Incidence of Urease Producing Bacteria in Saliva

Abstract

The use of carbamide (synthetic urea) in a mouth rinse has been suggested because in the mouth the carbamide is converted into ammonium carbonate which acts as an efficient buffer for acids. The combination of carbamide and quinine has been recommended as an antiseptic for oral use; the alkalinity resulting from the conversion of carbamide makes the quinine much more germicidal (2). Other therapeutic properties of carbamide such as ability to increase capillary proliferation, stimulate tissue granulations and dissolve necrotic tissue are probably of minor importance in the use of carbamide as an oral rinse.Carbamide is converted into ammonium carbonate by heat or by the action of an enzyme called urease, which is found in saliva in minute quantities and also is produced by many species of proteolytic bacteria. No investigations of the urease-producing bacteria of the mouth could be found in the literature, so this study was undertaken to determine their incidence in the oral flora.Shulte and Thompson (3) studied the urea-splitting bacteria in urine and found potent urea-splitting organisms as part of the normal urethral flora in fifteen of two hundred cases. They also found such bacteria associated with renal calculae of the calcium carbonate and calcium phosphate type, and believed the presence of these bacteria predisposed to severe infection. To prevent and treat such infections, these men used a weak lactic acid solution (0.25 to .5%). Proteus ammoniae, Proteus morganie, Micrococcus ureae, certain strains of Staphylococcus aureus and certain strains of diphtheroids were found to be of clinical significance. The method used by Shulte and Thompson (3) has been adapted for this study. METHOD OF STUDYTo study the incidence of urease-producing organisms in the oral flora unstimulated salivary samples were collected from a total of 82 patients and inoculated into "carbamide media." The media used to test for presence of ureaseproducing bacteria was similar to that prepared by Laidley and modified by Thompson and Shulte (3) (peptone 2 gms., sodium chloride 5 gms., distilled water 1000 cc., 20 cc. of a 0.2% alcoholic solution of thymol blue). The media was adjusted to pH 6.8. Ten cc. of this media was poured into each tube and sterilized by heat. After sterilization, 0.5 cc. of a Seitz filtered 10% carbamide (C.P.) solution was added to each tube and incubated for 24 hours. If not contaminated, tubes were stored in a refrigerator until used. This media is very selective for bacteria able to split carbamide.

Comparison between a new 13C-urea breath test, using a film-coated tablet, and the conventional 13C-urea breath test for the detection of Helicobacter pylori infection

“…There have been reports stating urease-producing bacteria are present in the oral cavity, [15][16][17] which may lead to false-positive results if breath samples are collected soon after administration of 13 C-urea in solution. 2,3,18 Therefore, in with most 13 C-urea breath-testing, a study meal is given to patients to delay the excretion of 13 Curea from the stomach, 2,6 and an interval of 20-30 min is allowed to elapse between the administration and the breath-sampling time.…”

A rapid, low‐dose, 13C‐urea tablet for the detection of Helicobacter pylori infection before and after treatment

“…13 When administered as a drink, interference from urease-producing bacteria in the oro-pharynx may cause false positive results in early breath tests. 14,15 Therefore, most UBT protocols do not obtain the diagnostic breath sample until 20-30 min after administration. In contrast, when using a capsule or tablet, the problem of oropharyngeal bacteria is eliminated.…”

The relationship between dental caries status and dental plaque urease activity

“…Although there is enough indirect evidence to suggest that ammonia production from bacterial ureolytic activity in the oral cavity may inhibit the development of dental caries, clinical studies directly evaluating the association of urease activity with dental caries have been very few and inconclusive. Hine and O'Donnell (15) noticed a possible inverse association between caries activity and salivary urease activity, although other investigators (2, 22) did not confirm this observation. Frostel in 1960 (13) measured urease levels in plaque from caries‐active and caries‐inactive human volunteers using an antimony electrode and found no statistically significant differences.…”