IADR Abstract Archives
D-Galactose and Obesity Induce Aging and Pathologies in Dental Pulp
Objectives: We previously demonstrated that both D-galactose (Dgal) induced aging and obesity caused pathological conditions as indicated by increased inflammation and impaired mitochondrial function in several vital organs. We also reported that Dgal-induced aging aggravated obesity-induced bone dyshomeostasis. However, the dental pulp pathologies including aging, inflammation, and mitochondrial dynamics imbalance in Dgal-induced aging, obesity and combined conditions still remain unclear. This study aimed to investigate the effects of Dgal-induced aging and high-fat diet (HFD)-induced obesity and combined conditions on aging, inflammation, mitochondrial dynamics, apoptosis, and mitophagy in dental pulp of male Wistar rats.
Methods: Twenty-four male Wistar rats were randomly fed with normal diet (ND) or HFD for 20 weeks. At week 13, each dietary group (ND or HFD) was subdivided into 2 subgroups (n=6/subgroup). Each subgroup was treated with either vehicle (0.9% normal saline, subcutaneous injection, once daily) or Dgal (150 mg/kg/day, subcutaneous injection, once daily) for 8 weeks. At the end of protocol, all rats were sacrificed. The pulp tissues from rats’ incisors were collected for investigation of aging, inflammation, mitochondrial dynamics, apoptosis, and mitophagy.
Results: Pulpal tissues of Dgal-treated HFD-fed rats significantly 1) increased aging markers, including p16 and RAGE expressions; 2) increased inflammatory levels, such as TNF-α, IL-1β, and IL-6 expressions; 3) imbalanced mitochondrial dynamics, as indicated by decreased mitochondrial fusion proteins (MFN1, 2); 3) increased pulpal apoptosis: increased Bax/Bcl-2 ratio, and 4) impaired mitophagy as indicated by decreased the expressions of PINK1 and Parkin, when compared to vehicle-treated ND-fed rats (p<0.05), as shown in Table 1. Dgal administration and HFD-induced obesity alone did not induce aging in dental pulp, however obese condition led to increase pulpal inflammation and pulpal apoptosis, when compared to vehicle-treated ND-fed rats (p<0.05).
Conclusions: These findings suggest that Dgal-induced aging aggravates obesity-induced pulpal pathologies.
Methods: Twenty-four male Wistar rats were randomly fed with normal diet (ND) or HFD for 20 weeks. At week 13, each dietary group (ND or HFD) was subdivided into 2 subgroups (n=6/subgroup). Each subgroup was treated with either vehicle (0.9% normal saline, subcutaneous injection, once daily) or Dgal (150 mg/kg/day, subcutaneous injection, once daily) for 8 weeks. At the end of protocol, all rats were sacrificed. The pulp tissues from rats’ incisors were collected for investigation of aging, inflammation, mitochondrial dynamics, apoptosis, and mitophagy.
Results: Pulpal tissues of Dgal-treated HFD-fed rats significantly 1) increased aging markers, including p16 and RAGE expressions; 2) increased inflammatory levels, such as TNF-α, IL-1β, and IL-6 expressions; 3) imbalanced mitochondrial dynamics, as indicated by decreased mitochondrial fusion proteins (MFN1, 2); 3) increased pulpal apoptosis: increased Bax/Bcl-2 ratio, and 4) impaired mitophagy as indicated by decreased the expressions of PINK1 and Parkin, when compared to vehicle-treated ND-fed rats (p<0.05), as shown in Table 1. Dgal administration and HFD-induced obesity alone did not induce aging in dental pulp, however obese condition led to increase pulpal inflammation and pulpal apoptosis, when compared to vehicle-treated ND-fed rats (p<0.05).
Conclusions: These findings suggest that Dgal-induced aging aggravates obesity-induced pulpal pathologies.