Alveolar bone loss associated to periodontal disease in lead intoxicated rats under environmental hypoxia

Terrizzi, Antonela Romina; Fernández‐Solari, Javier; Lee, Ching M.; Bozzini, Clarisa; Mandalunis, Patricia; Elverdín, Juan C.; Conti, Maria; Martínez, María Pilar

doi:10.1016/j.archoralbio.2013.06.010

Cited by 23 publications

(19 citation statements)

References 23 publications

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“…Rats with LPS‐induced periodontitis exhibited a reduced total salivary response to pilocarpine and higher values of PGE 2 and NO in the SMG. It is well known that SMG is the major contributor to total saliva production in the oral cavity and that salivary secretion is an essential factor in the establishment and progression of oral infectious processes 30 , 45 . The influence of periodontitis on the pathophysiology of the SMG was evident in the present study.…”

Section: Discussionsupporting

confidence: 60%

“…Immediately after sacrifice of the rats, hemimandibles were resected, defleshed, and stained with 1% aqueous methylene blue to delineate the cemento‐enamel junction (CEJ) and the alveolar crest (AC) 29 . A stereomicroscope ‖ and stainless hardened digital caliper ¶ were used to measure three buccal and three lingual/palatal distances (mesial, central, and distal), from the CEJ to the AC 30 . The sum of the three distances of each side of molars was used as a measure of alveolar bone loss (ABL) in millimeters.…”

Section: Methodsmentioning

confidence: 99%

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Anti‐Inflammatory and Osteoprotective Effects of Cannabinoid‐2 Receptor Agonist HU‐308 in a Rat Model of Lipopolysaccharide‐Induced Periodontitis

Ossola

Surkin

Mohn

et al. 2016

Journal of Periodontology

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Section: Discussionsupporting

confidence: 60%

Section: Methodsmentioning

confidence: 99%

Anti‐Inflammatory and Osteoprotective Effects of Cannabinoid‐2 Receptor Agonist HU‐308 in a Rat Model of Lipopolysaccharide‐Induced Periodontitis

Ossola

Surkin

Mohn

et al. 2016

Journal of Periodontology

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“…Many epidemiological studies reported that the incidence of periodontitis in residents living in areas with altitudes over 4000 meters was significantly higher than that in residents living at sea level (Jian et al, 2014). Animal experiments also revealed that hypoxia may induce severe periodontitis (Xiao et al, 2012;Terrizzi et al, 2013). The abovementioned evidence showed that hypoxic microenvironments may contribute to periodontal cells' inability to regenerate.…”

Section: Introductionmentioning

confidence: 86%

Hypoxia enhances periodontal ligament stem cell proliferation via the MAPK signaling pathway

He¹,

Cao²,

Zhang³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. There is high incidence of periodontal disease in highaltitude environments; hypoxia may influence the proliferation and clone-forming ability of periodontal ligament stem cells (PDLSCs). The MAPK signaling pathway is closely correlated with cell proliferation, differentiation, and apoptosis. Thus, we isolated and cultured PDLSCs under hypoxic conditions to clarify the impact of hypoxia on PDLSC proliferation and the underlying mechanism. PDLSCs were separated and purified by the limiting dilution method and identified by flow cytometry. PDLSCs were cultured under hypoxic or normoxic conditions to observe their cloning efficiency. PDLSC proliferation at different oxygen concentrations was evaluated by MTT assay. Expression of p38/MAPK and MAPK/ERK signaling pathway members was detected by western blotting. Inhibitors for p38/MAPK or ERK were applied to PDLSCs to observe their impacts on clone formation and proliferation. Isolated PDLSCs exhibited typical stem cell morphological characteristics, strong abilities of globular clone formation and proliferation, and upregulated expression of mesenchymal stem cell markers. Stem cell marker expression was not statistically different between PDLSCs cultured under hypoxia and normoxia (P > 0.05). The clone number in the hypoxia group was significantly higher than that in the control (P < 0.05). PDLSC proliferation under hypoxia was higher than that of the control (P < 0.001). p38 and ERK1/2 phosphorylation in hypoxic PDLSCs was markedly enhanced compared to that in the control (P < 0.05). Either P38/MAPK inhibitor or ERK inhibitor treatment reduced clone formation and proliferation. Therefore, hypoxia enhanced PDLSC clone formation and proliferation by activating the p38/MAPK and ERK/MAPK signaling pathways.

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“…Environmental hypoxia increased iNOS activity in gingival tissue of rats, in agreement with the alveolar bone loss we observed under such condition. On the other hand, chronic lead intoxication did not significantly enhance iNOS activity in gingival tissue, according to the absence of bone damage previously observed (Terrizzi et al, 2013). It has been suggested that the increased expression of iNOS leads to the production of NO, a free radical that might be involved in bone destruction by modulating metalloproteinase synthesis (Jung et al, 2013).…”

Section: Discussionmentioning

confidence: 70%

“…Previously reported studies from this laboratory suggested that chronic intoxication with Pb in immature rats under hypoxic conditions impaired growth parameters, induced negative effects on mandibular structural properties that predispose to fractures, and produced alveolar and interradicular bone loss (Conti et al, 2012). Additionally, these environmental variables aggravated the pathophysiological alterations produced by periodontal disease when experimental periodontitis was induced (Terrizzi et al, 2013). Chronic exposure to Pb significantly affects oral health among exposed workers, increasing the prevalence of periodontal diseases (gingivitis and periodontitis), caries, missing and filled teeth, and dental LEAD AND HYPOXIA IMPAIR ORAL HEALTH 1305 abrasions (Won et al, 2013;El-Said et al, 2008).…”

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confidence: 95%

Lead Intoxication Under Environmental Hypoxia Impairs Oral Health

Terrizzi

Fernández‐Solari

Lee

et al. 2014

Journal of Toxicology and Environmental Health, Part A

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We have reported that chronic lead intoxication under hypoxic environment induces alveolar bone loss that can lead to periodontal damage with the subsequent loss of teeth. The aim of the present study was to assess the modification of oral inflammatory parameters involved in the pathogenesis of periodontitis in the same experimental model. In gingival tissue, hypoxia increased inducible nitric oxid synthase (iNOS) activity (p < .01) and meanwhile lead decreased prostaglandin E2 (PGE2) content (p < .05). In submandibular gland (SMG), iNOS activity was enhanced by lead and PGE2 content was increased by both lead and hypoxia (p < .01) and even more by combined treatments (p < .001). In the SMG, hypoxia stimulated angiogenesis (p < .01) with blood extravasation. Adrenal glands were 22% bigger in those animals exposed to lead under hypoxic conditions. Results suggest a wide participation of inflammatory markers that mediate alveolar bone loss induced by these environmental conditions. The lack of information regarding oral health in lead-contaminated populations that coexist with hypoxia induced us to evaluate the alteration of inflammatory parameters in rat oral tissues to elucidate the link between periodontal damage and these environmental conditions.

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Alveolar bone loss associated to periodontal disease in lead intoxicated rats under environmental hypoxia

Cited by 23 publications

References 23 publications

Anti‐Inflammatory and Osteoprotective Effects of Cannabinoid‐2 Receptor Agonist HU‐308 in a Rat Model of Lipopolysaccharide‐Induced Periodontitis

Anti‐Inflammatory and Osteoprotective Effects of Cannabinoid‐2 Receptor Agonist HU‐308 in a Rat Model of Lipopolysaccharide‐Induced Periodontitis

Hypoxia enhances periodontal ligament stem cell proliferation via the MAPK signaling pathway

Lead Intoxication Under Environmental Hypoxia Impairs Oral Health

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