CALCIUM HYDROXIDE
Antimicrobial activity of calcium hydroxide is related
to the release of hydroxyl ions in an aqueous
environment.
Hydroxyl ions are highly oxidant free
radicals that show extreme reactivity, reacting with
several biomolecules.
Their lethal effects on bacterial cells are probably due to the
following mechanisms:
1.Damage to the bacterial cytoplasmic membrane
2.Protein denaturation
3.Damage to the DNA
Damage to the bacterial cytoplasmic membrane
Hydroxyl ions induce lipid peroxidation, resulting in
the destruction of phospholipids.
Hydroxyl ions remove hydrogen atoms from unsaturated fatty acids,
generating a free lipidic radical.
This free lipidic radical reacts with oxygen, resulting in the formation of a
lipidic peroxide radical, which removes another hydrogen atom from a second fatty acid, generating another lipidic peroxide.
Thus, peroxides themselves act as free radicals, initiating an autocatalytic chain
reaction, and resulting in further loss of unsaturated
fatty acids and extensive membrane damage.
(Halliwell 1987, Cotran et al. 1999)
Protein denaturation
Cellular metabolism is highly dependent on enzymatic
activities.
The alkalinization provided by calcium
hydroxide induces the breakdown of ionic bonds that
maintain the tertiary structure of proteins
the enzyme maintains its covalent
structure but the polypeptide chain is randomly
unravelled in variable and irregular spacial conformation.
These changes frequently result in the loss of
biological activity of the enzyme and disruption of the
cellular metabolism.
(Voet & Voet 1995).
Damage to the DNA
Hydroxyl ions react with the bacterial DNA and induce
the splitting of the strands.
DNA replication is
inhibited and the cellular activity is disarranged. Free
radicals may also induce lethal mutations.
(Imlay & Linn 1988)
ANOTHER MECHANISM
It has been suggested that the ability of calcium
hydroxide to absorb carbon dioxide may contribute to
its antibacterial activity
(Kontakiotis et al. 1995)
calcium hydroxide impedes the carbon dioxide supply
to bacteria.
Reference
International Endodontic Journal, 32, 361-369, 1999
Monday, July 06, 2009
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