CARIDEX
The chemo-mechanical system for caries removal was published in 1975 by HABIB et al.
It is marketed under the trade name of Caridex.
Chemo-mechanical caries removal uses sodium hypochlorite (NaOCl), a non-specific proteolytic
agent (monoaminobutyric acid) removing organic components at room temperature
CARISOLV
Carisolv consists of a red gel and transperant fluid.
composition
Red gel
glutamic acid,
leucin,
lysine,
sodium chloride,
erythrosine,
water and sodium hydroxide
Transparent fluid
0.5% sodium hypochlorite
The chemical action of Carisolv is similar to that of Caridex in softening the carious dentin but leaving the healthy dentin unaffected
In caridex it was shown that, NaOCl was dissolving not only necrotic tissue but also sound dentin.
INSTRUMENTS
Special instruments designed to scrape in two or in several directions, which reduce the friction during caries excavation
MECHANISM OF ACTION
While mixing amino acids react with sodium hypochloride and forms chloromines.
chloromines seems to involve the chlorination of partially degraded collagen and the conversion of hydroxyproline to pyrrole-2-carboxylic acid, which initiates disruption of altered collagen fibres in carious dentin .
Saturday, February 07, 2009
Thursday, February 05, 2009
ACTION OF FLUORIDE ON TEETH
ACTION OF FLUORIDE ON TEETH
It is deposited on the enamel by the formation of a globular deposits of CaF2.
These globules do not dissolve as quickly as expected on their basis of their solubility.
The solubility is attributed to prescence of phosphate and proteins rich surface covering these globules.
The dissolution of fluoride from globules is pH dependent,because phosphate ions are released when they are protonated at low pH.
During a cariogenic challenge, F released from this globules may diffuse into the enamel promoting reformation of apatite.
It is known that the formation of the CaF2 reservoir is increased under acidic compared to neutral condition.
Fluoride from saliva or exogenous sources such as fluoride rinses, gels, varnishes and toothpastes is taken up preferentially by biofilms, lessens the effects of an acidogenic challenge and facilitates remineralization when the resting pH returns to 7.0.
INCREASED CONCENTRATION
Increased concentrations of calcium and phosphate in biofilms, saliva and artificial calcifying fluids, excessive levels of fluoride lead to rapid mineral precipitation on the enamel surface and owing to occlusion of surface porosities communicating with the subsurface leads to white-spots.
INCREASED CONCENTRATION
Increased concentrations of calcium and phosphate in biofilms, saliva and artificial calcifying fluids, excessive levels of fluoride lead to rapid mineral precipitation on the enamel surface and owing to occlusion of surface porosities communicating with the subsurface leads to white-spots.
So that high concentration topical fluoride results in unsightly white opacification of enamel lesions.
High frequency application of low F concentration agents has been considered the most beneficial treatment regime.
journal of de n t i s t r y, 2 0 0 8
Adv Dent Res ,1994
Wednesday, February 04, 2009
FLUORIDE MECHANISM
FLUORIDE
Fluoride ions promote the formation of fluorapatite in enamel in the presence of calcium and phosphate ions produced during enamel demineralization by plaque bacterial organic acids.
Fluoride ions can also drive the remineralization of previouslydemineralized enamel if enough salivary or plaque calcium and phosphate ions are available.
availability of calcium and phosphate ions can be the limiting factor for net enamel remineralization to occur
this is highly exacerbated under xerostomic condition.
FLUORAPATITE
when the fluoride is applied, for every two fluoride ions, 10 calcium ions and six phosphate ions are required toform one unit cell of fluorapatite (Ca10(PO4)6F2)..
Fluoride mechanisms
1) Free fluoride ion combines with H+ to produce hydrogen fluoride, which migrates throughout acidified plaque.
This ionized form is lipophilic and can readily penetrate bacterial membranes.
Bacterial cytoplasm is relatively alkaline, which forces the dissociation of H+ and F-.
Fluoride ion inhibits various cellular enzymes (enolase, proton extruding ATPase)key to sugar metabolism.
Hydrogen ions simultaneously acidify the cytoplasm, thus slowing cellular activities and inhibiting bacterial function
2) Fluoride integrated in the enamel surface (as fluorapatite, FAP) makes enamel more resistant to demineralization than HAP during acid challenge.
FLUORAPATITE formed is less soluble,this is due to incorporation of fluoride and carbonate is washed out (Tencate).
3) Fluoridated saliva not only decreases critical pH, but also further inhibits demineralization of the deposited CaF2 at the tooth surface.
DCNA,1999
Australian Dental Journal,2008
Fluoride ions promote the formation of fluorapatite in enamel in the presence of calcium and phosphate ions produced during enamel demineralization by plaque bacterial organic acids.
Fluoride ions can also drive the remineralization of previouslydemineralized enamel if enough salivary or plaque calcium and phosphate ions are available.
availability of calcium and phosphate ions can be the limiting factor for net enamel remineralization to occur
this is highly exacerbated under xerostomic condition.
FLUORAPATITE
when the fluoride is applied, for every two fluoride ions, 10 calcium ions and six phosphate ions are required toform one unit cell of fluorapatite (Ca10(PO4)6F2)..
Fluoride mechanisms
1) Free fluoride ion combines with H+ to produce hydrogen fluoride, which migrates throughout acidified plaque.
This ionized form is lipophilic and can readily penetrate bacterial membranes.
Bacterial cytoplasm is relatively alkaline, which forces the dissociation of H+ and F-.
Fluoride ion inhibits various cellular enzymes (enolase, proton extruding ATPase)key to sugar metabolism.
Hydrogen ions simultaneously acidify the cytoplasm, thus slowing cellular activities and inhibiting bacterial function
2) Fluoride integrated in the enamel surface (as fluorapatite, FAP) makes enamel more resistant to demineralization than HAP during acid challenge.
FLUORAPATITE formed is less soluble,this is due to incorporation of fluoride and carbonate is washed out (Tencate).
3) Fluoridated saliva not only decreases critical pH, but also further inhibits demineralization of the deposited CaF2 at the tooth surface.
DCNA,1999
Australian Dental Journal,2008
Tuesday, February 03, 2009
MECHANISM OF CALCIUM HYDROIDE IN ROOT CANAL
CALCIUM HYDROXIDE
Since its introduction in 1920 (Hermann 1920), calcium hydroxide has been widely used in
endodontics.
It is a strong alkaline substance, which has a pH of approximately 12.5. In an aqueous
solution, calcium hydroxide dissociates into calcium and hydroxyl ions.
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.
Damage to the bacterial cytoplasmic membrane
Hydroxyl ions induce lipid peroxidation, resulting in the destruction of phospholipids, structural components of the cellular membrane.
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.
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
The alkalinization provided by calcium hydroxide induces the breakdown of ionic bonds that maintain the tertiary structure of proteins.
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.
Genes are then lost , Consequently, DNA replication is inhibited and the cellular activity is disarranged.
Free radicals may also induce lethal mutations.
(Imlay & Linn 1988).
...
It has been suggested that the ability of calcium hydroxide to absorb carbon dioxide may contribute to
its antibacterial activity (Kontakiotis et al. 1995).
Since its introduction in 1920 (Hermann 1920), calcium hydroxide has been widely used in
endodontics.
It is a strong alkaline substance, which has a pH of approximately 12.5. In an aqueous
solution, calcium hydroxide dissociates into calcium and hydroxyl ions.
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.
Damage to the bacterial cytoplasmic membrane
Hydroxyl ions induce lipid peroxidation, resulting in the destruction of phospholipids, structural components of the cellular membrane.
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.
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
The alkalinization provided by calcium hydroxide induces the breakdown of ionic bonds that maintain the tertiary structure of proteins.
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.
Genes are then lost , Consequently, DNA replication is inhibited and the cellular activity is disarranged.
Free radicals may also induce lethal mutations.
(Imlay & Linn 1988).
...
It has been suggested that the ability of calcium hydroxide to absorb carbon dioxide may contribute to
its antibacterial activity (Kontakiotis et al. 1995).
Monday, February 02, 2009
AMELOGENESIS IMPERFECTA
CLASSIFICAION OF AMELOGENESIS IMPERFECTA
Weinmann et al., 1945 [4] Two types based solely on phenotype: hypoplastic and hypocalcified
Darling, 1956 [5] Five phenotypes based on clinical, microradiographic and histopathological findings.
Hypoplastic
Group 1 – generalised pitting
Group2 – vertical grooves (now known to be X-linked AI)
Group 3 – Generalised hypoplasia
Hypocalcified
Type 4A – chalky, yellow, brown enamel
Type 4B – marked enamel discolouration and softness with post-eruptive loss of enamel
Type 5 – generalised or localised discolouration and chipping of enamel
Witkop, 1957 [6] Classification based primarily on phenotype. 5 types:
1. Hypoplastic
2. Hypocalcification
3. Hypomaturation
4. Pigmented hypomaturation
5. Local hypoplasia
Added mode of inheritance as further means of delineating cases.
Schulze, 1970 [7] Classification based on phenotype and mode of inheritance.
Witkop and Rao, 1971 [8] Classification based on phenotype and mode of inheritance. Three broad categories: hypoplastic, hypocalcificied,
hypomaturation.
a. Hypoplastic
Autosomal dominant hypoplastic-hypomaturation with taurodontism (subdivded into a and b according to author)
Autosomal dominant smooth hypoplastic with eruption defect and resorption of teeth
Autosomal dominant rough hypoplastic
Autosomal dominant pitted hypoplastic
Autosomal dominant local hypoplastic
X-linked dominant rough hypoplastic
b. Hypocalcified
Autosomal dominant hypocalcified
c. Hypomaturation
X-linked recessive hypomaturation
Autosomal recessive pigmented hypomaturation
Autosomal dominant snow-capped teeth
White hypomature spots
Winter and Brook, 1975 [9] Classification based primarily on phenotype. Four main categories: hypoplasia, hypocalcification, hypomaturation,
hypomaturation-hypoplasia with taurodontism, with mode of inheritance as a secondary means of sub-classification.
a. Hypoplasia
Type I. Autosomal dominant thin and smooth hypoplasia with eruption defect and resorption of teeth
Type II. Autosomal dominant thin and rough hypoplasia
Type III. Autosomal dominant randomly pitted hypoplasia
Type IV. Autosomal dominant localised hypoplasia
Type V. X-linked dominant rough hypoplasia
b. Hypocalcification
Autosomal dominant hypocalcification
c. Hypomaturation
Type I. X-linked recessive hypomaturation
Type II. Autosomal recessive pigmented hypomaturation
Type III. Snow-capped teeth
d. Hypomaturation-hypoplasia with taurodontism
Type I. Autosomal dominant smooth hypomaturation with occasional hypoplastic pits and taurodontism
Type II. Autosomal dominant smooth hypomaturation with thin hypoplasia and taurodontism
Witkop and Sauk, 1976 [2] Classification based on phenotype and mode of inheritance, similar to classification of Witkop and Rao (1971)
Sundell and Koch, 1985 [10] Classification based solely on phenotype
Witkop, 1988 [11] Four major categories based primarily on phenotype (hypoplastic, hypomaturation, hypocalcified, hypomaturation-hypoplastic
with taurodontism) subdivided into 15 subtypes by phenotype and and secondarily by mode of inheritance.
Type I. Hypoplastic
Type IA. Hypoplastic, pitted autosomal dominant
Type IB. Hypoplastic, local autosomal dominant
Type IC. Hypoplastic, local autosomal recessive
Type ID. Hypoplastic, smooth autosomal dominant
Type IE. Hypoplastic, smooth X-linked dominant
Type IF. Hypoplastic, rough autosomal dominant
Type IG. Enamel agenesis, autosomal recessive
Type II. Hypomaturation
Type IIA. Hypomaturation, pigmented autosomal recessive
Type IIB. Hypomaturation, X-linked recessive
Type IIC. Hypomaturation, snow-capped teeth, X-linked
Type IID. Hypomaturation, snow-capped teeth, autosomal dominant?
Type IIIA. Autosomal dominant
Type IIIB. Autosomal recessive
Type IV. Hypomaturation-hypoplastic with taurodontism
Type IVA. Hypomaturation-hypoplastic with taurodontism, autosomal dominant
Type IVB. Hypoplastic-hypomaturation with taurodontism, autosomal dominant
Aldred and Crawford, 1995[12]
Classification based on:
Molecular defect (when known)
Biochemical result (when known)
Mode of inheritance
Phenotype
Hart et al., 2002 [13] Proposed a molecular defect sub classification of the AMELX conditions
1.1 Genomic DNA sequence
1.2 cDNA sequence
1.3 Amino acid sequence
1.4 Nucleotide and amino-acid sequences
1.5 AMELX mutations described to date
Aldred et al., 2003 [1] Classification based on:
Mode of inheritance
Phenotype – Clinical and Radiographic
Molecular defect (when known)
Biochemical result (when known)
Orphanet Journal of Rare Diseases 2007
Weinmann et al., 1945 [4] Two types based solely on phenotype: hypoplastic and hypocalcified
Darling, 1956 [5] Five phenotypes based on clinical, microradiographic and histopathological findings.
Hypoplastic
Group 1 – generalised pitting
Group2 – vertical grooves (now known to be X-linked AI)
Group 3 – Generalised hypoplasia
Hypocalcified
Type 4A – chalky, yellow, brown enamel
Type 4B – marked enamel discolouration and softness with post-eruptive loss of enamel
Type 5 – generalised or localised discolouration and chipping of enamel
Witkop, 1957 [6] Classification based primarily on phenotype. 5 types:
1. Hypoplastic
2. Hypocalcification
3. Hypomaturation
4. Pigmented hypomaturation
5. Local hypoplasia
Added mode of inheritance as further means of delineating cases.
Schulze, 1970 [7] Classification based on phenotype and mode of inheritance.
Witkop and Rao, 1971 [8] Classification based on phenotype and mode of inheritance. Three broad categories: hypoplastic, hypocalcificied,
hypomaturation.
a. Hypoplastic
Autosomal dominant hypoplastic-hypomaturation with taurodontism (subdivded into a and b according to author)
Autosomal dominant smooth hypoplastic with eruption defect and resorption of teeth
Autosomal dominant rough hypoplastic
Autosomal dominant pitted hypoplastic
Autosomal dominant local hypoplastic
X-linked dominant rough hypoplastic
b. Hypocalcified
Autosomal dominant hypocalcified
c. Hypomaturation
X-linked recessive hypomaturation
Autosomal recessive pigmented hypomaturation
Autosomal dominant snow-capped teeth
White hypomature spots
Winter and Brook, 1975 [9] Classification based primarily on phenotype. Four main categories: hypoplasia, hypocalcification, hypomaturation,
hypomaturation-hypoplasia with taurodontism, with mode of inheritance as a secondary means of sub-classification.
a. Hypoplasia
Type I. Autosomal dominant thin and smooth hypoplasia with eruption defect and resorption of teeth
Type II. Autosomal dominant thin and rough hypoplasia
Type III. Autosomal dominant randomly pitted hypoplasia
Type IV. Autosomal dominant localised hypoplasia
Type V. X-linked dominant rough hypoplasia
b. Hypocalcification
Autosomal dominant hypocalcification
c. Hypomaturation
Type I. X-linked recessive hypomaturation
Type II. Autosomal recessive pigmented hypomaturation
Type III. Snow-capped teeth
d. Hypomaturation-hypoplasia with taurodontism
Type I. Autosomal dominant smooth hypomaturation with occasional hypoplastic pits and taurodontism
Type II. Autosomal dominant smooth hypomaturation with thin hypoplasia and taurodontism
Witkop and Sauk, 1976 [2] Classification based on phenotype and mode of inheritance, similar to classification of Witkop and Rao (1971)
Sundell and Koch, 1985 [10] Classification based solely on phenotype
Witkop, 1988 [11] Four major categories based primarily on phenotype (hypoplastic, hypomaturation, hypocalcified, hypomaturation-hypoplastic
with taurodontism) subdivided into 15 subtypes by phenotype and and secondarily by mode of inheritance.
Type I. Hypoplastic
Type IA. Hypoplastic, pitted autosomal dominant
Type IB. Hypoplastic, local autosomal dominant
Type IC. Hypoplastic, local autosomal recessive
Type ID. Hypoplastic, smooth autosomal dominant
Type IE. Hypoplastic, smooth X-linked dominant
Type IF. Hypoplastic, rough autosomal dominant
Type IG. Enamel agenesis, autosomal recessive
Type II. Hypomaturation
Type IIA. Hypomaturation, pigmented autosomal recessive
Type IIB. Hypomaturation, X-linked recessive
Type IIC. Hypomaturation, snow-capped teeth, X-linked
Type IID. Hypomaturation, snow-capped teeth, autosomal dominant?
Type IIIA. Autosomal dominant
Type IIIB. Autosomal recessive
Type IV. Hypomaturation-hypoplastic with taurodontism
Type IVA. Hypomaturation-hypoplastic with taurodontism, autosomal dominant
Type IVB. Hypoplastic-hypomaturation with taurodontism, autosomal dominant
Aldred and Crawford, 1995[12]
Classification based on:
Molecular defect (when known)
Biochemical result (when known)
Mode of inheritance
Phenotype
Hart et al., 2002 [13] Proposed a molecular defect sub classification of the AMELX conditions
1.1 Genomic DNA sequence
1.2 cDNA sequence
1.3 Amino acid sequence
1.4 Nucleotide and amino-acid sequences
1.5 AMELX mutations described to date
Aldred et al., 2003 [1] Classification based on:
Mode of inheritance
Phenotype – Clinical and Radiographic
Molecular defect (when known)
Biochemical result (when known)
Orphanet Journal of Rare Diseases 2007
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