Periostin is essential for the integrity and function of the periodontal ligament during occlusal loading in mice.
BACKGROUND
The ability of the periodontal ligament (PDL) to absorb and distribute forces is necessary for periodontal homeostasis. This adaptive response may be determined, in part, by a key molecule, periostin, which maintains the integrity of the PDL during occlusal function and inflammation. Periostin is primarily expressed in the PDL and is highly homologous to betaig-H3 (transforming growth factor-beta [TGF-beta] inducible gene). Cementum, alveolar bone, and the PDL of periostin-null mice dramatically deteriorate following tooth eruption. The purpose of this study was to determine the role of periostin in maintaining the functional integrity of the periodontium.


METHODS
The periodontia from periostin-null mice were characterized followed by unloading the incisors. The effect of substrate stretching on periostin expression was evaluated using a murine PDL cell line. Real-time reverse transcription-polymerase chain reaction was used to quantify mRNA levels of periostin and TGF-beta. TGF-beta1 neutralizing antibodies were used to determine whether the effects of substrate stretching on periostin expression are mediated through TGF-beta.


RESULTS
Severe periodontal defects were observed in the periostin-null mice after tooth eruption. The removal of masticatory forces in periostin-null mice rescue the periodontal defects. Periostin expression was increased in strained PDL cells by 9.2-fold at 48 hours and was preceded by a transient increase in TGF-beta mRNA in vitro. Elevation of periostin in response to mechanical stress was blocked by the addition of 2.5 ng/ml neutralizing antibody to TGF-beta1, suggesting that mechanical strain activates TGF-beta to have potential autocrine effects and to increase periostin expression.


CONCLUSIONS
Mechanical loading maintains sufficient periostin expression to ensure the integrity of the periodontium in response to occlusal load.
Rios
H F
HF
Department of Periodontics and Oral Medicine, School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA. hrios@umich.edu
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Giannobile
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Bonewald
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Conway
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Feng
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D016301:Alveolar Bone Loss / Q000209:etiology; D000565:Ameloblasts / Q000473:pathology; D000818:Animals; D019898:Autocrine Communication / Q000502:physiology; D001696:Biomechanical Phenomena; D001732:Bite Force; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000502:physiology*; D002460:Cell Line; D003739:Dental Cementum / Q000473:pathology; D005347:Fibroblasts / Q000473:pathology; D007091:Image Processing, Computer-Assisted / Q000379:methods; D007150:Immunohistochemistry; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D017622:Periodontal Attachment Loss / Q000209:etiology; D010513:Periodontal Ligament / Q000502:physiology*; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012391:Root Resorption / Q000209:etiology; D013314:Stress, Mechanical; D014057:Tomography, X-Ray Computed / Q000379:methods; D014078:Tooth Eruption / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000032:analysis / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000037:antagonists & inhibitors
D015815:Cell Adhesion Molecules; C082838:Postn protein, mouse; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1