Inactivation of root canal medicaments by dentine, hydroxylapatite and bovine serum albumin.
OBJECTIVE
This study examined and compared the inhibition of the antibacterial effect of saturated calcium hydroxide solution, chlorhexidine acetate and iodine potassium iodide by dentine, hydroxylapatite and bovine serum albumin.


METHODS
Enterococcus faecalis strain A197A prepared to a suspension of 3 x 10(8) cells per ml in 0.5% peptone water was used. Fifty microL of saturated calcium hydroxide solution, 0.05% chlorhexidine acetate or 0.2/0.4% iodine potassium iodide were incubated at 37 degrees C with 28 mg dentine powder (DP), hydroxylapatite (HA) or bovine serum albumin (BSA) in 50 microL water for 1 h before adding 50 microL of the bacterial suspension. Samples for bacterial culturing were taken from the suspension 1 and 24 h after adding the bacteria. In further experiments, the amount of dentine was stepwise reduced from 28 mg 150 microL-1 to 2.8 mg 150 microL-1.


RESULTS
Calcium hydroxide was totally inactivated by the presence of 28 mg of DP, HA or BSA. Chlorhexidine (0.05%) was strongly inhibited by BSA and slowed down by dentine. However, HA had little or no inhibitory effect on chlorhexidine. The antibacterial effect of 0.2/0.4% iodine potassium iodide on E. faecalis was totally inhibited by dentine (28 mg), but was practically unaffected by HA or BSA. A stepwise reduction of dentine from 28 mg 150 microL-1 to 2.8 mg 150 microL-1 was followed by a similar reduction of the inhibition of the antibacterial activity of chlorhexidine. Iodine potassium iodide was not inhibited at all with dentine amounts less than 28 mg. However, the effect of saturated calcium hydroxide solution was totally eliminated by dentine, in all four concentrations.


CONCLUSIONS
Inhibition by dentine of the antibacterial activity of calcium hydroxide, chlorhexidine and iodine potassium iodide occurs by different mechanisms. Different components of dentine may be responsible for the inhibition of these three medicaments. Calcium hydroxide was particularly sensitive to inhibition by both inorganic and organic compounds.
Portenier
I
I
Department of Endodontics, Dental Faculty, University of Oslo, Oslo, Norway. isaport@odont.uio.no
Haapasalo
H
H
Rye
A
A
Waltimo
T
T
Ørstavik
D
D
Haapasalo
M
M
D000818:Animals; D000891:Anti-Infective Agents, Local / Q000037:antagonists & inhibitors; D001672:Biocompatible Materials / Q000494:pharmacology*; D002126:Calcium Hydroxide / Q000037:antagonists & inhibitors; D002417:Cattle; D002710:Chlorhexidine / Q000037:antagonists & inhibitors; D003804:Dentin / Q000502:physiology*; D004336:Drug Antagonism; D017886:Durapatite / Q000494:pharmacology*; D013293:Enterococcus faecalis / Q000187:drug effects / Q000254:growth & development; D017613:Iodine Compounds / Q000037:antagonists & inhibitors; D011193:Potassium Iodide / Q000037:antagonists & inhibitors; D012388:Root Canal Irrigants / Q000737:chemistry*; D012710:Serum Albumin, Bovine / Q000494:pharmacology*
D000891:Anti-Infective Agents, Local; D001672:Biocompatible Materials; D017613:Iodine Compounds; D012388:Root Canal Irrigants; C439385:iodine potassium iodide; D011193:Potassium Iodide; D012710:Serum Albumin, Bovine; D017886:Durapatite; D002126:Calcium Hydroxide; D002710:Chlorhexidine