title: Effect of ascorbic acid deficiency on primary and reparative dentinogenesis in non-ascorbate-synthesizing ODS rats.
abstract: Ascorbic acid is essential to the biosynthesis of collagen, the major organic matrix component of dentine. The ODS rat is a mutant strain of Wistar rat characterized by hereditary lack of L-gulono-gamma-lactone oxidase and thus is unable to synthesize ascorbic acid. ODS rats were given an ascorbic acid-free diet to investigate how ascorbic acid deficiency affects dentine formation in vivo. Histomorphometric analysis on their growing molars and incisors showed a significant reduction in both size and mineral apposition rate of dentine, as revealed by contact microradiography and fluorescent time-marking, respectively. A similar reduction in bone formation was simultaneously demonstrated in the mandible, confirming the previously reported osteopathic effects of ascorbic acid deficiency. When pulp inflammation was induced in lower first molars by making unsealed pulp exposures, specimens from control animals showed continuous deposition of an osteodentine-like tissue in the radicular pulp chamber; this type of mineralized tissue formation was greatly reduced in ascorbic acid-deprived animals. These results indicate that ascorbic acid deficiency hampers dentine formation under both physiological and pathological conditions of the dentine/pulp complex. ODS rats could be useful in investigating in vivo effects of ascorbic acid deficiency on the formation of dentine and other dental mineralized tissues.
authors.affiliation: Department of Endodontics, Faculty of Dentistry, Tokyo Medical and Dental University, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Ogawara
authors.forename: K
authors.initials: K
authors.lastname: Aoki
authors.forename: T
authors.initials: T
authors.lastname: Okiji
authors.forename: H
authors.initials: H
authors.lastname: Suda
mesh_terms: D000818:Animals; D001205:Ascorbic Acid / Q000096:biosynthesis; D001206:Ascorbic Acid Deficiency / Q000235:genetics / Q000503:physiopathology*; D003094:Collagen / Q000096:biosynthesis; D003786:Dental Pulp Cavity / Q000503:physiopathology; D003804:Dentin / Q000378:metabolism / Q000503:physiopathology; D003809:Dentin, Secondary / Q000378:metabolism / Q000503:physiopathology*; D003810:Dentinogenesis / Q000502:physiology*; D005456:Fluorescent Dyes; D007180:Incisor / Q000473:pathology / Q000503:physiopathology; D050544:L-Gulonolactone Oxidase; D008334:Mandible / Q000503:physiopathology; D008661:Metabolism, Inborn Errors / Q000235:genetics; D008852:Microradiography; D008903:Minerals / Q000378:metabolism; D008963:Molar / Q000473:pathology / Q000503:physiopathology; D009805:Odontogenesis / Q000502:physiology; D009811:Odontometry; D010012:Osteogenesis / Q000502:physiology; D011671:Pulpitis / Q000503:physiopathology; D051381:Rats; D011922:Rats, Mutant Strains; D017208:Rats, Wistar; D013401:Sugar Alcohol Dehydrogenases / Q000172:deficiency
chemical_list: D005456:Fluorescent Dyes; D008903:Minerals; D003094:Collagen; D013401:Sugar Alcohol Dehydrogenases; D050544:L-Gulonolactone Oxidase; D001205:Ascorbic Acid