2.5. Acid-base balance and teeth
There are numerous similarities between the osteoblasts and the odontoblasts. The principal difference between the osteogenesis and the odontogenesis lies in the fact that no remodelling nor osteoclast-like cells exist in the dentine (Fig 1.). However, microorganisms seem to be capable of destroying enamel and dentine structure by a direct action resembling osteoclasts dissolving bone (Brännström et al. 1980, Luoma et al.1984).
Figure 1. Schematic drawing of the dentine (left) and the bone (right). Gray area = mineralized tissue. Striped gray area = unmineralized new dentine (predentine) / bone (osteoid). Left: carious dentine and cariogenic bacteriae up, odontoblast cells (pulp) down. Odontoblast processes in tubules. Right: Active (round) and passive (flat) osteoblasts surround the bone. Osteocytes are located inside the bone. They are communicating via the bone canaliculi with each other and with the osteoblasts. In left upper corner, multinucleated osteoclast resorbs the bone.
The odontoblasts are partly under the same metabolic regulation as the osteoblasts (Linde & Goldberg 1993), and therefore the formation of the bone and the dentine are probably regulated by similar factors. Thus there is a reason to assume that the changes in acid-base balance have effects on dentine metabolism as they do on the bone. Indeed, in previous studies we have found that chronic metabolic acidosis slowed down the rate of dentine formation and the general body growth in the young rats (Bäckman et al. 1996).
In humans, several congenital chronic diseases, causing acid-base disturbances, result into changes in dental health and development and the structure of the teeth. Congenital persistent proximal type renal tubular acidosis causes enamel defects of the permanent teeth (Winsnes et al. 1979). Also, missing and peg-shaped teeth, enamel hypoplasias and excessive caries in carbonic anhydrase II deficiency syndrome with renal tubular acidosis have been reported (Ohlsson et al. 1986).
Severe symmetrically distributed enamel hypoplasia in the permanent teeth was found in a patient with chronic metabolic acidosis (congenital persistent renal tubular acidosis of proximal type, capillary blood pH 7.07-7.15) (Koppang et al. 1984). Delayed shedding and eruption, agenesia of a few permanent teeth and retarded tooth development were also reported. The primary teeth were normal except for an extremely thin enamel. From a 10-year old boy, several teeth had been extracted due to caries. His skeletal age was 3 years and dental age 2 years delayed.
Both chronic metabolic alkalosis (children with congenital chloride diarrhoea [E87.8];, Myllärniemi & Holmberg 1975) and chronic respiratory alkalosis (children with acyanotic congenital atrial septal defect in heart [Q21.1];, Bäckman et al. 1990) have been observed to increase caries resistance. Myllärniemi & Holmberg (1975) also reported enamel defects and hypoplasias of varying severity in both the deciduous and the permanent teeth. The timing of the deciduous and permanent teeth formation and eruption was normal.
Acid-base balance also affects the fluoride metabolism. The absorption rate of fluoride from the stomach is dependent on the pH of the gastric contents (Whitford & Pashley 1984). Plasma clearance of fluoride by the kidneys is related to urinary pH: acidosis induces reduction in the renal clearance of fluoride (Whitford et al. 1976). High concentrations of fluoride and magnesium are found in the bone and the enamel associated with the acidotic state (Angmar-Månsson & Whitford 1995).
Mineralization defects in the enamel of rats and dogs, resembling fluorosis, have also been found in acidosis without an exposure to fluoride (Angmar-Månsson & Whitford 1990). Both chronic metabolic acidosis (exposure to NH4Cl) and chronic respiratory acidosis (exposure to 10% CO2) result in major disturbances in the rat incisor enamel (Whitford & Angmar-Månsson 1995).
In an experiment with young pups, chronic metabolic acidosis was induced with NH4Cl (Angmar-Månsson & Whitford 1986, Angmar-Månsson & Whitford 1990). This resulted in an increase in the amount of fluoride in teeth with no change in the phosphorus concentration. Also in NH4Cl -induced acidosis with no fluoride supplementation, the mineralization of enamel was severely disturbed with alternating layers of hyper- and hypomineralization, having in some cases even cystic appearance in the microradiographic analyses. Chronic metabolic alkalosis (induced with NaHCO3) caused only minor changes in the mineralization pattern. The ratios of Ca/P or Ca/Na did not differ between these groups or compared to the controls.
With similar experimental setting, Driessens et al. (1987) found no differences in the Ca/P or Ca/Na ratios in the molar dentine between acidotic, alkalotic and control pups. Also, there was not a clear trend in these ratios as a function of the distance from the front of the mineralization.
Metabolic alkalosis enhances the excretion rate of fluoride by the kidneys, which is reflected in reduced fluoride levels in both soft and hard tissues. The disturbance in the enamel mineralization associated with alkalosis is additive to that produced by fluoride. In acidosis, the defective mineralization is attenuated by a supplementation with fluoride. (Angmar-Månsson & Whitford 1990)
Calcium phosphate supplementation of the diet did not mitigate the defects in the enamel mineralization associated with the chronic acid-base disturbances. Instead, it worsened them, especially in chronic acidosis. (Angmar-Månsson & Whitford 1990)
Chronic respiratory alkalosis, caused by living in low pressure corresponding 5490 meters above sea level, also results in disturbances in the mineralization of the rat incisor enamel. The enamel is severely damaged both macroscopically and microradiographically and uniformly bleached to the color of chalk. The incisor dentine contains numerous small lacunae. Like in metabolic acidosis, hard and soft tissues have a higher concentration of fluoride. (Angmar-Månsson et al. 1984, Angmar-Månsson & Whitford 1990)