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Advanced Dental Care 2018 Dentistry and Craniofacial Research
ISSN: 2576-392X Page 18
October 08-09, 2018
Moscow, Russia
26th International Conference on
Advanced Dental Care
Diabetic mellitus is a well-known systemic disease to
affect periodontal tissues behavior. However, underlying
mechanism of how this alters the alveolar bone tissue
homeostasis in a physiological condition or even under
a biophysical force loading such as orthodontic force
application is unknown. This study investigated the effect of
hyperglycaemia itself or glucose metabolites on biophysical
force-induced periodontal tissue remodelling. Alterations of
two key factors for the altered alveolar bone remodelling were
hypothesized: vascular endothelial growth factor (VEGF) and
colony stimulating factor-1 (CSF-1). The alteration mechanism
was investigated by examining the effects of hyperglycaemia
and advanced glycation end products (AGE) and their receptor
machineries. In vivo tissue responses were evaluated by
applying orthodontic appliances to molars in streptozotocin-
induced hyperglycaemic rats. Morphological features were
examined by light microscopy and immunofluorescence and
the gene alteration was determined by real-time RT-PCR. Also,
the in vitro effect of hyperglycaemia itself and biophysical
forces in a hyperglycaemic conditionwere determined in human
primary periodontal ligament (PDL) cells and mouse bone
marrow stromal cells. In vivo: In diabetic rats, tissue responses
were histologically characterized by augmented angiogenesis
in the PDL and additional undermining (or indirect) osteoclastic
bone resorption from bone marrow surface. By diabetes itself,
CSF-1, VEGF, AGE and AGER mRNA levels were upregulated,
whereas changes in expression of DDOST, a decoy receptor
for AGE and AGE-detoxifying Glo1 were not significant.
VEGF expression in the PDL was enhanced in diabetic rats.
Biophysical force-induced tooth movement (BTM) at day 6 was
augmented in diabetic rats, compared with normoglycemic
rats. In vitro: A hyperglycaemic condition (25 mM) itself
downregulated the VEGF and AGER transcription in human
PDL cells, compared with a normoglycemic condition (5 mM),
whereas (glucose transporter 1) Glut-1 and CSF-1 were not
varied. Furthermore, this hyperglycaemic condition decreased
RANKL/OPG ratio and inhibited osteoclast genesis in mouse
bone marrow stromal cells. In contrast, N-acetyl glucosamine
or PUGNAC, an OGA (β-D-N acetylglucosaminidase) inhibitor
treatment stimulated osteoclast genesis. Advanced glycation
end products and N-acetyl glucosamine upregulated the
expression of VEGF, CSF-1, receptors for AGE (AGER) and
Glut1 at specific time points. The VEGF and CSF-1 mRNA in
PDL cells was upregulated by either compression or tension
force and moreover, this upregulation was more altered at
the high glucose or glucose metabolites-treated conditions,
compared with a normoglycemic condition. This study
suggested that diabetic hyperglycaemia–induced metabolic
end products may alter periodontal tissue remodelling due to
augmented angiogenesis and macrophage activation and this
alteration can be further altered by biophysical forces including
orthodontic force.
Biography
Sun Hun Kim completed his DDS and MS., PhD from Chonnam National
University, School of Dentistry, Korea in the year 1980-1991. He is a Visiting
professor in UCSF medical school, USA; He is a Dean in School of Dentistry,
ChonnamNational University, Korea in 2013. He is a Head of Dental Science
Research Institute, School of Dentistry, Chonnam National University, Korea
from 2013. And also a professor in the Department of Oral Anatomy, school
of dentistry, Chonnam National University, Korea from 1989.
Alterations of VEGF and CSF-1 in periodontal
tissue remodeling following biophysical force
loading in hyperglycemia
Sun Hun Kim, SuYoung Lee, Jung Sun Moon and Min Seok Kim
Chonnam National University, Republic of South Korea
Sun Hun Kim et al., Dent Craniofac Res 2018, Volume 3
DOI: 10.21767/2576-392X-C4-011