Evaluation of <scp>DNA</scp> methylation of inflammatory genes following treatment of chronic periodontitis: A pilot case–control study

Asa’ad, Farah; Bollati, Valentina; Pagni, Giorgio; Castilho, Rogerio M.; Rossi, Eleonora; Pomingi, Francesca; Tarantini, Letizia; Consonni, Dario; Giannobile, William V.; Rasperini, Giulio

doi:10.1111/jcpe.12783

Cited by 27 publications

(30 citation statements)

References 51 publications

(78 reference statements)

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“…This is not surprising, as the expression of pro-inflammatory cytokines, and other inflammatory-related genes may be modulated by epigenetic mechanisms. [48][49][50] Furthermore, chronic inflammation triggered by various factors can induce aberrant DNA methylation, which in some cases may initiate cancer-specific epigenetic changes in epithelial cells. [51][52][53] In humans, an overlap between the DNA methylation pattern of chronic periodontitis and oral SCC has been previously reported.…”

Section: Discussionmentioning

confidence: 99%

Analysis of DNA methylation and TP53 mutational status for differentiating feline oral squamous cell carcinoma from non‐neoplastic mucosa: A preliminary study

Renzi

Morandi

Lenzi

et al. 2020

Vet Comparative Oncology

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Feline oral squamous cell carcinoma (FOSCC) is characterized by high local invasiveness and early bone lysis. The late diagnosis largely limits the efficacy of therapy and increases treatment-related morbidity. The aim of this exploratory study was to assess the methylation pattern of 10 candidate genes and TP53 mutational status in histologic samples of FOSCC. Results were compared with normal oral mucosa and oral inflammatory lesions, in order to establish a gene panel for FOSCC detection. For 10 cats, the above analyses were also performed on oral brushing samples, in order to explore the utility of these methods for screening purposes. Thirty-one FOSCC, 25 chronic inflammatory lesions and 12 controls were included. TP53 mutations were significantly more frequent in the FOSCC (68%) than in the non-neoplastic oral mucosa (3%; P <.001). Based on lasso regression analysis, a step-wise algorithm including TP53, FLI1, MiR124-1, KIF1A and MAGEC2 was proposed. The algorithm allowed to differentiate FOSCC with 94% sensitivity and 100% specificity (accuracy, 97%). When applying the proposed algorithm on 10 brushing samples, accuracy decreased to 80%. These results indicate that the altered DNA methylation of specific genes is present in FOSCC, together with a significant proportion of TP53 mutations. Such alterations are infrequent in normal oral mucosa and chronic stomatitis in cats, suggesting their involvement in feline oral carcinogenesis and their utility as diagnostic biomarkers. Further studies on a high number of brushing samples will be needed to assess the utility of a screening test for the early detection of FOSCC.

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Section: Discussionmentioning

confidence: 99%

Analysis of DNA methylation and TP53 mutational status for differentiating feline oral squamous cell carcinoma from non‐neoplastic mucosa: A preliminary study

Renzi

Morandi

Lenzi

et al. 2020

Vet Comparative Oncology

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“…Studies on DNA methylation in periodontal tissues identified hypomethylation profiles within the IFN‐γ , IL‐6 , and TNF‐α promoters that are associated with increased IFN‐γ, IL‐6, and TNF‐α transcription in gingival biopsies from patients with chronic PD . Interestingly, it was recently reported that periodontal therapy can reduce methylation status of prostaglandin‐endoperoxide synthase 2 (PTGS2) but not IFN‐γ and TNF‐α at healthy and PD sites over time . Despite its limitations in sample size, different sampling sites per time point and relatively short follow‐up, this study suggests that local disease activity influences the epigenetics of the tissues, which may be modulated by environmental factors, including the microbiota.…”

Section: Mac Functions In Inflammation Resolution and Osteoimmunologymentioning

confidence: 95%

Macrophage immunomodulation in chronic osteolytic diseases—the case of periodontitis

Sima

Viniegra

Glogauer

2018

Journal of Leukocyte Biology

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Periodontitis (PD) is a chronic osteolytic disease that shares pathogenic inflammatory features with other conditions associated with nonresolving inflammation. A hallmark of PD is inflammation‐mediated alveolar bone loss. Myeloid cells, in particular polymorphonuclear neutrophils (PMN) and macrophages (Mac), are essential players in PD by control of gingival biofilm pathogenicity, activation of adaptive immunity, as well as nonresolving inflammation and collateral tissue damage. Despite mounting evidence of significant innate immune implications to PD progression and healing after therapy, myeloid cell markers and targets for immune modulation have not been validated for clinical use. The remarkable plasticity of monocytes/Mac in response to local activation factors enables these cells to play central roles in inflammation and restoration of tissue homeostasis and provides opportunities for biomarker and therapeutic target discovery for management of chronic inflammatory conditions, including osteolytic diseases such as PD and arthritis. Along a wide spectrum of activation states ranging from proinflammatory to pro‐resolving, Macs respond to environmental changes in a site‐specific manner in virtually all tissues. This review summarizes the existing evidence on Mac immunomodulation therapies for osteolytic diseases in the broader context of conditions associated with nonresolving inflammation, and discusses osteoimmune implications of Macs in PD.

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“…As such, these epigenetically altered tissues subsequent to tooth extraction may differ from those not exposed to epigenetic cues such as histone deacetylation or DNA hypermethlyation. 23,24 This connection could be the missing link between periodontitis and peri-implantitis and could serve as a rationale for why patients with a history of periodontal disease, even with enhanced oral hygiene measures, should have more intense monitoring. This theory needs to be tested, given the very limited information available on epigenetic mechanisms and the initiation and progression of peri-implantitis.…”

mentioning

confidence: 99%

Editorial Epigenetics: A Missing Link Between Periodontitis and Peri-implantitis?

Monje¹,

Asa’ad²,

Larsson³

et al. 2018

Int J Periodontics Restorative Dent

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Evaluation of DNA methylation of inflammatory genes following treatment of chronic periodontitis: A pilot case–control study

Cited by 27 publications

References 51 publications

Analysis of DNA methylation and TP53 mutational status for differentiating feline oral squamous cell carcinoma from non‐neoplastic mucosa: A preliminary study

Analysis of DNA methylation and TP53 mutational status for differentiating feline oral squamous cell carcinoma from non‐neoplastic mucosa: A preliminary study

Macrophage immunomodulation in chronic osteolytic diseases—the case of periodontitis

Editorial Epigenetics: A Missing Link Between Periodontitis and Peri-implantitis?

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