title: Chronic glycine treatment inhibits ligature-induced periodontal disease in Wistar rats.
abstract: OBJECTIVE
  Dysregulation of immune and stress responses plays a significant role for the development and progression of inflammatory diseases, including periodontal disease. The non-essential amino acid glycine modulates immune and central nervous system (CNS) responses, and has been shown to beneficially affect tissue destructive inflammatory conditions. The purpose of this study was to test the ability of orally administered glycine to influence periodontal disease progression, as well as immune and hypothalamic-pituitary-adrenal (HPA) responses following lipopolysaccharide stimulation.
  
  
  METHODS
  Glycine was supplied in the drinking water during the whole experiment to male Wistar rats, starting 3 days before the induction of experimental ligature-induced periodontal disease. Control rats were given tap water only. The periodontal breakdown was assessed after the ligatures had been in place for 34 days. Following intraperitonal lipopolysaccharide stimulation, concentrations of the proximal cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin-10, as well as the HPA axis-derived hormone corticosterone, were measured in blood serum.
  
  
  RESULTS
  Orally administered glycine significantly reduced periodontal bone loss as measured by digital X-rays (p = 0.007). Bone loss was negatively correlated with increased serum glycine, whereas no significant relationship was found with TNF-alpha, interleukin-10, or corticosterone.
  
  
  CONCLUSIONS
  Chronic ingestion of glycine supplied in the drinking water significantly reduced periodontal bone loss. No effect of glycine on immune and HPA-axis responses was revealed. Further studies are needed to clarify the mechanisms of action.
authors.affiliation: Department of Periodontology, Faculty of Dentistry, University of Oslo, Oslo, Norway. tbreivik@odont.uio.no
authors.forename: Torbjørn
authors.initials: T
authors.lastname: Breivik
authors.forename: Yngvar
authors.initials: Y
authors.lastname: Gundersen
authors.forename: Frode
authors.initials: F
authors.lastname: Fonnum
authors.forename: Per
authors.initials: P
authors.lastname: Vaagenes
authors.forename: Per Kristian
authors.initials: PK
authors.lastname: Opstad
mesh_terms: D016301:Alveolar Bone Loss / Q000188:drug therapy; D000818:Animals; D003345:Corticosterone / Q000097:blood; D004353:Drug Evaluation, Preclinical; D005998:Glycine / Q000097:blood / Q000627:therapeutic use*; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects; D016753:Interleukin-10 / Q000097:blood; D008026:Ligation; D008297:Male; D010510:Periodontal Diseases / Q000097:blood / Q000188:drug therapy* / Q000517:prevention & control; D010913:Pituitary-Adrenal System / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D018709:Statistics, Nonparametric; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D005998:Glycine; D003345:Corticosterone