Lead Intoxication Under Environmental Hypoxia Impairs Oral Health

Abstract

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.

Epidemiologic evaluation of Nhanes for environmental Factors and periodontal disease

“…Terrizzi et al ., have reported that elevated lead levels under hypoxia induces alveolar bone resorption and periodontitis 47 . More recently they demonstrated that iNOS and PGE 2 levels are altered by lead and hypoxia as inflammatory responses that would contribute to damage of the periodontium 48 . Furthermore, the lead levels investigated in these previous studies generally targeted levels that have been shown in blood to have substantial neurotoxicity (≥10 µg/dL), although levels of >5 µg/dL are considered deleterious 49 .…”

Environmental lead effects on gene expression in oral epithelial cells

“…The original premise of the study was based upon data regarding elevated blood lead levels and an increased risk of periodontitis across populations . Thus, we hypothesized that increased lead levels would stimulate proinflammatory responses in cells of the periodontium that might contribute to the biologic dysregulation of the disease.…”

“…110,111 The original premise of the study was based upon data regarding elevated blood lead levels and an increased risk of periodontitis across populations. 29,34,36,112,113 Thus, we hypothesized that increased lead levels would stimulate proinflammatory responses in cells of the periodontium that might contribute to the biologic dysregulation of the disease. Interestingly, of the large number of genes involved in host responses, which were expressed by the oral epithelial cells and affected by treatment with biofilms, a rather limited array was altered in expression by environmental lead.…”

“…El‐Said et al reported that chronic occupational exposure of workers to lead resulted in increased blood lead levels and a significant negative impact on oral health. Finally, studies using a rat model reported that elevated lead levels elicited molecular changes in inflammatory responses that accompanied alveolar bone resorption . In translational research, additional studies are required to identify a causative relationship of blood lead levels to the severity of the periodontitis, age of onset and response to therapy.…”

“…Finally, studies using a rat model reported that elevated lead levels elicited molecular changes in inflammatory responses that accompanied alveolar bone resorption. 35,36 In translational research, additional studies are required to identify a causative relationship of blood lead levels to the severity of the periodontitis, age of onset and response to therapy. While various reports have indicated that elevated lead levels within a cellular environment alters normal functions, these in vitro studies generally focused on neuronal cell targets 37,38 and generally examined blood lead levels with substantial neurotoxicity.…”