MECHANISM OF ULTRASONICS - ACOUSTIC STREAMING

¢ Acoustic streaming is the rapid movement of particles of fluid in vortex(circular)-like motion about a vibrating object.

¢ When a vibrating file is immersed in a fluid, the file is observed to generate a streaming fluid comprising two components:

¢ Primary field consisting of rapidly moving eddies in which the fluid element oscillates about a mean position, and a superimposed secondary field consisting a patterns of relatively slow, time independent flow. Characteristically the fluid is transported from the apical end to the coronal end.

¢ In a endosonic file the greatest shear stresses will be generated around points of maximum displacement, such as the tip of the file and the antinodes along its length

¢ it is probable that will also be important in moving the associated irrigant around the canal so that maximum benefit is achieved from the chemical irrigant.

Martin H. the ultrasonic synergistic system. Int Dent J 1984;34:198 –203.

Martin H. the ultrasonic synergistic system of endodontics. Endod Dent Traumatol 1985;1:201– 6.

Ahmad M. Ultrasonic debridement of root canals: acoustic cavitation and its relevance. J Endod 1988;14:486 –93.

PROCEDURAL ERRORS DURING CLEANING AND SHAPING

TRANSPORTATION

It is moving the position of canal’s normal anatomic foramen to a new location on the external root surface.

It Occurs apical to curvature.

Transportation occurs when the angle of access and angle of incidence differ.

The angle of access refers to the orientation of the instrument as it slides down the body of the root canal.

The angle of incidence refers to the turn required to follow the path of the root canal.

EXTERNAL TRANSPORTATION

• Occurs mainly due to failing to precurve files, using large instruments.

Original apical foramen is torn.

• When the instrument is overused - the elastic memory of the instrument may create the teardrop and tearing of the apical foramen

• Another form of external transportation is direct perforation.

• begins with a ledge or apical blockage.

• continues its misdirection until it perforates the root surface.

INTERNAL TRANSPORTATION

• occurs when foramen is clogged with dentin mud.

• perforate the external root surface through a false path.

LEDGING

• leding is Iatrogenically created root canal wall irregularity .

• it Impedes the placement of instrument

• Caused by

– forcing uncurved instrument in a curved canal.

– Rapid advancement in file size.

• Identified by Loss of tactile sensation on instrument - loose feeling instead of binding at the apex.

ZIPPING

• It is transposition of the apical portion of the canal.

• Causes

– failure to precurve the files

– Forcing the instrument in curved canal.

– Use of large , stiff instruments.

files placed in a curved canal will cut more on the outer portion of the canal wall.

ELBOW

• Creation of an ‘elbow’ is associated with zipping

• narrow region of the root canal at the point of maximum curvature as a result of the irregular widening.

• Elbow prevents obturation in the apical portion of the canal

STRIP PERFORATION

Strip perforation occurs in the middle part of the inner curve of a root canal if excessive dentine is removed by over instrument.

cross section of hand instruments in endodontics

MECHANISM OF SODIUM HYPOCHLORITE

PECORA ET AL,1999

NaOCl + H2O « NaOH + HOCl « Na+ + OH- + H+ + OCl-

SODIUM HYPOCHLORITE EXHIBITS DYNAMIC BALANCE

Saponification reaction

Sodium hypochlorite acts on fatty acids, transforming them into fatty acid salts (soap) and glycerol (alcohol), that reduces the surface tension of the remaining solution.

Neutralization reaction

NaOCl neutralizes amino acids and forms water and salt. With the exit of hydroxyl ions, there is a reduction of ph.

Chloramination reaction

Hypochlorous acid, present in NaOCl solution, when in contact with organic tissue acts as a solvent, releases chlorine that, combined with the protein amino group, forms chloramines, that interfere in cell metabolism.

Hypochlorous acid (hocl-) and hypochlorite ions (ocl-) lead to amino acid degradation and hydrolysis.

Chlorine (strong oxidant) presents antimicrobial action inhibiting bacterial enzymes leading to an irreversible oxidation of SH groups (sulphydryl group) of essential bacterial enzymes.

Braz Dent J (2002) 13(2): 113-117

Mechanism of xylitol in remineralization

Xylitol prevents the decalcification by inhibiting the translocation of dissolved calcium(Ca2+) and phosphate(PO43–) ions from lesions.

Xylitol may act as Ca2+ ion carrier supplying the middle and deep layers with Ca2+ ions from the oral environment, thus enhancing remineralization by providing the Ca2+ ions for crystal repair.

It may also accelerate remineralization by lowering the diffusion coefficients of calcium and phosphate ions within the demineralized layers.

The greater extent of mineralization in seen in deeper layer.

Journal of Electron Microscopy 52(5): 471–476 (2003)

CRITERIA FOR EVALUATION OF RESTORATION

COLOUR MATCH

CPP-ACP - RECALDENT- REMINERALIZING MECHANISM

CPP-ACP IS CALLED AS RECALDENT

MOST COMMONLY USED REMINERALIZING AGENT IN DENTAL PRACTICE

Recaldent was developed by Professor Eric Reynolds in the School of Dental Science at the University of Melbourne.

The CPP-ACP (casein phosphopeptide-amorphous calcium phosphate) nanocomplex is found in the casein protein of cows milk. These peptides are responsible for carrying the calcium phosphate in milk and are what give milk its white colour.

The casein phosphopeptides can be easily prepared from a tryptic digest of caseinate by selective precipitation with Ca2+ in the presence of ethanol (Reynolds, 1991). This produces a casein phosphopeptide (CPP) fraction rich in the phosphopeptides aLS-CN(59-79) and PCN(l /2-25)

CPP containing the cluster sequence –Ser(P)-Ser(P)-Ser(P)-Glu-Glu- stabilize ACP in metastable solution. Through the cluster sequence the CPP bind to forming nanoclusters of ACP preventing their growth to the critical size required for nucleation and phase transformation.

Casein phosphopeptides (CPP) stabilize high concentrations of calcium and phosphate ions, together with fluoride ions, at the tooth surface by binding to pellicle and plaque, significantly increase the levels of calcium and phosphate ions in supragingival plaque.

Although the calcium, phosphate and fluoride ions are stabilized by the CPP from promoting dental calculus, during acidogenic challenges, nano-complexes release calcium and phosphate ions via a pH or concentration gradient mechanism to maintain a supersaturated environment with respect to hydroxyapatite

CPP-ACP was incorporated into supragingival dental plaque by binding onto the surfaces of bacterial cells, as well as to components of the intercellular plaque matrix, and significantly increased the plaque levels of calcium (Ca) and inorganic phosphate (Pi).

CPP are responsible for not only the stabilization and water solubility of ACP but also the incorporation of ACP into plaque by binding to bacterial cell surfaces and onto adsorbed macromolecules on the tooth surface.

The bacterial cell contains both hydrophilic and hydrophobic molecules on its surface (Rose et al., 1997). The CPP molecules also contain hydrophilic and hydrophobic regions, and it is possible that binding to the bacterial cell surface is mediated by Ca2+ cross-linking of the negative charges on the peptide and the cell surface molecules (e.g,phosphoryl and carboxylate groups) as well as by hydrophobic and hydrogen-bond-mediated interactions.

CPP-ACP would compete with calcium for plaque Ca binding sites. This will reduce the amount of calcium bridging between the pellicle and adhering cells and between cells themselves

As the pH decreases CPP-ACP residues become protonated thereby releasing calcium together with its associated anions. Hence, CPP can act as a reservoir for calcium, phosphate and fluoride ions.

remineralized enamel indicated that the mineral deposited was hydroxyapatite with a higher Ca:P ratio than normal apatite. remineralized apatite was more resistant to acid challenge than the normal calciumdeficient carbonated tooth enamel.

CPP act as a delivery vehicle to co-localize bioavailable calcium,fluoride and phosphate ions at the tooth surface.

casein proteins are capable of decreasing the rate of precipitation of calcium phosphate from a moderately supersaturated solution at concentrations, suggesting that the very rapid interaction of the phosphoprotein with calcium phosphate nuclei in such solutions is aided by the open and generally flexible conformation of casein produce nanometre-sized particles of calcium phosphate stabilized by a casein phosphopeptide.

IT IS COMMERCIALLY AVAILABLE AS TOOTH MOUSE

Tooth Mousse is NOT a toothpaste and should not be applied like toothpaste i.e. do not brush your teeth with it. MI paste is applied to the tooth with either a finger or can be applied in either a custom whitening tray if you have one .Mi paste can also be professionally applied by the hygienist with a polishing cup during your prophylaxis (tooth cleaning). Recommended to leave on the tooth for 3-5 minutes and then expectorate (spit out). For maximum benefit, do NOT rinse with water after application

Tooth Mousse plus is a water-based cream containing Recaldent with incorporated fluoride (CPP-ACPF - casein phosphopeptide – amorphous calcium phosphate fluoride). The level of fluoride is 0.2% (900ppm), similar to the level in adult-strength toothpastes

The sugar-free gums (control and CPP-ACP containing gums) were chewed for either 20- minute periods, four times a day or for 5-minute periods, seven times a day.

Supplies calcium and phosphate needed for patients with poor saliva flow.

GIC CONTAINGING CPP-ACP

The CPP-ACP nanoparticles may have been physically encapsulated into the set GIC, as has been found with
unreacted glass particles (Matsuya et al., 1984), and therefore released as the acid eroded the cement in the acidic buffer.

The acid-catalyzed release of the CPP-ACP nanoparticles from the GIC is consistent with the protection of the adjacent dentin observed during acid challenge

The CPP-ACP in the GIC may have also directly increased microtensile bond strength by the incorporation of the CPP-ACP nanoparticles into the crosslinked matrix of the GIC.

reference

Australian Dental Journal 2008; 53: 268–273

J. Biol. Chem., Vol. 280, Issue 15, 15362-15369, April 15, 2005

Biochem. J. (1996) 314 (1035–1039)

Arch Oral Biol 45:569-575 (2000).

J Am Dent Assoc 2008;139;25S-34S

J Dent Res 82(3):206-211, 2003

J Dent Res 82(11):914-918, 2003

The journal of nutrition 2004 989s-95s

Caries Res 2004;38:551–556

CVD DIAMOND TIPS IN APICOECTOMY & ROOT END PREPARATION

CVD DIAMOND TIPS are newer instruments used in dental practice for conservative cavity preparation.

chemical vapor deposition (CVD)- coated diamond tips adaptable to conventional ultrasound devices are developed by brazilian company.

These tips are manufactured by the deposition of continuous diamond coatings onto molybdenum shafts in an excess hydrogen environment.

After some physicochemical interactions, a pure diamond film is covalently formed on metal surface and strongly adhered to the shaft without metallic binder between the crystals.

CVD diamond TIPS are also applied in endodontic practice for apicoectomy and root end cavity preparation.

the ultrasoundactivated CVD-coated tips produced rough root-end surfaces probably because the longer time required for ultrasonic root-end resection makes it difficult to maintain a uniform and continuous cutting, IN CONTRAST TO CARBIDE BURS WHICH produce smoother and more regular root-end surfaces

the use of the ultrasonic tip in the analysis of the cutting time, ultrasonic root-end resection took the longest time to be performed, which discourages its indication as the main choice for apicoectomy.

ultrasonic root-end resection WITH CVD DIAMOND TIPS took a longer time and resulted in rougher surfaces compared with the use of carbide burs at both high and low speeds.

REFERENCE
Braz Oral Res 2006;20:155– 61.

JOE — Volume 35, Number 2, February 2009

REPARATIVE DENTINE FORMATION - CALCIUM HYDROXIDE MECHANISM

The calcium hydroxide is most commonly used material in dental practice for pulp capping.

The mechanism by which calcium hydroxide initiates the reparative process is unclear. It has been suggested that a rise in pH as a result of the free hydroxyl ions may initiate or favour mineralization (Tronstad et al. 1981).

calcium hydroxide may act as a local buffer against the acidic reactions produced by theinflammatory process (Heithersay 1975). An alkaline pH may also neutralize the lactic acid secreted by osteoclasts, and this may help to prevent further destruction of mineralized tissue.

It has been speculated that the material exerts a mitogenic and osteogenic effect, the high pH combined with the availability of calcium and hydroxyl ions having an effect on enzymatic pathways and hence mineralization (Torneck et al. 1983).

The high pH may also activate alkaline phosphatase activity which is postulated to play an important role in hard tissue formation (Guo & Messer 1976). The optimum pH for alkaline
phosphatase activity is 10.2 (Gordon et al. 1985), a level of alkalinity which is produced
by many calcium hydroxide preparations.

Heithersay (1975) suggested that calcium ions may reduce the permeability of new capillaries, so that less intercellular serum is produced, thus increasing the concentration of calcium ions at the mineralization site.

The presence of a high calcium concentration may also increase the activity of calcium dependent
pyrophosphatase, which represents an important part of the mineralization process.

The reduced capillary permeability following the increase in the number of calcium ions could reduce serum flow within the dental pulp, and consequently the concentration of the inhibitory pyrophosphate ion would be reduced.

This would coincide with an increase in levels of calcium-dependent pyrophosphatase as promulgated by Heithersay (1975), and would result in uncontrolled mineralization of the pulp tissue (Fig. 1). This could possibly explain the high incidence of mineralized canals observed following pulpotomy and direct pulp capping (Langeiand et al. 1971, Seltzer & Bender 1984)

SOME VARIATION in the way in which a dentine bridge is formed, depending on the pH of the material that is used to dress the tooth.

high pH material such as pulpdent
Necrotic zone is formed adjacent to the material, and the dentine bridge then forms between this layer and the underlying vital pulp. The necrotic tissue eventually degenerates and disappears, leaving a void between the capping material and the bridge.

lower pH, such as Dycal
The necrotic zone is similarly formed but is resorbed prior to the formation of the dentine bridge, which then comes to be formed directly against the capping material.

Dentine bridges formed by the high pH materials are histologically identical to those produced by lower pH materials, but are easier to distinguish on a radiograph because of the space between the bridge and the calcium hydroxide.

reference
International Endodontic Journal ,1990,23,283-297

BIOACTIVE GLASSES - NOVAMIN

The bioactive glasses is introduced by HENCH in 1969

Bioactive glass containing calcium sodium phosphosilicate (NovaMinTM) that the glass particles release calcium and phosphate ions intra-orally to promote remineralization.

NovaMin releases fully active calcium and phosphorus ions when in contact with water.This provides a higher concentration of the same ions that are naturally found in saliva. This ensures and enhances the natural self-repair of your tooth surface, crystalline hydroxyl-carbonate apatite (HCA) layer that is chemically and structurally the same as tooth mineral.

The silica containing Ca, PO and Na bind to the tooth surface. The Na buffers the pH above 7, sodium ions (Na+) in the bioactive glass exchanges with H+ ions in body fluids causing pH to increase. (the pH is needed to be above 7 to allow for the precipitation of crystals onto the tooth surface).

ANTIBACTERIAL MECHANISM

The short-term antimicrobial effect of these glasses has been attributed exclusively to their ability to raise pH in an aqueous environment (Allan et al. 2001).

This pH increase results from the release of alkali ions, mainly Na+, and the incorporation of protons (H+) into the corroding material.

(i) the immediate killing effect of glasses on microbiota is related to their sodium content and thus their alkaline capacity.

(ii) the effect with a slow onset after several days is related to apatite precipitation on the bacteria.

(iii) the latter effect is promoted by soluble ionic species rather than the calcium and phosphate ions.

MECHANISM OF ACTION

As bioactive glass is mixed with distilled water rapid dissolution and breakdown of silica network, accompanied by the release of Ca2+, PO4 3- and Si4+ occurs at the glass surface.

Then, sodium ions are leached, leaving behind a silica-rich surface.

Finally, a polycondensated silica-rich gel layer is formed on the glass bulk.

The latter may act as a template for apatite nucleation [11] that grow by assuming more Ca2+ and PO4 3- from the surrounding fluid.

Therefore, the formation of apatite on glass surface is related to the concentration of the effective ions of Ca2+, PO4 3- and OH- released in the reaction medium,as its solution is saturated with calcium and phosphate, which might drive mineral back into the tooth.

ADVANTAGE
Benefits in patients experience reduced calcium, phosphate and fluoride ions caused by hyposalivation resulting from old age, prescription drug use, Sjögren’s Syndrome, diabetes and radiation therapy.

APPLICATION
Increased exposure time yields increased mineralization, at least up to 40 minutes. Exposure time has a generally linear effect on new mineral formation, up to 40 minutes of exposure time, indicating that users of NovaMin dentifrice would be best served to maximize dwell time by refraining from rinsing, drinking, etc. for some time after brushing.

REFERENCE
Australian Dental Journal 2008; 53: 268–273
Acta Biomaterialia , Volume 3 , Issue 6 , Pages 936 - 943
International Endodontic Journal. 41(8):670-678, August 2008
Egypt. J. Solids, Vol. (29), No. (1), (2006) 69
Hench LL, Wilson J, An Introduction to Bioceramics Singapore, World Scientific Publishing, 1993.

BUONOCORE - ACID ETCHING MECHANISM

Method of surface treatment employed 85 per cent phosphoric acid for 30 seconds to determine the effect of a simple acid decalcification on adhesion.

The increased adhesion obtained intraorally on treated enamel surfaces may be due to several factors...

(a) a tremendous increase in surface area due to the acid etching action.

(b) the exposing of the organic framework of enamel which serves as a network, in and about which the acrylic can adhere.

(c) the formation of a new surface due to precipitation of new substance, for instance, calcium oxalate, organic tungstate complex, and so on,to which the acrylic might adhere.

(d) the removal of old, fully reacted, and inert enamel surface, exposing a fresh, reactive surface more favorable for adhesion.

(e) the presence on the enamel surface of an adsorbed layer of highly polar phosphate groups, derived from the acid used.


J. D. Res. December, 1955,849-853

Antimicrobial mechanism of CALCIUM HYDROXIDE

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

CHEMICOMECHANICAL CARIES REMOVAL (CARISOLV)

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 .

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.

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

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

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).

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