title: The molecular and cellular effects of ageing on the periodontal ligament.
abstract: OBJECTIVE
  Many in vitro studies have investigated age-related biological changes in cells comprising the periodontium but the basic question of whether the periodontium can maintain its integrity with age remains unanswered. Thus, the aim of this study was to understand how, in the absence of disease, advancing age impacts the structure of the periodontium.
  
  
  METHODS
  Of 4, 10, 25, and 50-week-old mice were examined using histology and immunohistochemical analyses for cell proliferation, cell turnover, collagen quantity and quality, osteogenic markers, bone turnover, and cytokine expression.
  
  
  RESULTS
  The periodontal ligament (PDL) space shows a gradual decrease in width over the lifespan of the mice. Cell proliferation as well as the quantity and quality of collagen fibres decreased with age although cell density did not appear to be altered. Osteoprogenitor markers in the PDL maintained their expression with increasing age. Alkaline phosphatase (ALP) activity decreased, but osteoclast activity increased with age.
  
  
  CONCLUSIONS
  Ageing is associated with a decline in the quality and quantity of collagen and an increase in bone resorption, all of which can diminish the function of the periodontium even in the absence of disease.
authors.affiliation: Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford School of Medicine, Stanford, CA, USA; Department of Orthodontics, School of Dentistry & Dental Research Institute, Seoul National University, Seoul, Korea.
authors.forename: Won Hee
authors.initials: WH
authors.lastname: Lim
authors.forename: Bo
authors.initials: B
authors.lastname: Liu
authors.forename: Su-Jung
authors.initials: SJ
authors.lastname: Mah
authors.forename: Serafine
authors.initials: S
authors.lastname: Chen
authors.forename: Jill A
authors.initials: JA
authors.lastname: Helms
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000375:Aging / Q000235:genetics / Q000473:pathology*; D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D016723:Bone Remodeling / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000032:analysis; D002452:Cell Count; D016923:Cell Death / Q000502:physiology; D049109:Cell Proliferation; D003094:Collagen / Q000032:analysis / Q000737:chemistry; D050659:Core Binding Factor Alpha 1 Subunit / Q000032:analysis; D016207:Cytokines / Q000032:analysis; D016326:Extracellular Matrix Proteins / Q000032:analysis; D005347:Fibroblasts / Q000473:pathology; D000071235:Fibromodulin; D053582:Interleukin-1alpha / Q000032:analysis; D007527:Isoenzymes / Q000032:analysis; D019394:Ki-67 Antigen / Q000032:analysis; D051379:Mice; D010010:Osteoclasts / Q000473:pathology; D010012:Osteogenesis / Q000502:physiology; D053495:Osteopontin / Q000032:analysis; D010513:Periodontal Ligament / Q000737:chemistry / Q000166:cytology* / Q000378:metabolism; D011509:Proteoglycans / Q000032:analysis; D053245:RANK Ligand / Q000032:analysis; D000076182:Sp7 Transcription Factor; D000071681:Tartrate-Resistant Acid Phosphatase; D014157:Transcription Factors / Q000032:analysis; D016335:Zinc Fingers / Q000235:genetics
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; D050659:Core Binding Factor Alpha 1 Subunit; D016207:Cytokines; D016326:Extracellular Matrix Proteins; C000604332:Fmod protein, mouse; D053582:Interleukin-1alpha; D007527:Isoenzymes; D019394:Ki-67 Antigen; C498355:Mki67 protein, mouse; C082838:Postn protein, mouse; D011509:Proteoglycans; D053245:RANK Ligand; C493716:Runx2 protein, mouse; D000076182:Sp7 Transcription Factor; C479466:Sp7 protein, mouse; C506896:Spp1 protein, mouse; C505689:Tnfsf11 protein, mouse; D014157:Transcription Factors; D053495:Osteopontin; D000071235:Fibromodulin; D003094:Collagen; D000469:Alkaline Phosphatase; D000135:Acid Phosphatase; D000071681:Tartrate-Resistant Acid Phosphatase
keywords: age; collagen fibre; osteogenic factor; periodontal ligament; width