous inhibitor of NOS, were recently reported in serum from young women with chronic AP, compared to healthy volunteers Cotti et al.

Oxidative stress links oral infections and cardiovascular diseases. On one hand, oral infections and cardiovascular diseases share a number of risk factors. On the other hand, oral infections may contribute to the development of several cardiovascular risk factors.

relationship between periapical and periodontal status

The processes that mediate the association between the two disease categories and involve oxidative stress are inflammation, redox disturbances, and autoimmunity. Categorically antioxidants, acquired either endogenous or supplemented, decrease oxidative stress. Oxidative stress is strongly involved in the pathology of atherosclerosis, where a chronic inflammatory process develops in the arterial wall. In its early phases, the areas that are susceptible for lesion formation display diffuse intimal thickening that are sites for low density lipoprotein LDL particle retention.

The retention predisposes LDL to oxidative modifications, especially during hyperlipidemia. On one hand, enzymes that can mediate the oxidation of LDL include lipoxygenase, MPO and peroxidase-like activity of hemoglobin Tsimikas and Miller, On the other hand, free radicals that are generated in the presence of hydrogen peroxide, nitric oxide, and superoxide mediate the non-enzymatic oxidation of LDL Tsimikas and Miller, Oxidized LDL oxLDL plays an essential role in atherogenesis as it represents a crucial pro-inflammatory stimulus and is recognized by various arms of the immune system Matsuura et al.

OxLDL is a ligand for cellular scavenger receptors, such as, CD36, and binding leads to accelerated LDL uptake by the arterial wall macrophages, foam cell formation, and generation of ROS, producing the vicious circle.

Oxidized structures also activate TLR further promoting inflammation in the atherosclerotic lesions Miller et al.

relationship between periapical and periodontal status

The signaling is essential for adaptive immune system to activate dendritic cells and macrophages, and subsequently T and B cells Huang and Pope, The concept of oxLDL refers to a wide range of reaction products in the particle: They are also recognized by natural antibodies, mainly of IgM isotype, which are transcribed from the germ-line genes and do not require prior exposure to foreign antigens to be secreted Baumgarth et al.

They bind to oxidatively modified structures due to their specificity against highly conserved structures that are present on pathogen surfaces or endogenously generated by oxidative reactions.

Sequence similarity or structural resemblance between self and non-self antigens leads to immune response called molecular mimicry Cusick et al.

This is also considered as a potential mechanism behind the association of periodontitis and CVD Schenkein and Loos, Similar or closely related, conserved molecules among the self-antigens can be found in bacteria leading to production of autoantibodies Leishman et al. Such antibodies described in periodontitis patients include anti-phosphorylcholine Schenkein et al. The epitope was identified as gingipain, one of the most important virulence factor and protease of the bacterium.

To directly link this observation with atherosclerosis, immunization of mice with MDA-LDL was shown to reduce the aortic lipid deposition area after P. In addition to oxLDL, other major molecules giving rise to molecular mimicry are members of the heat-shock protein Hsp families. Hsp are highly conserved stress molecules present both in humans and bacteria.

The antibody response to them is implicated in atherosclerosis Pockley et al. After taking into account age, sex, smoking, and number of teeth, A. A recent study from our group also demonstrated an association between ALs, P. Importantly, a significant association between AL and risk of coronary artery disease was reported.