tetracycline and Hypocalcemia

The aetiological factors in enamel defects of a non-fluoride nature can be divided into systemic and local. The systemic factors comprise a variety of conditions: genetically determined, chromosomal anomalies, congenital defects, inborn errors of metabolism, neonatal disturbances, infectious diseases, neurological disturbances, endocrinopathies, nutritional deficiencies, nephropathies, enteropathies, liver diseases and intoxications. The genetically determined enamel defects include amelogenesis imperfecta, which may occur as an isolated phenomenon or as part of other disorders such as epidermolysis bullosa, pseudohypoparathyroidism and taurodontism. The congenital defects include heart disorders and unilateral facial hypoplasia and hypertrophy. Among the inborn errors of metabolism are: galactosaemia, phenylketonuria, alkaptonuria, erythropoietic porphyria and primary hyperoxaluria. Neonatal disturbances are important in the development of enamel hypoplasia, foremost among these are premature birth and hypocalcaemia. The latter causes postnatal hypoplasias, which, however, are never seen in breast-fed children. Haemolytic anaemia, mostly in conjunction with erythroblastosis foetalis, may cause enamel hypoplasia. In children with neurological disturbances a rather large number have enamel hypoplasias, and these changes may be a significant aid in neurological diagnosis. When the tetracyclines were introduced, many children had these drugs prescribed in the period when the teeth were undergoing mineralization. The result was a yellow-brown stain of the affected teeth. In recent years, however, there appears to have been a reduction in the incidence of tetracycline staining. As for local causes the most important are traumatic injuries and periapical osteitis of primary teeth.

Topics: Amelogenesis Imperfecta; Communicable Diseases; Congenital Abnormalities; Dental Enamel; Dental Enamel Hypoplasia; Fluorosis, Dental; Humans; Hypocalcemia; Tetracycline

Topics: Aged; Aminosalicylic Acids; Anti-Bacterial Agents; Berlin; Clinical Trials as Topic; Cycloserine; Drug Resistance, Microbial; Ethambutol; Humans; Hypocalcemia; Hypokalemia; Kidney Diseases; Middle Aged; Rifampin; Tetracycline; Tuberculosis, Pulmonary; Urea; Vision Disorders

The acute effects of parathyroid extract (PTE) were studied repeatedly in young dogs (prelabeled with 45Ca and [3H]tetracycline) during the development of calcium (Ca) and vitamin D deficiency. Blood Ca and radioactivity changes were monitored sequentially after subcutaneous PTE, injected seven times over 63 days. In control dogs, all sequential responses to acute PTE challenges were constant in both magnitude of increase and time at which maximum response occurred over the entire experiment. Under chronic Ca and D deficiency, plasma 25-hydroxyvitamin D in experimental dogs decreased continuously to very low levels at 63 days, whereas 1,25-dihydroxyvitamin D initially increased to a maximum at 32 days and thereafter decreased. In response to an acute challenge of PTE, dogs on the deficient diet for 3 and 10 days showed a greater response of blood Ca and 45Ca than the controls but subsequently showed a smaller response than controls after 49 and 63 days on the deficient diet. Compared with control dogs, the time of maximal response of blood Ca and 45Ca to PTE occurred much earlier in dogs that were on the deficient diet for 35-63 days. The blood [3H]tetracycline response (index of bone resorption) to exogenous PTE in the deficient dogs, however, was constant and similar to that of the control dogs during the entire period. The data suggest that the bone resorption response to PTE was normal in Ca- and D-deficient puppies with hypocalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Bone and Bones; Bone Resorption; Calcifediol; Calcium; Dogs; Humans; Hypocalcemia; Parathyroid Hormone; Tetracycline; Vitamin D; Vitamin D Deficiency

Topics: Animals; Bone Development; Bone Matrix; Bone Resorption; Calcium; Hyperparathyroidism, Secondary; Hypocalcemia; Male; Parathyroid Glands; Phosphorus; Rats; Tetracycline

Topics: Adrenal Cortex Hormones; Blood Protein Disorders; Capillaries; Colchicine; Epithelial Cells; Estrogens, Conjugated (USP); Female; Humans; Hydroxyurea; Hypocalcemia; Iodoquinol; Leukocytes; Methotrexate; Microcirculation; Microscopy, Electron; Middle Aged; Psoriasis; Serum Albumin; Skin; Tetracycline

Topics: Calcium; Dental Enamel Hypoplasia; Humans; Hypocalcemia; Tetracycline

Topics: Animals; Body Weight; Bone Development; Bone Resorption; Calcification, Physiologic; Calcium, Dietary; Computers; Epiphyses; Fluorescence; Hypocalcemia; Periosteum; Rats; Stress, Mechanical; Tetracycline; Tibia; Time Factors

Topics: Animals; Bone and Bones; Calcium; Dextrans; Female; Femur; Forelimb; Hindlimb; Hypocalcemia; Male; Osteoporosis; Parathyroid Glands; Phosphorus; Radiography; Rats; Tetracycline; Tibia

Topics: Animals; Autoradiography; Bone Resorption; Calcitonin; Calcium Isotopes; Cats; Epiphyses; Femur; Gelatin; Hyperparathyroidism, Secondary; Hypocalcemia; Microradiography; Nephrectomy; Osteogenesis; Parathyroid Glands; Phosphates; Swine; Tetracycline; Thyroidectomy

Quantitative histologic methods have been devised to measure several processes dealing with formation and mineralization of matrix and bone resorption. In vitamin D-deficient rats, the total osteoblastic matrix formation rate was 20% less and the total osteoclastic bone resorption rate was 80% more than in pair-fed control rats. These changes were found to be primarily because of changes in the rates of matrix formation and of bone resorption per unit area of forming or resorbing surfaces rather than to changes in the areas of these surfaces. The rate of maturation of osteoid and the rate of initial mineralization both were reduced to half of normal in the vitamin D-deficient rats. These variables related to matrix formation and mineralization were significantly correlated with the concentration of calcium but not with the concentration of phosphate in serum. The occurrence of hypocalcemia is interpreted as the consequence, both of reduced calcium absorption and of inadequate resorptive response of bone cells to homeostatic stimuli, such that, although bone resorption was greater than normal, it did not adequately compensate for the reduced intestinal absorption.

Topics: Animals; Bone and Bones; Bone Development; Bone Resorption; Calcification, Physiologic; Hypocalcemia; Microscopy, Fluorescence; Minerals; Phosphorus; Rats; Tetracycline; Vitamin D Deficiency