Various attempts have been made to study the effect of acids on decalcification of tooth enamel. Head (1) showed that saliva had a neutralizing power on acid phosphate solution in its decalcifying activity. This we know now is due to the buffering action of saliva. Others have found that saliva neutralizes lactic and other acids to such an extent that decalcification does not occur (2). Head's work was discounted by Pickerill on the ground that the acidity of the saliva and acid mixture was not determined and consequently the total effective acidity of the saliva was not known.McClelland (3) weighed pieces of enamel and immersed them in buffered solutions for various lengths of time, finding that the pieces in solutions of pH 6.0 and below are decalcified at a rate proportional to the degree of acidity. Dobbs (4) surmises that carbohydrates pass through dental plaques and are converted into acids by fermentation. If this is true, the pH of the dental plaque is more important than the pH of the saliva in tooth decalcification. Thus, the pH of a person's saliva might be high enough that no decalcification would occur and yet the pH of the plaque would be low enough to permit decalcification. Karshan and Rosebury (5) have studied the relationship of pH, calcium, and phosphorus to solubility of enamel with lactic, succinic, and malic acids on powdered enamel without addition of calcium andphosphorus.They stated that "the pH change at each time-level is strictly proportional to dissolved phosphorus at that level dissolved in the case of lactate buffers." However, this work was not performed in the presence of saliva. They stated that the calcium values are about 1
Experimental inflammatory edema was induced by injecting an irritant solution into the pleural cavity of rats. The volume of fluid found in the pleural cavity after a specified time interval was used as a measure of the degree of inflammation produced. The effect of counterirritants on reducing pleural inflammation was studied. Injection of irritants into the knee joint of the rat was found to reduce the amount of pleural inflammation formed. The anti-inflammatory effect observed could not be explained by loss of fluid into the injected knee, nor by stimulation of the pituitary-adrenal axis. The effect was still present in hypophysectomized rats and adrenalectomized rats. The use of plaster casts to prevent fluid loss into the injected leg did not block the reduction in pleural inflammation. It was suggested that counterirritants release some substance or substances from the tissues which they damage, which is carried by the blood and can exert an anti-inflammatory effect in another part of the animal.
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