Assessment of Salivary Levels of RANKL and OPG in Aggressive versus Chronic Periodontitis

Teodorescu, Alexandra Cornelia; Mârțu, Ioana; Teslaru, Silvia; Kappenberg‐Niţescu, Diana Cristala; Goriuc, Ancuța; Luchian, Ionuț; Mârțu, Maria-Alexandra; Solomon, Sorina Mihaela; Mârţu, Silvia

doi:10.1155/2019/6195258

Cited by 33 publications

(30 citation statements)

References 21 publications

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“…Furthermore, the expression levels of RANKL and OPG were respectively decreased and increased upon disease development. These findings were in contrast with the results of some studies indicating the elevated level of RANKL accompanied by a significant reduction in OPG level during disease progression [33][34][35]. However, immunohistochemical studies on periodontal tissues have revealed a negative expression of RANKL and a positive expression of OPG in both oral and periodontal pocket epithelium [36].…”

Section: Discussioncontrasting

confidence: 77%

The expression levels of MicroRNA-146a, RANKL and OPG after non-surgical periodontal treatment

et al. 2021

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Objective MicroRNA-146a (miR-146a) is a regulator of inflammatory response. Periodontitis is a disease with immune pathophysiology of the periodontium in which the inflammation results in the destruction of the soft tissues and alveolar bone. Therefore, the aim of this study was to investigate the expressions of miR-146a, OPG, and RANKL in diseased and healthy periodontal tissues to understand whether miR-146a expression level may associate with OPG and RANKL mRNA levels and OPG/RANKL ratio after non-surgical periodontal treatment. Methods The levels of miR-146a, RANKL, and OPG in gingival tissues from patients with generalized periodontitis stages II and III and grades A and B (n = 15, group A), patients with generalized periodontitis stages III and IV and grade C (n = 15, group B), and healthy individuals (n = 10) were determined by real-time PCR. The associations of miR-146a expression with OPG and RANKL levels were evaluated. Results The levels of miR-146a in two subgroups within periodontitis patients were significantly higher than healthy subjects (P < 0.0001). MiR-146a showed the increased level in group A of patients compared with group B (P < 0.05). Clinical parameters such as probing depth (PD) and clinical attachment loss (CAL) were significantly higher in patients than control group (P < 0.05). The levels of OPG and RANKL were increased in patients compared with healthy subjects, although the elevated levels were not statistically significant. MiR-146a was not associated with OPG and RANKL levels and OPG/RANKL ratio. Conclusions The results of this study failed to show the associations of miR-146a level with OPG and RANKL levels and OPG/RANKL ratio in periodontitis after non-surgical periodontal treatment.

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Section: Discussioncontrasting

confidence: 77%

The expression levels of MicroRNA-146a, RANKL and OPG after non-surgical periodontal treatment

et al. 2021

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“…Furthermore, the expression levels of RANKL and OPG were respectively decreased and increased upon the disease development. These ndings were in contract with the results of some studies indicating the elevated level of RANKL accompanied by a signi cant reduction in OPG level during the disease progression (32)(33)(34). However, immunohistochemical studies on periodontal tissues have revealed a negative expression of RANKL and a positive expression of OPG in both oral and periodontal pocket epithelium (35).…”

Section: Discussionsupporting

confidence: 88%

Micro RNA-146a effect on Periodontitis is Independent on OPG/RANKL Axis

Sattari¹,

Ghotloo²,

Taheri³

et al. 2021

Preprint

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Background MicroRNA-146a (miR-146a) is a regulator of inflammatory response. Periodontitis is a disease with immune pathophysiology of the periodontium in which the inflammation results in the destruction of the soft tissues and alveolar bone. Therefore, this study was investigated whether miR-146a may contribute to periodontitis through affecting the levels of OPG and RANKL. Methods The levels of miR-146a, RANKL, and OPG in gingival tissues from patients with generalized periodontitis stages II and III and grades A and B (n = 15, group A), patients with generalized periodontitis stages III and IV and grade C (n = 15, group B), and healthy individuals (n = 10) were determined by real-time PCR. The associations of miR-146a expression with OPG and RANKL levels were evaluated. Results The levels of miR-146a in two subgroups within periodontitis patients were significantly higher than healthy subjects (P < 0.0001). MiR-146a showed the increased level in group A of patients compared with group B (P < 0.05). Clinical parameters such as probing depth (PD) and clinical attachment loss (CAL) were significantly higher in patients than control group (P < 0.05). The levels of OPG and RANKL were increased in patients compared with healthy subjects, although the elevated levels were not statistically significant. MiR-146a was not associated with the levels of OPG and RANKL. Conclusion The results of this study failed to show the effect of miR-146a on the pathophysiology of disease through OPG/RANKL axis. Clinical Relevancy: MiR-146a may participate in the pathophysiology of disease through independent mechanism(s) of OPG/RANKL axis.

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“…. This RANKL-mediated T-reg activation is further sustained in PD by the downregulation of osteoprotegerin that can block RANKL in the saliva and GCF of patients with PD [115,116]. This RANKL-RANK signaling in OSCC has been shown to stimulate cancer metastasis in concert with the presence of active tumor-infiltrating T-regs [117].…”

Section: Rankl Which Is Upregulated In Pd Promotes T-reg Induction While Rankl Inhibition Interferes With the Migration Of Tregs And Indumentioning

confidence: 99%

The Crossroads of Periodontitis and Oral Squamous Cell Carcinoma: Immune Implications and Tumor Promoting Capacities

Elebyary

Barbour

Fine

et al. 2021

Front. Oral. Health

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Periodontitis (PD) is increasingly considered to interact with and promote a number of inflammatory diseases, including cancer. In the case of oral squamous cell carcinoma (OSCC) the local inflammatory response associated with PD is capable of triggering altered cellular events that can promote cancer cell invasion and proliferation of existing primary oral carcinomas as well as supporting the seeding of metastatic tumor cells into the gingival tissue giving rise to secondary tumors. Both the immune and stromal components of the periodontium exhibit phenotypic alterations and functional differences during PD that result in a microenvironment that favors cancer progression. The inflammatory milieu in PD is ideal for cancer cell seeding, migration, proliferation and immune escape. Understanding the interactions governing this attenuated anti-tumor immune response is vital to unveil unexplored preventive or therapeutic possibilities. Here we review the many commonalities between the oral-inflammatory microenvironment in PD and oral-inflammatory responses that are associated with OSCC progression, and how these conditions can act to promote and sustain the hallmarks of cancer.

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Assessment of Salivary Levels of RANKL and OPG in Aggressive versus Chronic Periodontitis

Cited by 33 publications

References 21 publications

The expression levels of MicroRNA-146a, RANKL and OPG after non-surgical periodontal treatment

The expression levels of MicroRNA-146a, RANKL and OPG after non-surgical periodontal treatment

Micro RNA-146a effect on Periodontitis is Independent on OPG/RANKL Axis

The Crossroads of Periodontitis and Oral Squamous Cell Carcinoma: Immune Implications and Tumor Promoting Capacities

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