Calcium Hydroxide in Endodontics: A literature Review

CALCIUM HYDROXIDE AS INTRACANAL MEDICAMENT:- 

A medicament is an antimicrobial agent that is placed inside the root canal between treatment appointments in an attempt to destroy remaining microorganisms and prevent reinfection (Weine 2004). Thus, they may be utilized to kill bacteria, reduce inflammation (and thereby reduce pain), help eliminate apical exudate, control inflammatory root resorption and prevent contamination between appointments. When intracanal medicaments were not used between appointments, bacterial numbers increased rapidly (Bystrom & Sundqvist 1981).

Among the available intracanal dressings, calcium hydroxide is the most indicated and frequently used in the clinical practice. Calcium hydroxide with its antimicrobial property and protein denaturing ability facilitates pulpal tissue dissolution and has been widely used for interappointment intra-canal dressing.

Dressing of the root canal

Vital teeth: Normal, vital pulp is sterile. If pulpectomy is performed under controlled, aseptic conditions, the superficial bacterial flora and affected pulp will be removed, leaving a bacteria-free canal. Therefore, in root canal treatment of teeth where vital pulp tissue exists, it is questionable whether an intracanal medicament is needed. Since intracanal medicaments have the potential to do more harm than good, they are not indicated in vital teeth, where a bacteria-free canal is achievable by controlled asepsis without the need for medicaments.

Infected teeth: In infected root canals, intracanal medication has been advocated for many reasons. An intracanal medicament is used to:

(i) eliminate any remaining bacteria after canal instrumentation;

(ii) reduce inflammation of periapical tissues and puip remnants;

(iii) render canal contents inert and neutralize tissue debris;

(iv) act as a barrier against leakage from the temporary aiing;

(v) help to dry persistently wet canals

Anti-bacterial activity :- is related to its high alkalinity, which results in the inactivation of bacterial membrane enzymes.  It is well recognized that chemo-mechanical instrumentation alone is unable to completely disinfect the root canal system. The bacteria surviving root canal instrumentation proliferate between appointments.

Calcium hydroxide will exert an antibacterial effect in the root canal system as long as a high pH is maintained. In their in vivo study, Bystrom et al. (1985) reported that root canals treated with Ca(OH)2 had fewer bacteria than those dressed with camphorated phenol or camphorated monochlorophenol (CMCP). They attributed this to the fact that Ca(OH)2 could be packed into the root canal system allowing hydroxyl ions to be released over time. When compared with 2% iodine-potassium iodide solution, calcium hydroxide-dressed root canals yielded fewer culture reversals (Safavi et al. 198 5). Shuping et al. (2000) showed that placement of Ca(OH)2 for at least 1 week rendered 92.5% of canals bacteria free.

Behnen et al. (2001) demonstrated that Ca(OH)2 decreased the numbers of E. faecalis at all depths within dentinal tubules up to 24 h and that less viscous preparations of Ca(OH)2 were more effective in the elimination of E. faecalis from dentinal tubules than viscous preparations.

Lin et al. (2005) reported that treatment with electrophoresis was significantly more effective than pure Ca(OH)2 up to depths of 200–500 lm. Specimens treated with electrophoretically activated Ca(OH)2 revealed no viable bacteria in dentinal tubules to a depth of 500 lm from the root canal space within 7 days.

Weiger et al. (2002) concluded that the viability of E. faecalis in infected root dentine was not affected by Ca(OH)2.  The failure of calcium hydroxide to eliminate enterococci effectively has also been reported by other workers (Bystrom et al 1985, Haapasalo & Orstavik 1987, 0rstavik & Haapasalo 1990, Safavi et al 1990). Calcium hydroxide, although suitable as an intracanal medicament, cannot be considered as a universal intracanal medicament (Reit&Dahlenl988).

Intracanal medication does not 'sterilize' the root canal (Treanor & Goldman 1972), and is no substitute for thorough canal cleaning and adequate canal preparation.

Anti-endotoxin activity :- Endotoxin (LPS) is released during multiplication or bacterial death causing a series of biological effects, which lead to an inflammatory reaction and periapical bone resorption. Endotoxins from vital or nonvital, whole or fragmented bacteria act on macrophages, neutrophils and fibroblasts, leading to the release of a large number of bioactive or cytokine chemical inflammatory mediators, such as tumour necrosis factor (TNF), interleukin- 1 (IL-1), IL-5, IL-8, alpha-interferon and prostaglandins (Leonardo et al. 2004).

Currently, one of the concerns in endodontics is the treatment of teeth with necrotic pulps and periapical pathosis because post-treatment disease persists more often than in cases without periapical disease. In teeth with chronic periapical lesions, there is a greater prevalence of Gram-negative anaerobic bacteria disseminated throughout the root canal system (dentinal tubules, apical resorptive defects and cementum lacunae), including apical bacterial biofilm. Because these areas are not reached by instrumentation, the use of a root canal medicament is recommended to aid in the elimination of these bacteria and thus increase the potential for clinical success. Where bone loss has occurred, the use of a root canal medicament between treatment sessions is recommended, because the success of treatment in cases with periapical pathosis is directly related to the elimination of bacteria, products and subproducts from the root canal system. The procedures and medicaments used in root canal treatment should not only lead to bacterial death, but also to the inactivation of bacterial endotoxin.

In a laboratory study, Safavi & Nichols (1993) evaluated the effect of Ca(OH)2 on bacterial LPS and concluded that it hydrolysed the highly toxic lipid A molecule that is responsible for the damaging effects of endotoxin.

Silva et al. (2002) analysed histopathologically periapical tissues of teeth in dogs in which the root canals were filled with bacterial LPS and Ca(OH)2. They reported that LPS caused the formationof periapical lesions and that Ca(OH)2 detoxified this endotoxin in vivo.

In summary, endotoxin, a component of the cell wall of Gram-negative bacteria, plays a fundamental role in the genesis and maintenance of periapical lesions because of the induction of inflammation and bone resorption. Ca(OH)2 inactivates endotoxin, in vitro and in vivo, and appears currently the only clinically effective medicament for inactivation of endotoxin.

Anti-fungal activity :- Fungi constitute a small proportion of the oral microbiota and are largely restricted to Candida albicans. It is the fungal species most commonly detected in the oral cavity of both healthy and medically compromised individuals. The incidence of C. albicans in the oral cavity has been reported to be 30–45% in healthy adults and 95% in patients infected with human immunodeficiency virus. Fungi have occasionally been found in primary root canal infections, but they are more common in filled root canals in teeth that have become infected some time after treatment or in those that have not responded to treatment. A large number of other yeasts have also been isolated from the oral cavity, including C. glabrata, C. guilliermondii, C. parapsilosis, C. krusei, C. inconspicua, C. dubliniensis, C. tropicalis and Saccharomyces species.

Waltimo et al. (1999a) reported that C. albicans cells were highly resistant to Ca(OH)2 and that all Candida species (C. albicans, C. glabrata, C. guilliermondii, C. krusei and C. tropicalis) were either equally high or had higher resistance to aqueous calcium hydroxide than did E. faecalis. Because C. albicans survives in a wide range of pH values, the alkalinity of saturated Ca(OH)2 solution may not have any effect on

C. albicans. In addition, Ca(OH)2 pastes may provide the Ca2+ ions necessary for the growth and morphogenesis of Candida. These mechanisms may explain why

Ca(OH)2 has been found to be ineffective against C. albicans (Siqueira & Sen 2004).

Combinations of Ca(OH)2 with camphorated paramonochlorophenol or CHX have the potential to be used as effective intracanal medicaments for cases in which fungal infection is suspected.

As an anti-inflammatory agent, to reduce inflammation of pulp remnants or periapical tissues :- The reduction of inflammation is primarily aimed at alleviation of pain and any acute exacerbation.  Trope (1990) compared the effect of formocresol, a corticosteroid/antibiotic formulation and calcium hydroxide on the incidence of post-instrumentation 'flare-ups', and found no significant difference in the 'flare-up' rate between the three intracanal medicaments. A corticosteroid-antibiotic mixed with calcium hydroxide has also been advocated as an intracanalmedicament (Heithersay et al. 1990). However, addition of calcium hydroxide to the corticosteroid-antibiotic decreased their individual antibacterial effectiveness (Seow 1990). It was concluded that the combination of two medicaments did not produce any additive or synergistic effects, and should not be used in combination, since the antibacterial activity of the individual components may be affected.

Dissolution of necrotic material:- The ability of calcium hydroxide to dissolve necrotic material was reported by Hasselgren et al. (1988). Its action is similar to that of sodium hypochlorite, but is less effective. However, its prolonged presence in the root canal, where it has a continuous therapeutic effect, must largely compensate for this.

Diffusion of hydroxyl ions through dentine:- For calcium hydroxide to act effectively as an intracanal medicament, hydroxyl ions must be able to diffuse through dentine.  Nerwich et al. (1993) investigated pH change over a 4-week period after application of a Ca(OH)2 dressing and concluded that hydroxyl ions derived from Ca(OH)2 dressings diffused in a matter of hours into the inner root dentine but required 1–7 days to reach the outer root dentine and 2–3 weeks to reach peak levels. Hydroxyl ions diffused faster and reached higher levels cervically more than apically. Saif et al. (2008) indicated that a final canal rinse with 3 mL 17% EDTA and 10 mL 6% NaOCl before Ca(OH)2 placement allowed the greatest hydroxyl ion diffusion to the root surface.

In summary, it seems that diffusion of hydroxyl ions through dentine depends on the period of medication, diameter of dentinal tubules (cervical versus apical) and smear layer removal (patency of dentinal tubules).

Buffering effect of dentine on Ca(OH)2:- The root canal milieu is a complex mixture of a variety of organic and inorganic components. Hydroxyapatite is the major representative of the inorganic components, whilst pulp tissue, micoorganisms and inflammatory exudate, rich in proteins such as albumin, are the major organic components. The substantial effect of dentine on the antibacterial activity of Ca(OH)2 can be attributed to the buffering action of dentine against alkali (Wang & Hume 1988). Both laboratory and in vivo studies have shown that buffering by dentine, particularly in the subsurface layers of the root canal walls, might be the main factor behind the reduced antibacterial effect of Ca(OH)2 (Haapasalo et al. 2000). Besides dentine, remnants of necrotic pulp tissue as well as inflammatory exudate might affect the antibacterial potential of endodontic disinfectants (Haapasalo et al. 2007).

In summary, it seems that dentine, hydroxyapatite and remnants of necrotic pulp tissue as well as inflammatory exudate decrease the antibacterial potential of Ca(OH)2. In other words, Ca(OH)2 is likely to be effective under laboratory conditions but relatively ineffective as a medicament in vivo.

Physical barrier:- In addition to eliminating remaining viable bacteria unaffected by the chemomechanical preparation of the root canal, calcium hydroxide also act as a physicochemical barrier, precluding the proliferation of residual microorganisms and preventing the reinfection of the root canal by bacteria from the oral cavity.

Because calcium hydroxide has low water solubility, it is slowly dissolved in saliva, remaining in the canal for a long period, delaying the bacterial progression toward the apical foramen. Despite the vehicle used, calcium hydroxide seems to act as an effective physical barrier and kill remaining microorganisms by withholding substrate for growth and by limiting space for multiplication. It certainly may be one of the possible antimicrobial actions of calcium hydroxide.

Synergism between Ca(OH)2 and sodium hypochlorite:- Chemicals should be used to supplement mechanical cleansing of canals, and irrigation with sodium hypochlorite and/or intracanal placement of Ca(OH)2 are used as therapeutic agents in an attempt to alter the properties of tissue remnants and microorganisms so as to facilitate their removal/killing (Yang et al. 1995). The synergy between Ca(OH)2 and sodium hypochlorite is controversial. Hasselgren et al. (1988) reported an enhancement of the tissue-dissolving capability of sodium hypochlorite when the tissue was pretreated with Ca(OH)2 for 30 min, 24 h and 7 days.

Wadachi et al. (1998) evaluated the tissue-dissolving ability of NaOCl and Ca(OH)2 in a bovine tooth model and reported that the amount of debris was reduced remarkably in teeth treated with NaOCl for >30 s or Ca(OH)2 for 7 days. However, the combination of Ca(OH)2 and NaOCl was more effective than the separate treatments.

In summary, the pretreatment of root canals with Ca(OH)2 enhances the tissue-dissolving capability of sodium hypochlorite, and this may confer an advantage to multiple-visit root canal treatment where NaOCl would be used following a period of Ca(OH)2 medication.

Ca(OH)2 and chlorhexidine :- Chlorhexidine is a cationic biguanide whose optimal antimicrobial activity is achieved within a pH range of 5.5–7.0. Therefore, it is likely that alkalinizing the pH by adding Ca(OH)2 to CHX will lead to precipitation of CHX molecules, thereby decreasing its effectiveness (Mohammadi & Abbott 2009). It has been demonstrated that the alkalinity of Ca(OH)2 when mixed with CHX remained unchanged (Haenni et al. 2003). Therefore, the usefulness of mixing Ca(OH)2 with CHX still remains unclear and controversial.

When used as an intracanal medicament, CHX was more effective than Ca(OH)2 in eliminating E. faecalis from inside dentinal tubules (Athanassiadis et al.2007).

In a study using agar diffusion, Haenni et al. (2003) could not demonstrate any additional antibacterial effect by mixing Ca(OH)2 powder with 0.5% CHX and reported that CHX had a reduced antibacterial action. However, Ca(OH)2 did not lose its antibacterial properties in such a mixture. This may be because of the

deprotonation of CHX at a pH >10, which reduces its solubility and alters its interaction with bacterial surfaces as a result of the altered charge of the molecules. In a laboratory study using human teeth, Ercan et al. (2006) reported that 2% CHX gel was the most effective agent against E. faecalis inside dentinal tubules, followed by a Ca(OH)2/2% CHX mixture, whilst Ca(OH)2 alone was totally ineffective, even after 30 days. The 2% CHX gel was also significantly more effective than the Ca(OH)2/2% CHX mixture against C. albicans at 7 days, although there was no significant difference at 15 and 30 days. Ca(OH)2 alone was completely ineffective against C. albicans.

In summary, the descending order of the antimicrobial activity of Ca(OH)2, CHX and their combination is as follows: CHX, Ca(OH)2/CHX and Ca(OH)2.

Influence of the vehicle on the antimicrobial activity :- A plethora of substances have been used as vehicles for calcium hydroxide. They ideally must not change the pH of calcium hydroxide significantly. They include distilled water, saline solution and glycerine, camphorated paramonochlorophenol (CMCP) and metacresylacetate. Siqueira & Uzeda (1996) verified that calcium hydroxide/saline solution paste was ineffective in eliminating E. faecalis and F. nucleatum from dentinal tubules even after 1 week of exposure. In contrast, a calcium hydroxide/CMCP/glycerine paste effectively killed bacteria in the tubules after 1 h exposure, except for E. faecalis that required 1 day of exposure.

Siqueira & Uzeda (1998) evaluated the influence of three different vehicles on the antibacterial activity of calcium hydroxide and found that calcium hydroxide with CMCP has a broader antibacterial spectrum, a higher radius of antibacterial action, and kills bacteria faster than mixtures of calcium hydroxide with inert vehicles. Therefore, CMCP cannot be considered a vehicle for calcium hydroxide, but an additional medicament. Although CMCP has strong cytotoxic activities, the association of calcium hydroxide/CMCP mixtures owes its biocompatibility to:

1. the small concentration of released paramonochlorophenol (MCP). Calcium hydroxide plus CMCP yields calcium paramonochlorophenolate, which is a weak salt that progressively releases MCP and hydroxyl ions to the surrounding medium. The low release of MCP from the paste might not be sufficient to have cytotoxic effects.

2. the denaturing effect of calcium hydroxide on connective tissue, which may prevent the tissue penetration of MCP, reducing its toxicity.

Toxicity of Ca(OH)2 in medicaments:- Early reports on the outcome of Ca(OH)2 extruded into the periapical region concluded it was well tolerated and was resorbed (Martin & Crabb 1977). Pissiotis & Spangberg (1990) evaluated mandible bone reactions of guinea pigs to implants of hydroxyapatite, collagen, and Ca(OH)2, alone or in different  combinations, over a period of 16 weeks. Findings revealed that no major inflammatory reactions occurred in any of the implant combinations. Hydroxyapatite was not resorbed over the examination periods, but Ca(OH)2 and collagen implants were partially or totally resorbed and replaced by bony tissue.

Calcium oxide is converted into Ca(OH)2 when the paste is prepared with water. In contact with tissue fluids, this mixture would dissociate into calcium and hydroxyl ions. The calcium ions reacting with the carbonic gas of the tissues would originate the calcite granulations. Close to these granulations, there is accumulation of fibronectin, which allows cellular adhesion and differentiation.

In summary, it seems that Ca(OH)2 paste is well tolerated by bone and dental pulp tissues. However, its effect on the periodontal tissue is controversial.

Calcium hydroxide points:- Despite its good anti microbial effect, it exhibits poor handling properties and its distribution throughout the entire canal is problematic. Another challenge is the complete removal of the suspension. Presence of residual calcium hydroxide can impede the properties of endodontic sealers or its distribution into the lateral canals. An innovative solution to these drawbacks was the introduction of calcium hydroxide releasing gutta percha points which contain calcium hydroxide instead of zinc oxide at a concentration of 50-54% (wt %). They can be easily inserted and removed form the pulp space when their role is accomplished.

The temporary calcium hydroxide points combine the efficiency of calcium hydroxide in matrix of bio-inert gutta-percha. The points are 28mm in length and a distinctive brown color differentiates the calcium hydroxide points form the gutta percha points (GPP). They serve as an effective alternative to calcium hydroxide paste and are available in ISO sizes of 15 to140.

An improved version of calcium hydroxide points is the calcium hydroxide plus points (CHPP) which additionally contain sodium chloride and tensides. The tensides reduce the surface stress of liquids thereby allowing a more efficient penetration into the dentinal tubules. Thus these points are capable of maintaining a high pH over a long period of time. This effect was also a reason for enhanced alkalization of outer dentin by calcium hydroxide plus points for up to 7 days.

Advantages of Calcium hydroxide points

1. Minimal or no residue left

2. No smearing around the access cavity during insertion

3. Firm for easy insertion and flexible enough to follow the natural canal curvature

4. Time saving as the points are:

_ Ready to use

_ No mixing required

_ Ease of insertion and removal with help of tweezers

5. Insertion of points down the apex is easy and ensures that calcium hydroxide is released through out the canal.

6. In addition the calcium hydroxide plus points have shown to have:

_ Three fold high calcium release than calcium hydroxide points due to highly water soluble components like tensides and sodium chloride

_ Superior pH values

_ Increased wettability of canal surfaces

_ Increased release of zinc oxide compared to normal gutta percha points thus increasing its antibacterial effects

_ Sustained alkaline pH for 7 days as against 3 days which was seen with calcium hydroxide points.

Disadvantages

1. Action is short lived

2. Lack of sustained release

3. Radiolucent

Removal of Ca(OH)2 from canals :- Remnants of Ca(OH)2 can hinder the penetration of sealers into the dentinal tubules, hinder the bonding of resin sealers to dentine, increase the apical leakage of root fillings and potentially interact with zinc oxide eugenol sealers and make them brittle and granular. Therefore, complete removal of Ca(OH)2 from the root canal before filling is recommended.

Nandini et al. (2006) reported that the vehicle used to prepare Ca(OH)2 paste was important for its removal. Oil-based Ca(OH)2 paste was more difficult to remove than Ca(OH)2 powder mixed with distilled water. Both 17% EDTA and 10% citric acid were found to remove Ca(OH)2 powder mixed with distilled water, whereas 10% citric acid performed better than EDTA in removing an oil-based Ca(OH)2 paste.

Another method to remove remnants of Ca(OH)2 from the root canal involved the use of ultrasonic devices. Overall, no technique removed the Ca(OH)2 entirely. Rotary and ultrasonic techniques, whilst not different from each other, removed significantly more Ca(OH)2 than passive irrigation.

Summary:- Bacteria vary in their pH tolerance ranges and most grow well within a range of 6±9 pH. Some strains of Escherichia coli, Proteus vulgaris, Enterobacter aerogenes and Pseudomonas aeruginosa can survive in pH 8 or 9. These bacterial species have been occasionally isolated from infected root canals, usually causing secondary infections. Certain bacteria, such as some enterococci, tolerate very high pH values, varying from 9 to 11. Bacterial tolerance to pH changes may be because of activation of specific proton pumps, specific enzymatic systems and/or buffering devices, which help to keep the internal pH practically constant. In addition to these mechanisms, some bacterial products generated during growth may help bacteria to neutralize the environmental pH.

Therefore, in order to have antibacterial effects within dentinal tubules, the ionic diffusion of calcium hydroxide should exceed the dentine buffer ability, reaching pH levels sufficient to destroy bacteria. After short-term use of calcium hydroxide, microorganisms are probably exposed to lethal levels of hydroxyl ions only at the tubule orifice. Another factor can also help to explain the inefficacy of calcium hydroxide in disinfecting dentinal tubules. The arrangement of the bacterial cells colonizing the root canal walls can reduce the antibacterial effects of calcium hydroxide, since the cells located at the periphery of colonies can protect those located more deeply inside the tubules. On the other hand, the low solubility and diffusibility of calcium hydroxide may make it difficult to reach a rapid and significant increase in the pH to eliminate bacteria located within dentinal tubules and enclosed in anatomical variations. Likewise, the tissue buffering ability controls pH changes. Because of these factors, calcium hydroxide is a slowly working antiseptic. Prolonged exposure may allow for saturation of the dentine and tissue remnants.

CALCIUM HYDROXIDE IN WEEPING CANAL: 

A persistently 'weeping/wet' canal results from seepage of apical fluids into the root canal. Calcium hydroxide is widely used as an intracanal medicament to control this continuous exudation. The elimination of exudation facilitates permanent filling of the root canal. The exact mechanism of action of calcium hydroxide is unknown, but it may be due to its antibacterial properties. Another possible explanation is that the release of hydroxyl ions and the pH shift in the process of alkaiization of calcium hydroxide provides an environment that favours repair and calcification. Other suggested mechanisms of action include the contraction of capillaries, the formation of a fibrous barrier,or formation of an apical plug by calcium hydroxide.

CALCIUM HYDROXIDE IN PERIPAICAL LESION: 

Periapical granuloma may be formed by the immunological responses of the apical tissues to chronic infection within the root canal. When small they are probably sterile, but as they increase in size they may contain an increasing variety of bacteria. Heithersay (1975) recommended that calcium hydroxide be used as a root canal dressing in teeth with large periapical lesions, and in cases where it was necessary to control the passage of periapical exudate into the canal. It is speculated that it would have a direct effect on inflamed tissue and epithelial cystic linings and in this manner would favour periapical healing and encourage osseous repair.

The osteogenic potential was recognized and reported in 1958 by Mitechell & Shankwalkar, Shah N in 1982 conducted a clinical study to evaluate efficacy of Ca(OH ) in treating periapical lesions The high alkaline ph of 8.6 to 10.3 activates alkaline phosphatase, a hydrolytic enzyme, which separates phosphoric esters, freeing phosphate ions which then react with calcium ions from the blood stream to form a precipitate, calcium phosphate in the organic matrix. This precipitate is related to the process of mineralization.

Ghose et al. (1987) has advocated that direct contact between the calcium hydroxide and the periapical tissue was necessarily beneficial for osseoinductive reasons. It is suggested that if the calcium hydroxide is confined to the root canal, it is possible that the inflammation created by the diffusion of the calcium hydroxide through the apical foramen may be sufficient to cause break-up of the cystic epithelial lining, thereby allowing a connective tissue invagination into the lesion with ultimate healing. Moreover, Souza et al. (1989) suggested that the action of calcium hydroxide beyond the apex may be fourfold: (i) anti-inflammatory activity; (ii) neutralization of acid products; (iii) activation of the alkaline phosphatase, (iv) antibacterial action.

It is apparent that its use beyond the apex intentionally or accidentally has been

associated with the successful nonsurgical management of many cases of large periapical lesions. Teeth with periapical lesions, in which calcium hydroxide paste was extruded, did not show a different healing pattern from the ones treated conventionally. Such deliberate overextension is not, however, widely advocated, since periapical extrusion of calcium hydroxide can have damaging effects.

CALCIUM HYDROXIDE IN APEXIFICATION:

The use of calcium hydroxide for apical closure was first reported by Granath (1959), and later by Frank (1966). The favourable clinical, radiographic and histological responses obtained with calcium hydroxide are related to the Ca++ and OH—ions in several mechanisms (I) control of  inflammatory reaction (by hygroscopic action; formation of calcium proteinate bridges and inhibition of phopholipase); (II) the neutralization of acidic products of osteoclasts (acidic hydrolases and lactic acid); (III) the induction of mineralization ( activation of alkaline phosphtase and calcium-dependant ATPases); (IV) the induction of cell differentiation; (V) the depolymerization of endotoxins; and (VI)antibacterial action by means of irreversible damage to DNA, proteins, enzymes and bacterial lipids.

High alkaline pH of 8.6 - 10.3 activates alkaline phosphatase (hydrolytic enzyme) which separates phosphoric esters, freeing phosphate ions which then react with calcium ions from the blood stream to form a precipitate, calcium phosphate in the organic matrix. This precipitate is related to the process of mineralization.

The average time taken for apexification to complete using CaOH is 5-20 months. So in this period, how frequently the CaOH dressing should be changed is a controversy in the endodontic literature. Majority of studies have suggested that, the initial change should be at 1 month and subsequent 3-month intervals, while others advocate changing at 1 month and again at 6-8 month intervals until apical barrier formation takes place. The original concept says that Calcium hydroxide progressively solubilises and diffuses into the tissue fluids, especially via the apical foramen, so it should be periodically renewed. But now days it is believed that there is no solubilization and dissolution of calcium hydroxide over a period of time. This may be attributed to the fact that calcium hydroxide could possibly establish zones of tissue response through the formation of calcium carbonate (CaCo3 ) as a result of the reaction of Ca(OH)2 with tissue Co2. Thus calcium hydroxide would diffuse through the hidden, microscopic spaces of the root canal system, providing continuous disinfection throughout the structure of the dentin, and ultimately obturation, by hardening in place by formation of calcium carbonate.

After apical root closure because of the physical and chemical barriers posed by the

dentine, dissolution decreased and calcium hydroxide converted into hard setting calcium carbonate which stopped its dissolution. The resultant mineralized tissue can be composed of osteocementum, osteodentine, or bone or some combination of the three. The calcific bridge can be a complete or an incomplete hard tissue bridge at the root end or a few millimeters short of it.

Chawla (6) has suggested that the amount of CaOH in the single root canal dressing was sufficient to initiate and complete the bridge in 92.3% of the teeth in his study.

Chosack et al. (12) suggested that repeated root filling are not required as CaOH is only required to initiate healing process. They also reported that the CaOH has to be replaced if there are any symptoms or displacement of the medicament. Hence it is confirmed that, if the root apex is disturbed by repeated instrumentation and dressing changes, then the time required for apex formation prolongs. Thus a single dressing is enough to induce the apical barrier formation.

CALCIUM HYDROXIDE IN PERFORATION REPAIR: 

Iatrogenic root perforations can occur during root canal treatment or when preparing a canal for a post. Perforations can be treated nonsurgically in a similar way to apical closure of immature apices, using the mineralization potential of calcium hydroxide. The timing of the procedure is similar in both cases, and success is related to the size of the perforation and avoidance of extrusion of excess material through the perforation.

Hartwell & England (1993) stated that ‘the ideal repair material should induce osteogenesis and cementogenesis, be biocompatible, non-toxic, non-carcinogenic easily obtainable, convenient to use, and be relatively inexpensive’.

The necrosis layer, formed in direct contact with calcium hydroxide, is a prerequisite for mineralization, and the tissue dissolving capacity of calcium hydroxide can be useful in the presence of ingrowth of granulation tissue into the perforation defect. Finally, because of its bactericidal properties, calcium hydroxide will disinfect ‘old’ perforations. Some authors (El Deeb et al. 1982, Himel et al. 1985) have expressed their concern about using calcium hydroxide in close proximity to the attachment apparatus because of the necrotizing properties of the material and the inflammatory reaction to it. On the other hand, the use of hard-setting calcium hydroxide to repair furcation perforations ‘did not appear to alter the pattern of healing, except to prevent ingrowth of granulation tissue into the instrumented root canal’ and was followed by a ‘high rate of repair’ (Beavers et al. 1986). Kvinnsiand et al. (1989) also found that the success rate for non-surgical treatment of perforated root canals, which included calcium hydroxide dressing, was poorest in the cervical region, and could be attributed to the close proximity of the epithelial attachment leading to a permanent periodontal defect.

Treatment of horizontal root fractures:

When root canal therapy is required it is difficult to retain the root filling, particularly the sealer, within the coronal section of the root, from which it tends to extrude into the fracture site. In these cases it has been suggested that a preliminary dressing of calcium hydroxide left in place for 3 months may encourage soft tissue healing and possibly mineralization at the fracture site. This will provide a barrier for subsequent condensation of the filling material.

CALCIUM HYDROXIDE IN ROOT RESORPTION: 

Calcium hydroxide is frequently used as a dressing for the treatment of both internal and external inflammatory root resorption, in order to halt the process and encourage remineralization.

It is doubtful whether the material has any real beneficial effect on internal resorption, as this is now considered to be sustained by infection within the dentinal tubules coronal to the resorptive process. At one time it was thought that osteoclasts

and osteocytes originated from the same progenitor cells, and that osteoclasts could divide into osteoblasts, presumably under the influence of calcium hydroxide.

However, it is now considered that these two cell types have different origins. Whether the resorption is external, or internal with communication to the periodontal membrane, calcium hydroxide is probably the initial treatment of choice, and is used in the same manner as described for closure of the apex. Andreasen (1971) was able to arrest external inflammatory root resorption following replantation, in nine cases out often, by the use of calcium hydroxide.

However, -work carried out by Cvek (1973) indicated that early obturation with gutta-percha could achieve the same result. The important aspect of treatment seems to be the elimination of the source of infection from the root canal, and obturation with gutta-percha.

CALCIUM HYDROXIDE AS ROOT CANAL SEALER: 

Among the desired biological properties of an ideal sealer is a prolonged antibacterial effect that will maintain the root canal free from micro-organisms or will prevent their proliferation when they survive instrumentation. Calcium hydroxide has been used extensively in dentistry and has also been added to several endodontic sealers to improve their biological properties and to enhance antibacterial activity. The beneficial antibacterial effect of Ca(OH)2 is attributable to its ionic constituents calcium and hydroxyl ions and to the hydroxyl alkalinising properties during its diffusion through dentine.

Caicium-hydroxide-based root canal sealers have recently been introduced as an alternative to the conventional zinc oxide-eugenol based sealers. These have a pH ranging between 8 and 9 and consist of the following:

Base paste	Catalyst paste
Calcium hydroxide 32%	Disalicylates 36%
Colophony 32%	Bismuth carbonate 18%
Silicon dioxide 6%	Silicon dioxide 15%
Zinc oxide 6%	Colophony 5%
Others 16%	Tricalcium phosphate 5%
	Others 21%

Two such materials are Sealapex and Calciobiotic Root Canal Sealer (CRCS).

CRCS: (calcibiotic root canal sealer)- takes 3 days to set fully in either dry or humid environment.

Seal apex (Sybron endo) : in 100% humidity it takes upto 3 weeks to reach a final set. In the dry atmosphere, it never sets. It is also the only sealer that expands while setting.

When the pattern of release of calcium and hydroxyl ions from different sealers was investigated by Tagger et al. (1988) it was found that Sealapex released ions and disintegrated more rapidly than CRCS, It was also found that, although the release of calcium ions from CRCS was negligible, the material continued to alkalize its environment, possibly due to free eugenol combining with calcium ions as they were released. Sonat et al. (1990) reported that hard tissue formation was more pronounced after root filling with Sealapex than with calcium hydroxide or gutta-percha.

LIFE: commonly used as a liner and pulp capping material similar in formulation to seal apex has also been suggested as a sealer.

Iodoform: containing sealers – Metapex, Vitapex, Calciform-RC, contain 40% Iodoform and silicone oil amongst other components.

MCS: medicated canal sealer  (mediadenta) contains Iodoform to go along with MGP gutta percha points that also contain 10% Iodoform.