The more slowly developing dentition, in myxoedema congenitale (a- and hypo-function of thyroid gland), makes the teeth resistant to caries. Con‑trary to general pediatric opinion, the author’s findings indicate that caries is not a symptom of myxoedema congenitale, although mouth hygiene in this disease is unsatisfactory.
Frequency of caries in permanent teeth is greatest among those having myxoedema congenitale who, since childhood, received thyroidal medicinal treatment. The total caries percentage (30.04 percent of teeth) among the author’s cases is lower than for ordinary people. In the oldest diagnosed case of myxoedema congenitale in Finland (age 52 years, 23 teeth in place) only 8.7 percent of the teeth are carious. In many myxedema patients, as late as age 30, the persisting milk teeth are often free from caries.
Reference: Ann. Acad. Sci. Fennicae, Series A, 1934.
YOUNGBURG, GUY E.: Medical School, University of Buffalo, Buffalo, N. Y. (May 9, 1938).
There is no reason to believe that phosphate in saliva is a factor in caries. There is no characteristic difference in ammonia content in salivas of cariesimmunes and caries-susceptibles, and no indication that ammonia, per se, is a determining factor in susceptibility to caries.
Of the phosphorus in saliva of normal persons, of persons having caries, and of nephritics, 96 percent is present as inorganic orthophosphate ; the remainder is in protein combination. Inorganic phosphorus increases in saliva slightly but definitely with age. There is appreciable variation for the same individual during the day and on different days. In phosphate content, the average saliva of persons having caries (or nephritis) was not appreciably different from normals, but there were greater variations. Average values for inorganic phosphorus per 100 cc. of saliva are : normal, 17.50 mgm.; caries, 18.13 mgm.; nephritis, 17.54 mgm. Amounts of ammonia in saliva of normal individuals ranged from 1.28 mgm. to 13.66 mgm. (ammonia N) per 100 cc. Meals nearly always caused striking decrease in salivary ammonia; bicarbonate ingestion also diminished it. The effect of ingesting ammonium chloride was neither striking nor constant ; that of holding various stimulating substances in the mouth varied with different individuals. Change from normal to acid- or alkaline-diet, for a week, had little influence on salivary ammonia, but it tended to decrease on alkaline diet. During protracted secretion (two subjects), non-mucin-N and ammonia-N of saliva diminished considerably, and ran nearly parallel. Ammonia-N in saliva of 45 individuals having active caries varied from 3.57 to 16.96 mgm. per 100 cc. There is no relation between amount of ammonia in saliva and the ” alkaline tide.” The body mechanism that regulates concentration of ammonia in saliva has not been elucidated.
References: J. Den. Res., 12, 267, 1932 ; 15, 247, 1936.