Streptococci isolated from plaque in subjects rinsing with chlorhexidine.
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The rates of three processes associated with the rise and fall in plaque pH, that normally occur following a urea rinse, were determined: (i) disappearance of urea from plaque, (ii) disappearance of urea from saliva and (iii) formation and disappearance from plaque of the ammonia produced by the plaque bacteria from the urea. Also examined were two processes associated with the fall and rise in pH following a glucose rinse: the disappearance of glucose from plaque and from saliva. Entry into plaque of either urea or glucose during rinsing was immediate; the subsequent disappearance of both from the plaque was slow and followed first-order kinetics. The ammonia formation and urea-disappearance results suggested that clearance of urea from the plaque occurred mainly by bacterial degradation and not by diffusion out of the plaque. The rate constants for ammonia formation and for its subsequent disappearance from the plaque made it clear why a rapid rise and a slow subsequent fall in the pH occurs after urea rinsing. The rate constants enabled calculation of the ammonia produced as a percentage of the urea utilized. Only 16-26 per cent of the urea was recovered as ammonia and the remainder of the urea-N was stored probably as NH2 moieties of certain amino acids. Such storage may enable the plaque bacteria to maintain the pH at an elevated level for an extended period of time by bacterial production of ammonia from these stored compounds after the urea ceases to be available as a source of substrate.
The effects on the metabolism of starch by plaques formed in human subjects during periods of dietary sucrose limitation or supplementation were studied. High sucrose (HS) plaques showed lower resting pH and pH minima, and higher concentrations of lactate ion after the starch mouth-rinse than low sucrose (LS) plaques. Plaque samples incubated with starch solutions in vitro showed no differences in final pH or acid-anion concentrations between HS and LS diets. Plaque-amylase activity was higher on HS than LS diets. Thus starch was more acidogenic when consumed as part of a diet already rich in sucrose, but it is unclear whether this was a specific or non-specific effect of starch on plaque metabolism.
Saliva at four buccal sites [between the upper (UC) and lower (LC) central incisors, and between the upper (UM) and lower (LM) second premolar and first molar], and also whole saliva, was collected from 10 subjects at 0.5, 2.5, 5.5 and 10.5 min after a rinse with 10 ml of 0.3 mol/l sucrose solution. After 0.5 min, unstimulated salivary flow rate was inversely correlated with sucrose concentration in whole saliva (p less than 0.05). Sucrose concentration decreased faster at LC than at other sites. Sucrose dilution at UC and LC was inversely correlated (p less than 0.05) with salivary flow rate at times after 0.5 min. At 10.5 min, the sucrose concentration at all sites was significantly correlated (p less than 0.05) with the salivary flow rate.
The object was to find out whether site-specific variations of pH might correlate with those of oral clearance as indicated by past studies using fluoride, sucrose and glucose as markers. Eleven subjects with 24 h growth of dental plaque rinsed the mouth with a 10% solution of sucrose. The pH of plaque, harvested from the labial or buccal cervical and approximal regions of certain teeth or groups of teeth, was then measured. The results confirmed previous reports that plaque pH varies from site to site in the mouth; the pattern observed was similar in each of the subjects. In the anterior part of the mouth, concentrations of hydrogen ion were invariably higher in plaque from the upper than from the lower surfaces of the teeth. The reverse pattern was found in the posterior part. This site-specific pattern was similar to that of oral clearance, as indicated by comparison with known values for glucose concentrations, a finding consistent with the view that site-specific pattern of plaque pH may reflect or at least be influenced by such differential clearance patterns.
Cell cultures were established from small samples of buccal tissue, using a 3T3 fibroblast feeder-layer technique. After exposure to increasing dilutions of three proprietary oral rinses for 22 h or 2 h, the effects upon cell proliferation were studied by measurement of [3H]-thymidine incorporation into cellular DNA. Cell membrane damage was assessed by measurement of lactate dehydrogenase content. Cultures exposed to hexetidine-containing or chlorhexidine-containing rinses for 22 h at dilutions of 250-fold or lower showed almost complete inhibition of [3H]-thymidine incorporation. Cultures treated with benzydamine-containing rinse at the same dilutions showed no significant inhibition of incorporation. Exposure to the same dilutions of hexetidine- and chlorhexidine-containing rinses for 2 h resulted in 65% and 20% inhibition of incorporation, respectively. Lactate dehydrogenase content decreased to negligible levels after exposure to the rinse containing hexetidine at a 250-fold dilution, but was unaffected by the other two rinses. Thus dividing buccal epithelial cells in vitro may be adversely affected by exposure to certain commercial oral rinses.