Effects of occlusal disharmony on cardiac fibrosis, myocyte apoptosis and myocyte oxidative DNA damage in mice

PLoS One. 2020 Jul 27;15(7):e0236547. doi: 10.1371/journal.pone.0236547. eCollection 2020.

Abstract

Occlusal disharmony leads to morphological changes in the hippocampus and osteopenia of the lumbar vertebra and long bones in mice, and causes stress. Various types of stress are associated with increased incidence of cardiovascular disease, but the relationship between occlusal disharmony and cardiovascular disease remain poorly understood. Therefore, in this work, we examined the effects of occlusal disharmony on cardiac homeostasis in bite-opening (BO) mice, in which a 0.7 mm space was introduced by cementing a suitable applicance onto the mandibular incisior. We first examined the effects of BO on the level of serum corticosterone, a key biomarker for stress, and on heart rate variability at 14 days after BO treatment, compared with baseline. BO treatment increased serum corticosterone levels by approximately 3.6-fold and the low frequency/high frequency ratio, an index of sympathetic nervous activity, was significantly increased by approximately 4-fold by the BO treatment. We then examined the effects of BO treatment on cardiac homeostasis in mice treated or not treated with the non-selective β-blocker propranolol for 2 weeks. Cardiac function was significantly decreased in the BO group compared to the control group, but propranolol ameliorated the dysfunction. Cardiac fibrosis, myocyte apoptosis and myocyte oxidative DNA damage were significantly increased in the BO group, but propranolol blocked these changes. The BO-induced cardiac dysfunction was associated with increased phospholamban phosphorylation at threonine-17 and serine-16, as well as inhibition of Akt/mTOR signaling and autophagic flux. These data suggest that occlusal disharmony might affect cardiac homeostasis via alteration of the autonomic nervous system.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis*
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism
  • Corticosterone / blood
  • DNA Damage*
  • Electrocardiography
  • Fibrosis
  • Mice
  • Mice, Inbred C57BL
  • Myocardium / metabolism
  • Myocardium / pathology*
  • Myocytes, Cardiac / cytology
  • Myocytes, Cardiac / metabolism
  • Oxidative Stress
  • Phosphorylation
  • Proto-Oncogene Proteins c-akt / metabolism
  • Proto-Oncogene Proteins c-bcl-2 / metabolism
  • Signal Transduction
  • Stress, Physiological*
  • TOR Serine-Threonine Kinases / metabolism

Substances

  • Proto-Oncogene Proteins c-bcl-2
  • mTOR protein, mouse
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • Corticosterone

Grants and funding

This work was supported by Japan Society for the Promotion of Science (JSPS) KAKENHI Grant [20K10305 to Dr. Kenji Suita, 20K10304 to Dr. Yoshiki Ohnuki, 17K17342 to Dr. Daisuke Umeki., 17K11977 to Dr. Megumi Nariyama., 19K24109 to Dr. Aiko Ito, 18K06862, 19H03657 to Dr. Satoshi Okumura]; the MEXT-Supported Program for the Strategic Research Foundation at Private Universities 2015-2019 (S1511018 to Dr. Satoshi Okumura); an Academic Contribution from Pfizer Japan (AC190821 to Dr. Satoshi Okumura); Research Promotion Grant from the Society for Tsurumi University School of Dental Medicine (28006 to Dr. Yuka Yagisawa). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. All authors approve of the contents and agree to coauthorship.