Overexpression of the receptor for resolvin E1 (ERV1) prevents early alveolar bone loss in leptin receptor deficiency-induced diabetes

Autores organización

• David Augusto Diaz Baez

  Autor

Autores

• Suárez L.J.
• Hasturk H.
• Tubero Euzebio Alves V.
• Van Dyke T.
• Kantarci A.

Unidades de investigación

• Unidad de Investigación Básica Oral UIBO

  

  Investigador

  Gloria Ines Lafaurie Villamil

Resumen

Background: This study was designed to test the hypothesis that the leptin receptor (LepR) regulates changes in periodontal tissues and that the overexpression of the receptor for resolvin E1 (ERV1) prevents age- and diabetes-associated alveolar bone loss. Methods: LepR-deficient transgenic (TG) mice were cross-bred with those overexpressing ERV1 (TG) to generate double-TG mice. In total, 95 mice were divided into four experimental groups: wild type (WT), TG, LepR deficient (db/db), and double transgenic (db/db TG). The groups were followed from 4 weeks up to 16 weeks of age. The natural progression of periodontal disease without any additional method of periodontitis induction was assessed by macroscopic and histomorphometric analyses. Osteoclastic activity was measured by tartrate-resistant acid phosphatase (TRAP) staining. Results: At 4 weeks, ERV1 overexpression prevented weight gain. From Week 8 onward, there was a significant increase in the weight of db/db mice with or without ERV1 overexpression compared to the WT mice, accompanied by an increase in glucose levels. By 8 weeks of age, the percentage of bone loss in the LepR deficiency groups was significantly greater compared to WT mice. ERV1 overexpression in the db/db TG mice prevented early alveolar bone loss; however, it did not impact the development of diabetic bone loss in aging mice after the onset of weight gain and diabetes. Conclusions: The findings suggest that the overexpression of ERV1 prevents LepR-associated alveolar bone loss during the early phases of periodontal disease by delaying weight gain, diabetes onset, and associated inflammation; however, LepR deficiency increases susceptibility to naturally occurring inflammatory alveolar bone loss as the animal ages, associated with excess weight gain, onset of diabetes, and excess inflammation. © 2024 American Academy of Periodontology.

Keywords

• alveolar bone loss; diabetes mellitus; leptin receptor deficiency; periodontitis; resolvin E1;Acid Phosphatase; Alveolar Bone Loss; Animals; Diabetes Mellitus, Experimental; Disease Progression; Eicosapentaenoic Acid; Isoenzymes; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Osteoclasts; Receptors, Leptin; Tartrate-Resistant Acid Phosphatase; Weight Gain; leptin receptor; protein; receptor; receptor for resolvin E1; unclassified drug; 5S,12R,18R-trihydroxy-6Z,8E,10E,14Z,16E-eicosapentaenoic acid; acid phosphatase; acid phosphatase tartrate resistant isoenzyme; Acp5 protein, mouse; icosapentaenoic acid; isoenzyme; leptin receptor; leptin receptor, mouse; aging; alveolar bone loss; animal experiment; animal model; animal tissue; Article; body weight gain; bone demineralization; bone radiography; cementoenamel junction; controlled study; diabetes mellitus; ERV1 gene; gene; gene overexpression; genotyping; glucose blood level; histology; morphometry; mouse; nonhuman; os