Sasaki T, Ramamurthy N S, Golub L M
Second Department of Oral Anatomy, School of Dentistry, Showa University, Tokyo, Japan.
J Biol Buccale. 1990 Sep;18(3):215-26.
Insulin-deficient, adult, diabetic rats were administrated a tetracycline (either minocycline or a chemically-modified non-antimicrobial tetracycline: CMT) by oral gavage over a 3-week period. Untreated diabetic and non-diabetic rats served as controls. On day 21, all rats received an intravenous injection of 3H-proline, as a radioprecursor of procollagen in bone, dentine and periodontal ligament (PDL) or of amelogenin in enamel; perfusion fixation with an aldehyde mixture was carried out at 20 minutes and 4 hours after isotope injection. The parietal bones (calvaria), mandibules including molars, and lower incisors of these rats were dissected and processed for light microscopic autoradiography to study 3H-proline utilization by osteoblasts, PDL fibroblasts, odontoblasts and ameloblasts. In the control rats, at 20 minutes after 3H-proline injection, silver grains of labeled precursor were detected in the osteoblasts of the periosteal surfaces of the parietal bones. At the 4 hour time period, although some radioprecursor was still present in the osteoblasts, most had progressed to the osteoid matrix. In contrast, the flattened bone-lining cells in the untreated diabetics showed minimal uptake and secretion of labeled proline at both time periods. In both minocycline- and CMT-treated diabetic rats, the labeled proline was localized in the osteoblasts and the osteoid in a pattern reminiscent of that seen in the control rats at both time periods. Of interest, CMT administration appeared to increase the labeling of the osteoid matrix more than minocycline treatment. In non-diabetic control rats, the PDL fibroblasts exhibited a polarized elongated profile and incorporated and secreted radioprecursor similar to that described for the osteoblasts in these animals. The PDL fibroblasts in the untreated diabetics lost their regular arrangement and incorporated little if any 3H-proline; once again, tetracycline administration appeared to normalize, at least in part, the structure and 3H-proline incorporation by these connective tissue cells. In contrast, diabetes and tetracycline administration did not affect the incorporation and secretion of radioprecursor by odontoblasts and secretory ameloblasts during tooth development.
将胰岛素缺乏的成年糖尿病大鼠通过灌胃给予四环素(米诺环素或化学修饰的非抗菌四环素:CMT),持续3周。未治疗的糖尿病大鼠和非糖尿病大鼠作为对照。在第21天,所有大鼠静脉注射3H-脯氨酸,其作为骨、牙本质和牙周韧带(PDL)中前胶原或釉质中釉原蛋白的放射性前体;在同位素注射后20分钟和4小时用醛混合物进行灌注固定。解剖这些大鼠的顶骨(颅骨)、包括磨牙的下颌骨和下切牙,并进行处理以用于光学显微镜放射自显影,以研究成骨细胞、PDL成纤维细胞、成牙本质细胞和成釉细胞对3H-脯氨酸的利用情况。在对照大鼠中,3H-脯氨酸注射后20分钟,在顶骨骨膜表面的成骨细胞中检测到标记前体的银颗粒。在4小时时间段,尽管一些放射性前体仍存在于成骨细胞中,但大多数已进入类骨质基质。相比之下,未治疗的糖尿病大鼠中扁平的骨衬细胞在两个时间段内对标记脯氨酸的摄取和分泌都很少。在米诺环素和CMT治疗的糖尿病大鼠中,标记的脯氨酸在成骨细胞和类骨质中的定位模式在两个时间段内都让人想起对照大鼠中的情况。有趣的是,CMT给药似乎比米诺环素治疗更能增加类骨质基质的标记。在非糖尿病对照大鼠中,PDL成纤维细胞呈现极化的细长形态,并摄取和分泌与这些动物中成骨细胞类似的放射性前体。未治疗的糖尿病大鼠中的PDL成纤维细胞失去了规则排列,几乎不摄取3H-脯氨酸;同样,四环素给药似乎至少部分地使这些结缔组织细胞的结构和3H-脯氨酸摄取恢复正常。相比之下,糖尿病和四环素给药在牙齿发育过程中不影响成牙本质细胞和分泌性成釉细胞对放射性前体的摄取和分泌。