International Endodontic Journal {Wm) 23,283-297

A review of calcium hydroxide p. C. FOREMAN & I. E. BARNES Department of Operative Dentistry, Dental School, University ofNeivcastle upon Tyne, Netvcastle upon Tyne, UK Summary. Calcium hydroxide is a material which has been used for a variety of purposes since its introduction into dentistry in the early part of the twentieth century. In its pure form, the substance has a high pH, and its dental use relates chiefly to its ability to stimulate mineralization, and also to its antibacterial properties. A range of products has been formulated with different therapeuric actions, the effects of which are partially dependent upon the tissue to which they are applied. The material is reviewed under the following general headings: biochemical actions; dental formulation; uses.

Biochemical actions Initiation ofmineralization Before considering the specific effects of calcium hydroxide, it will be helpful to describe briefly the theories of mineratization within mesenchytnal tissues. It is now widely accepted that an epitactic mechanism operates following the initial seeding of a coUagenous tissue. Only certain types of collagen, such as those found in dentine and hone, mineralize in this way. The process is probably the result of the juxtaposition of charged groups on adjacent macromolecules which give rise to the epitactic centres. These centres require a nucleation site from which hydroxyapatite crystal growth can proceed. Numerous theories abound as to the initiator of the process. Some workers have implicated chondroitin sulphate as the seed (Sohel 1955) whilst others, conversely, considered it to be an inhibitor of mineralization (Irving 1981). Other substances which have been postulated as initiators of mineralization include a vitamin D dependent protein which is capable of binding calcium (Hauschka & Reid 1978), phosphoproteins (Spector & Glimcher 1972) and phospholipids (Irving & Wuthier 1968). Correspondence: Dr P. C. Foreman, Department of Operative Dentistry, Dental School, Framlington PUce, Newcastle upon Tyne NE2 4BW, UK,

Of equal importance to the induction of mineralization is the ability to halt the process. One safety factor may be the presence in the blood and tissue of substances such as pyrophosphate ions which act as inhibitors. This action is lost when pyrophosphates are metabolized at the mineralization sites by pyrophosphatase (Fleisch & Bisaz 1962). Pyrophosphatase is a member of the alkaline phosphatase group, which may explaiti why these enzymes are invariably present in mineralizing tissues. Most of the research on mineralized tissues has been carried out on the normal mineralized tissues of the hody. Occasionally, however, other tissues such as the aorta develop a dystrophic mineralization and the presence of type 1 collagen has been implicated as an important factor in this process (Wadkins 1981). The dental pulp is also prone to dystrophic mineralization which may be either spherical or diffuse in nature, and so extensive as to obliterate the entire root canal system (Foreman & Soames 1988). Calcium hydroxide induced mineraltzation

It seems that calcium hydroxide has the unique potential to induce mineralization, even in tissues which have not been programmed to mineralize (Mitchell & Shankwaiker 1958, Binnie 1967). However, Rasmussen & Mjor (1971) could not verify that calcium hydroxide induced mature bone formation under these circumstances, but found that when the material was placed in direct conUct with hc^ tissue it induced the formation of fibrous tissue, with the occasional formation of areas of immature bone. These workers also found that when calcium hydroxide was separated from host tissue by milliporefilters,no significant reactions occurred, indicating that the material did not have any effect once it had diffused some distance. 283


P. C. Foreman S I. E. Barnes

It is atso likely that the calcium ions present in the applied calcium hydroxide do not become incorporated in the mineralized repair tissue, which derives its mineral content solely from the dental pulp, presumably via the blood supply (Sciaky & Pisanti 1960, Pisanti & Sciaky 1964). These observations indicate that calcium hydroxide is an initiator rather than a substrate for repair. The mechanism by which calcium hydroxide initiates the reparadve 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). There is a problem in accepting the hydroxyi ion as the sole initiator of the process, as it has been shown that other highly alkaline compounds such as barium hydroxide and calcium phosphate fail to initiate mineralization (Mitchell & Shankwalker 1958). However, calcium hydroxide may act as a local buffer against the acidic reactions produced by the inflammatory process (Heithersay 1975). An alkaline pH may also neutralize the lactic acid secreted by osteociasts, and this may help to prevent further destruction of mineralized tissue. Although calcium hydroxide does not become incorporated in the mineralized repair, it does appear to be involved in the initiation of the process. 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 atso 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 calciumdependent pyrophosphatase, which represents an important part of the mineralization process.

Once mineralization has been initiated, it can continue unabated if the normal selflimiting enzymes (pyrophosphates) fail to operate. The reduced capillary permeability following the increase in the number of calcium ions could reduce serumflowwithin 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). Uncontrolled mineralization of the pulp would therefore be dependent on a reduced blood supply to the remaining vital tissue and not necessarily on the amount of reparative dentine formed with time (Heide & Kerekes 1987). Andreasen (1989) also considered that mineralization of the pulp was initiated by a reduced flow in pulpal blood vessels, in this case as a result of loss of parasympathetjc inhibition. This would result in cellular respiratory depression, leading to pathological calcification of the pulp and eventual obliteration of the root canal. Recently, the mechanism of calciumhydroxide-induced mineralization has been the subject of review. Ida et al. (1989) found that the pH of setting calcium hydroxide materials with a high pH was reduced to almost neutral when the materials were placed in contact with dentine. If this is the case, it would suggest that a high pH is unnecessary for continuous mineralized tissue formation. There does, however, appear to be some conflict between this work and that of Hassetgren et al. (1982), who demonstrated an increase in the pH of calcium-hydroxide-treated dentine. Paradoxically, calcium hydroxide sometimes appears to stimulate resorption. Andreasen (1981) reported that external replacement resorption (ankylosis) of the roots of avulsed teeth may occur if they are replanted and filled immediately with calcium hydroxide. However, if the placement of the root filling is delayed for 2 weeks, resorption is less likely to occur. He si^ested that when calcium hydroxide was placed immediately.

A review of calcium hydraxide


Co (OH),


Reduced capillary permeobijity

\ \

Meutralizes acid produced by ostecclas^s

I Reduced serjm flow

Optimum pH for pyrophosphatQse oclivity

Reduced levels of ^ inhibi'ory pyrophosphate

. Increased levels cf Ca2+ dependent

» UncontrOllea

Fig. 1. Calcium hydroxide-induced mineralization.

the material diffused through the apical foramen, damaging the cementocytes. Internal resorption may follow pulpotomies performed on deciduous teeth. This commonly occurs near the iunction of the coronal and radicular pulp (Hannah & Rowe 1971, Rule 1974). Although it is possible that the high pH of calcium hydroxide may cause further irritation to already damaged tissue, internal resorption is now considered to be sustained by bacterial infection in the dentinal tubules which fortuitously communicate between necrotic and vital areas of the pulp (Tronstad !988). The dentine bridge

A mineralized barrier or 'dentine bridge' is usually produced following the application of calcium hydroxide to a vital pulp (pulpotomy). This repair material appears to be the product ofodontoblasts and connective tissue cells. The barrier may not always be complete (Holland etal. 1979). There appears to be 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. In the case of a highpH material such as fulpdent a 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. In the case of a material of 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 (Stanley & Lundy 1972, Tronstad 1974, Heys et al. 1981, Jerrelt et al. 1984, Pitt Ford 1985, Tagger & Tagger 1985). Dentine bridges formed by the highpH 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. Jean et al. (1988) have expressed doubt as to whether calcium hydroxide is the best material for inducing dentine bridge formation. In their investigation it was found that when calcium hydroxide was compared with a mixture of 50 per cent tricalcium phosphate and 50 per rent hydroxyapatite, the latter produced a thicker bridge and more rapid formation of normal tubular dentine. Other materials such as zinc oxide-eugenol cement and silicate cement have been investigated in this respccr


P. C. Foreman C /. £. Barnes

(GJX et al. 1987), but although not causing pupal inflammation (providing that they were free from bacterial contamination), the dentine bridge formation was often weak or absent. Destruction of bacteria (i) As a puip dressing. Some of the heat-

ing properties of calcium hydroxide may be attributed to its bactericidal effects. Studies on gnotobiotic rats have shown that when traumatically exposed teeth in germ-free animals were dressed, healing occurred irresjjective of the capping material used (Paterson 1972), This infers that under normal conditions healing is due to the antibacterial activity of calcium hydroxide, rather than any effect it may exert on mineralization. The bactericidal properties of calcium hydroxide have also been demonstrated by King et al. (1965) and by Fisher (1972). These properties are thought to be directly related to pH, and are directly proportional to the ability of calcium hydroxide to diffuse from the set material (Fisher & McCabe 1978). There would appear to be no clinical indications for the use of calcium hydroxide in targe old exposures with deep penetration of bacteria and chronic inflammation of the pulp, unless a radical pulpotomy is first performed. In this situation, calcium hydroxide does not have the same heating potential that it exhibits when used as a root canal dressing to treat chronically inflamed periapicat tissue. This is possibly because of the ready availability of healthy blood vessels in the periapical tissue, compared with their paucity in dying tissues in the enclosed environment of the pulp. It has been found that calcium hydroxide kilts only the bacteria on the surface of the pulp and not those that have penetrated necrotic tissue (Cox et al. 1982). Thus the material has no beneficial effect on the healing of an inflamed pulp, and its use would appear to be indicated for the treatment of healthy or superficially contaminated pulps where bacteria have not penetrated into the deeper part (Watts & Paterson 1987). (ii) As a root canal medicament. There is some uncertainty as to the efficacy of calcium hydroxide compared with other medicaments when used as an intra-canal dressir^ (Stevens & Grossman 1983, Bystrom et al. 1985, Safavi

etat. 1985). However, much of this uncertainty can be explained by the varying responses of different bacteria to antiseptic materials (Tobias f/a/. 1988). When used as a root canal dressing any material must be judged entirely as an antibacterial agent, acting without support from the tissue defence mechanisms. Thus in contrast to its mode of action in mineralization, calcium hydroxide has a non-specific bactericidal action within the confines of the root canal, alkalis in general having a pronounced destructive effect on cell membranes and protein structure (Gordon et al. 1985). Although most micro-organisms are destroyed at pH 9.5, a few can survive at pH 11 or higher (Hugo 1971). The main issue is not 'how bacteria are killed' but 'how the vital tissues can be protected from the toxicity of calcium hydroxide'. The separation of the material from the vital tissues by a zone of necrosis (Seltzer & Bender 1984) probably prevents gross tissue damage. 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. Dental formulation of calcium hydroxide (pastes) Calcium-hydroxide-containing pastes can be classified according to whether they are setting or non-setting materials. The former are generally used for the lining or sub-lining of cavities, or as root canal sealers, while the latter are used for dressing root canals. Setting materials (Table I) Therapeutic effect. The therapeutic properties of the setting calcium hydroxide materials are related to their pH. The latter is dependent on the levels of unbound calcium and hydroxyl ions that remain after the material has set, and it follows that the egress of ions from the set material will lead to a reduction of its mass. One factor which increases the availability of the hydroxyi ion is the hydrophobic nature

A review of calcium hydroxide

Table I. Antibacteriai effect of setting calcium hydroxide materials (Fisher & Shortall 1984) Strong effect Dycal (original formula) Reocap* Procal Medium effect Dycai (new formula) Lifet RenewJ Reolit* No effect iWPCf Hydrex Cal-Mer vii§ *Vivadent, Schaan/Liechtenslein. tKerr, Romulus. Michigan. tJSA. JS.S. White Co./Dentomax, Bradford, UK. ((Experimental cement devised by: Laboratory of Government Chemist, Comwali House, Stamford St, London, UK.

of the material. The more hydrophobic the latter, the less likely is diffusion to occur, A now withdrawn product, Hydrex, for example, was more hydrophobic than Dycal due to the presence of a paraffin solvent which prevented the diffusion of water into the set material (Fisher & McCabe 1978). An additional factor to be considered in the dissolution of calcium hydroxide is the effect of bacteria, associated with microleakage, on the set material. Watts & Paterson (1987) established that bacteria may be present in contact with calcium hydroxide. This could lower the pH of the material by converting it to calcium carbonate, and might explain why early Dycai preparations seemed to disappear from beneath permanent restorations (Akester 1979, Barnes &Kidd 1979). It is possible to rank the setting calcium hydroxide pastes according to the availability of their hydroxyl ions (de Freitas 1982). This ranking also corresponds with the antibacterial activities of the materials, as shown in Table I (Fisher & Shortall 1984). It is evident that if antibacterial activity is required (as in direct pulp capping), the paste should be


selected from near the top of this list, where diffusion of hydroxyl ions is greatest, whereas if an antibacterial effect is not required (when the material is to be used merely as a lining) the calcium hydroxide paste should be selected from near the bottom of the list, because such materials are less likely to leach out from beneath the restoration. The rationale for inclusion of calcium hydroxide in such nontherapeutic materials, where its high antibacterial effect is not required, is said to be its ability to react readily in the setting process (Fisher & Shortall 1984). One inherent problem in attempts to list proprietary setting type materials according to their composition is the lack of consistency in their formulation (Watts & Paterson 1987), One particular example is Dycal, which has undergone considerable changes in the percentage composition of most of its constituents since it was first introduced. It can therefore be seen that the problem for the manufacturer is to establish a balance between a material that is sufficiently soluble to exert a therapeutic effect, yet which is not so soluble that it dissolves away, thus vitiating its desired use as a mechanical lining. Setting mechanisms of calctum-hydroxidecontaining materials. There are two basic setting mechanisms. (i) The two-paste system, which is based on the reaction between calcium and zinc ions and a salicytate chelating agent, and is accelerated by the presence of water (Lim & McCabe 1982). (ii) The single-paste system, which utilizes the polymerization of a dimethacrylate by means of light, and is represented by Prisma VLC Dycal'. A potential disadvantage of the dimethacrylate systems, when used as a base beneath composite restorations, is their adherence to the composite material and subsequent withdrawal from the base of the cavity during polymerization (Papadakou 1989). Calcium hydroxide materials have also been developed for use as root canal sealers (Caiciobiodc Root Canai Sealer^, Sealapex^). " Caulk, Ltentsply, Milford, Delaware, USA. ^ Hygenic Co., Akron, Ohio, USA. 'Kerr, Sybron, Michigan, USA.


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Table II, Noti-setting calcium hydroxide materials

Uses of calcium hydroxide Lining of cavities

Material Analar CaOHj PuSfident* Hypo-Calf Reogan

Vehicle Water ,Methyl cellulose Methyl celiulose Methyl cellulose

*Pulpdent Corp. of America, Brookline, New York, USA. tEliman Dental Manufacturing Co. tnt., PO Box 68, Cedarhurst, New York, USA.

In these preparations the setting time is increased, probably by replacing calcium hydroxide with calcium oxide, in order to allow adequate time for the gutta-percha root filling to be condensed.

Non-settingmatertats (Table II) Most simply, Analar calcium hydroxide may be applied either dry, or using distilled water as the vehicle. Clinically, this has the disadvantage that the mixture forms a slurry which may separate and can be difficult to manipulate within the root canal by puddling; alternatively, it may be mixed into a very thick paste which can be placed into the root canal with an amalgam carrier and condensed with root canal pluggers. Proprietary brands overcome this problem by using methyl cellulose as a vehicle, with varying amounts of water. This results in homogeneous pastes of varying consistency, with good handling properties, such as Reogan' (Stock 1985). Other admixtures have been suggested, such as local anaesthetic solution, camphorated monochlorphenol (CMCP), beechwood creosote, Ledermix^ and radiopacifiers. With the possible exception of the last, where barium sulphate may be mixed with calcium hydroxide in a ratio of i:8 (Stock 1985), these mixtures are now out of favour because the additives may achieve very little, and indeed could adversely influence the beneficial effects of the calcium hydroxide (Magnusson 1980). ' Vivadent, Schaan, Liechtenstein. •Lederle Laboratories-Cyatmtnid of G.B. Ltd, Bush House, London, UK.

The setting calcium hydroxide pastes are now in general use as lining materials. Their perceived advantages, in addition to their therapeutic effects, are as follows. (i) They have a rapid initial set in the cavity under the accelerating effect of moisture in the ambient air of the orai cavity and from within the dentinal tubules, (ii) They do not interfere with the setting reaction of Bis-GMA resins, and are therefore the lining material of choice under composite resin material, (iii) It is generally considered that the initial set of the material in thin sections is sufficiently hard to resist the applied condensation pressures that are required even for lathe cut amalgam alloys (Lim & McCabe 1982). (iv) It has been shown that the light-cured resins are biocompatible (Cox et al. 1987) and will not cause pulpal damage. However, it is possible that detrimental effects may occur, particularly in deep cavities close to the pulp, as a result of the effects of heat generated during setting. The disappearance of the early versions of these materials from beneath restorations was probably due to the effects of bacteria and microleakage. Indirect pulp capping

In this procedure, grossly carious dentine is removed and the underlying soft dentine is covered with either calcium hydroxide or zinc oxide-eugenol cement. Both materials have bactericidal properties (King et al. 1965, Fisher 1972) which help to control (Fisher 1977) but not entirely eliminate (Watts & Paterson 1987) the few viable organisms that may remain. Calcium hydroxide may have a slight advantage in this situation as it can also stimulate the healing of a minute pulpal exposure which may have been overlooked. There is also evidence that calcium hydroxide stimulates an increase in mineralization within the dentine that remains at the base of a cavity (Eidelman et al. 1966, Mjor 1967). This mechanism may explain the reported reduction in permeability (in vitro) of both dentine and the smear layer when calcium

A review of calcium hydroxide

hydroxide is applied (Pashley et al. 1986). However, a similar increase in mineralization has been reported to follow the application of zinc oxide-eugenol cement (Kerkhove et at. 1967, Stewart & Richardson 1968). Direct pulp capping

Direct pulp capping is undertaken in an attempt to maintain the health of an exposed vital pulp. The advent of the setting materials simplified the placement of calcium hydroxide because no further reinforcement was necessary. The following criteria must be observed if successful direct pulp capping is to be achieved. (i) There must be no symptoms of pulpitis (Nyborg 1955, 1958). If calcium hydroxide is used to cap an inflamed pulp, necrosis will probably occur due to the presence of bacterial infection. Under these conditions, Tronstad & Mjor (1972) found zinc oxide-eugenol cement to be more effective, although this would normally be regarded as the wrong material to use (Cox et al. 1987). (ii) In the case of a carious exposure, there is general agreement that the larger the exposure the poorer the prognosis, because of the magnitude of contamination by micro-organisms (Seltzer & Bender 1984). In the case of a traumatic exposure with no bacteria! contamination, the size of the exposure is immaterial (Cvek 1978). (iii) Bacterial contamination from saliva should be prevented if possible (Seltzer & Bender 1984). However, work by Cox et al. (1982) demonstrated that the pulp still healed when a traumatic exposure was exposed to saliva for periods of up to 7 days, because the bacteria had not penetrated deep into the pulp tissue, (iv) Young permanent teeth are more successfully treated than older permanent teeth because of the open apical foramen and the improved blood supply to the pulp. In deciduous teeth, the operation of pulpotomy is more successful than pulp capping when there is carious involvement of the pulp (Massler 1967).


It has been reported that pulp capping procedures on trautnaticaliy exposed teeth, in which bacterial contamination is minimal, can produce successful results in 96 per cent of cases (Cvek 1978). The size of the exposure was found to have no bearing on the results, and the study included both mature and immature teeth. However, pulps with mineralized deposits within the canal are not recommended for pulp capping procedures because their repair potential is considered to be reduced. (Cvek 1981). Pulpotomy The operation of pulpotomy differs from direct pulp capping in that surgical removal of part of the coronal pulp is undertaken. It used to be standard clinical practice to amputate the entire coronal pulp prior to application of the calcium hydroxide dressing. However, work by Cvek (1978) on traumatically exposed, non-carious pulps showed that it was only necessary to remove the inflamed tissue, which extended merely a few millimetres into the pulp, regardless of the size of the exposure or the length of time that it had been left untreated. In the case of a carious exposure, the area of inflammation extends further into the pulp and it is probable that rather more pulp tissue would need to be removed (Camp 1987). Calcium hydroxide, for covering the amputated pulp, may be in the form of a hard setting material, a non-setting material, or a slurry of freshly mixed powder and saline. The use of calcium hydroxide mixed with medicaments for pulpotomy dressing is no longer recommended because there is little possibility of improving the properties of the material (Magnusson 1980), The healing process is similar to that which occurs in direct pulp capping. Dressing of the root canal

Routine dressing. It is doubtful whether routine dressings (medicaments) are necessary for root canal therapy in root canals that contain vital pulp tissue as these are not infected prior to instrumentation, or in contaminated canals which have been cleaned and shaped with modem instrumentation techniques combined with the copious use of sodium hypochlorite.


P. C. Foreman (£ I. E. Barnes

However, if a root canal is heavily infected prior to instrumentation, it is highly probable that a few bacteria will remain (Bystrom & Sundqvist 1981, PittFord 1982, Bystrom et al. 1985). In these circumstances, a dressing with calcium hydroxide which can be placed the full length of the canal is the treatment of choice. If the material is inadvertently forced through the apical foramen it is soon absorbed. An inflammatory cell response has been observed in the periapical tissues of dogs' teeth when calcium hydroxide was extruded through the apical foramen (Sonat et al. 1990); in addition to this response, periodontal fibre organization and formation of new cementum and alveolar bone was also seen.

hydroxide is now widely used to reduce the seepage of apical fluids into the canal so as to allow the placement of a satisfactory root filling. The mechanism whereby the reduction of seepage occurs is probably due to the fibrous barrier that is formed when calcium hydroxide is placed in direct contact with host tissues (Rasmussen & ,Mjor 1971), or to the contraction of capillaries, as suggested by Heithersay (1975), or simply to the effect of mechanical blockage. The ability of calcium hydroxide to dissolve necrotic tissue (Hasselgren et al. 1988) is useful, as anatomical problems often make it difficult for irrigating solutions to reach ail areas of the root canal. In this respect, it has been found that when a calcium hydroxide Long-term temporary dressing. When a dressing dressing was used in addition to irrigation with sodium hypochlorite, the canal was cleaned as is placed in a root canal it is usually removed effectively as when ultrasonic instrumentation after a few days and the canal permanently was used (Metzler & Montgomery 1989). filled with gutta-percha. On occasion it is necessary, for reasons of personal convenience, to leave the dressing in the canal for a considerApical closure. The closure of the apex of able period of time. Under these circumstances a non-vital tooth, following dressing of the calcium hydroxide may be regarded as the root canal with calcium hydroxide, may occur dressing material of choice because its antimieither by continued root development if formacrobial effect may last for weeks, whilst that of tive elements (Hertwig's sheath) remain, or by other chemicals is relatively brief (Bystrom et the formation ofa calcific barrier ofmineralized al. 1985). scar tissue across the apical foramen. This barrier may be quite deep, and is formed by a cementum-like tissue with loose connective Treatment of infected root canals and periapical tissue inclusions (Heithersay 1975). As a lesions. Periapical granulomata may be formed result, the length of the ultimate root filling by the immunological responses of the apical could be considerably short of the radiographic tissues to chronic infection within the root apex. In both types of closure of the apex it is canal. When small they are probably sterile, invariably found that lateral canals are formed but as they increase in size they may contain at the junction between the original root and an increasing variety of bacteria (Sundqvist the newly formed tissue (Heithersay 1975). 1976). In such cases it seems reasonable to use a dressing which can be placed as close to The use of calcium hydroxide for apical the lesion as possible. Heithersay (1975) recclosure was first reported by Granath (1959), ommended that calcium hydroxide be used as and later by Frank (1966). Closure of the apex a root canal dressing in teeth with large perihas been successfully completed to a similar apical lesions, and in cases where it was necessdegree when calcium hydroxide has been comary to control the passage of periapical exudate bined with other materials such as CMCP into the canal, Matsumiya & Kitamura (1960) (Frank 1966) and Ringer's solution (Cvek et al. considered that calcium hydroxide acceler1976). In addition to these admixtures, equal ated the natural healing of periapicai lesions, success has been achieved with tricalcium regardless of the bacterial status of the root phosphate (Koenigs et al. 1975) and zinc oxide canal at the time of placement of the material. pastes (Cooke & Rowbotham 1960). Apical However, there has been some doubt expressed closure has been reported to occur even withconcerning the ability of tissues to heal under out the presence of a root filling material these circumstances (Pitt Ford 1982), Calcium (England & Best 1977), and it would appear

A review of calcium hydroxide

that success depends more upon the thorough cleaning of the canal than on the type of dressing inserted. According to Tziafas et al. (1987), there is some doubt as to whether truly pulpless teeth are capable of normal apex formation, as a small amount of residual apical pulp is required. It is probable that in cases where an increase in root length occurs, elements of the root sheath have survived the initial inflammation and endodontic instrumentation. In the remainder of cases, in which a calcific barrier forms across the root-end, the process is not true apex formation, but rather formation of a calcific barrier of cementum. Because calcium hydroxide materials are inherently soluble, they must be replaced at 3-monthly intervals until closure of the apex has occurred, usually after 6-24 months (Yates 1988). Prevention ofroot resorption (i) Idiopathic. 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 dentinat tubules coronal to the resorptive process (Tronstad 1988). At one time it was thought that osteociasts and osteocytes originated from the same progenitor cells (Kember 1960), and that osteociasts could divide into osteoblasts (Rasmussen&Bordier 1974), presumably under the influence ofcalcium hydroxide. However, it is now considered that these two cell types have different origins (Bonucci 1981, Marks 1983). 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. Recently, further doubt has been expressed about the usefulness of calcium hydroxide in cases of early external cervical inflammatory resorption, where there is no direct communication with the surface of the root, as it has been shown that the calcium ion cannot diffuse through dentinal tubules (Fuss et at. 1989). This view has also been supported by the work of Wang & Hume (1988), who demonstrated that hydroxyl ions would not pass through dentine. The important aspect of treatment seems to be the elimination of the source of infection from the root canal, and obturation with gutta-percha. (ii) Follomftg the replacement of an avulsed tooth, or transplantation of a tooth. Once an avulsed tooth has been splinted in position for about 2 weeks the root canal should be thoroughly cleaned and dressed with calcium hydroxide for a period of 3-6 months, prior to the placement of a conventional rootfilling.Although it has been shown that calcium and hydroxyl ions do not diffuse through the dentine, the calcium hydroxide may still permeate through lateral canals, Andreasen (1981) has warned that immediate placement of calcium hydroxide can stimulate early resorption. He postulated that when placed into the root canal immediately after replacing the tooth, calcium hydroxide diffuses through the apical foramen, further injuring the cementum and initiating resorption. Calcium hydroxide treatment has no effect on replacement r^orption (ankylosis) once it has become established. The principles of managing transplanted teeth, once pulpal necrosis has been confirmed, are essentially the same as those that relate to replantation. Repair of iatrogenic perforations. It has been reported that ]>erfDrations of the root canal wall, by instruments or by posts, may be treated in a similar way to apical dosure, in an attempt to obtain hard tissue formation (Heithersay 1975, Zeigler & Serene 1987). The timing of the procedure is similar in both cases, and success is very much related to


P. C. Foreman !S I. E. Barnes

the size of the perforation (Stock 1985) and the avoidance of extrusion of excess material through the perforation (Bergenholtz et al. 1979), It is also important to consider the position of the perforation. Beavers et al. (1986) reported necrosis of the periodontal membrane coronal to perforated areas subsequent to the placement of calcium hydroxide. They also stressed the importance of an early preliminary dressing of the perforation with calcium hydroxide to prevent the ingrowth of granulation tissue. These findings were attributed to the fact thatfibroblastsfrom the periodontal membrane lack the capacity of pulpal fibroblasts to differentiate into odontobtasts. 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. The calcium hydroxide sealer, Sealapex, was used by Beavers et at. (1986) to treat root canal perforations. They observed bone healing and ingrowth of trabeculae into the perforation after 42 days. There was also reparative cementum formation and ankylosis. The use of calcium hydroxide in the treatment of root perforations has been questioned by Himel et al. (1985), who found that when the material was compared with tricalcium phosphate the latter caused less tissue destruction and provided a better matrix against which the canal could be obturated. However, Sinai et at. (1989), in a study using the rat model, found no significant differences between calcium hydroxide and tricalcium phosphate in the repair of perforations of the root canal, with no bone formation occurring over the 1-month period of the investigation. This issue as yet appears to be unresolved. Treatment of horizontal root fractures. When root canal therapy is required it is difficult to retain the root filling, particularly the seaier, 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 - ^ mcmths may encourage soft tissue healing and possibly mineralization at

Table III. Formula of Sealapex (as supplied by Kerr UK Ltd March 1990) Paste


Base paste Calcium oxide Butyl benzene sulpbonamide Zinc oxide Zinc stearate Sub micron silica

46.0 38.5 12.0 2.0 1.5

Catalyst paste Barium sulphate Life resin Isobutyl salicylate Sub micron silica Titanium dioxide Iron oxide pigment

39.3 33.0 17.0 6.5 4.0 0.2

the fracture site. This will provide a barrier for subsequent condensation of the filling materia! (Cvek 1974, 1981). Constituent of root canal sealers

Caicium-hydroxide-based root canal sealers have recently been introduced as an alternative to the conventional zinc oxide-eugenol based sealers. Two such materials are Sealapex (Table 3) and Caiciobiotic Root Canal Sealer (CRCS). In the case of the former the setting mechanism is retarded, by the replacement of the hydroxide with calcium oxide, compared with the lining cement. The rationale for the use of these materials is that if they are used in canals with wide apical foramina, perforations or fractures, mineralized repair tnay be further induced (Holland & de Souza 1985). However, the lack of success reported by Beavers et al. (1986) in the treatment of iatrogenic perforations has already been mentioned. In addition, Pitt Ford & Rowe (1989) reported that the success rate of these materials did not differ from that with zinc oxide-eugenol cement. 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

A review of calcium hydroxide free eugenol combining with calcium ions as they were released. The rise in pH caused by two calcium-hydroxide-containing sealers was investigated by Gordon & Alexander (1986). They found that it was insufficient to produce beneficial biological changes, although Zmener & Cabrini (1987) observed adverse effects when blood monocytes and lymphocytes were maintained in contact with these materials. Sonat et al. (1990) reported that hard tissue formation was more pronounced after root filling with Sealapex than with calcium hydroxide or gutta-percha, at least in dogs' teeth. Tests on both sealers suggested that only a small amount of apical leakage occurred (Cohen et at. 1985). Zmener (1987) compared these sealers with Tubli-Seal\ and found that the degree of leakage of all materials, including Tubli-Seal, was similar and increased with time. Hovland & Dumsha (1985) aiso showed that there was no significant difference between the apical seals produced by these materials compared with that produced by Tubli-Seal. It must be pointed out that all these assessments were short-term studies, and the question of what happens in the long term has yet to be resolved.


ANDREASEN, J . O . (1971) Treatment of fractured and avulsed teeth. Journal of Dentistry for Children, 38,29-31,45-48. ANDREASEN, J.O. (1981) Traumatic Injuries of the Teeth, 2nd edn, pp, 203-236. Munksgaard, Copenhagen. BARNES, t.E. & KIDD, E . A . M . (1979) Disappearing

Dycal (letter). British Dental Journal. 147, U1. BEAVERS, R.A., BERGENHOT-TZ, G . 8e Cox, C.F.

(1986) Periodontal wound healing following intentional root perforations in permanent teeth of Macaca muiatta. International Endodontic Journal, 19,36-44. BERGENHOLTZ, G . , LEKHOLM, U . , MILTHON, R. &

ENGSTROM, B . (1979) Influence of apical overinstrumentation and overfilling on re-treated root catials. Journal of Endodontics 5,310-314. BtNNiE, W.H. (1967) A histological study of induced calcification in the subdermal tissues of the rat. MSD Thesis. Indiana University' School of Dentistry, IndiatiapoUs, tndiatia. BONUCCI, E. (1981) New knowledge on the origin, function and fate of osteociasts. Clinical Orthopaedics and Related Research, 158,252-269. BvsTROM, A. & SUNDQVIST, G, (1981) Bacteriologic evaluation of the efficacy of mechanical root canal instrumentation in endodontic therapy. Scandinavian Journal ofDental Research, 89,321-328. BvsTROM, A. & SUNDQVIST, G. (1985) The antibacterial action of sodium hypochlorite and EDTA in 60 cases of endodontic therapy. International Endodontic Journal, 18,35-40. BYSTROM, A., CLAESSON, R . & SUNDQVIST, G .

Conclusions The uses of calcium hydroxide have been described. The material appears to be of particular value in dentistry, both in its pure form and as a constituent of proprietary cements. However, a less empirical and more scientific evaluation of the mechanisms of its effects and efficacy is required, and is currently being undertaken. Although the material is not a panacea for dental problems, it is possible that in the future further applications will be developed. References AKESTER, J. (1979) Disappearing Dycal (Setter). British Dental Journal, 146,369. ANDREASEN, F . M . (1989) Pulpal healing after luxation injuries and root fracture in the permanent dentition. Endodontics and Dental Traumatology, S, ttl-13L

(1985) The antibacterial effect of camphorated paramonochlorophenol, camphorated phenol and calcium hydroxide in the treatment of infected root cattals. Endodontics and Dental Traumatolog), 1, 170-175. CAMP, J.H. (1987) Pedodontic-endodontic treatment. In Pathways of the Pulp, (eds S. Cohen and R.C. Burns). 4th edn, pp. 685-722. C.V. Mosby Co., St Louis. COHEN, T . , GUTMANN, J . L . & WAGNER, M . (1985)

,^n assessment in vitro of the sealing properties of Calciobiotic Root Canal Sealer. International Endodontic Journal, 18,172-178. CooKE, C. & ROWBOTHAM, T . C . (1960) Root canal therapy in tion-vital teeth with open apices. British Dental Journal, 108,147-150. Cox, C.F., BERGENHOLTZ, G . , FITZGERALD, M . , HEVS, D.R., HEYS, R.J., AVKY, J.K., BAKER,

J.A. (1982) Capping of the dentai pulp mechanically exposed to the oral microflora—a 5-week observation of wound healing in the monkey. Journal of Oral Pathology, 11,327-339. Cox, C,F., KEALL, C.L., KEALL, H.J., OSTRO, E .

' Kerr, Romulus, Michigan, USA.

& BEHGEJJHOLTZ, G , (1987) Biocompatibility of


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surface-seated dental materials against exposed pulps. Journal of Prosthetic Dentistry, 57,1-8. CVEK, M . (1973) Treatment of non-vital permanent incisors with calcium hydroxide. tL Effect on external root resorption in luxated teeth compared with effect of root filling with guttapercha. A follow-up. Odontologisk Revy, 24, 343-354. CVEK, M . (1974) Treatment of non-vital permanent incisors with calcium hydroxide. IV. Periodontal healing and closure of the root canal in the coronal fragment of teeth with intra-alveolar fracture and vital apical fragment. A foilow-up. Odontologisk Revy, 25,239-246. CVEK, M . (1978) A clinical report on partial pulpotomy and capping witb calcium hydroxide in permanent incisors with complicated crown inaxae. Journal of Endodontics, 4,232-237. CVEK, M . (1981) Endodontic treatment of traumatized teeth. In Traumatic Injuries of the Teeth (ed. j . O . Andreasen), 2nd edn, pp. 321-383. Munksgaard, Copenhagen. CVEK, M . , HOLLENDER, L . & NORD, C . E . (1976)

Treatment of non-vital permanent incisors with calcitmi hydroxide. VI. A clinical, microbiological, radiological evaluation of treatment in one sitting of teeth witb mature and immature root. Odontologisk Revy, 27, 93-108. EIDELMAN, E . , FINN, S . B . & KOULOURIDES, T .

(1966) Remineralization of carious dentin treated with calcium hydroxide.J'ourBa/ of Dentistry for Children, 32, ll»-225. ENGLAND, M . C . & BEST, E . (1977) Non-itiduced

apical closure in immature roots of dogs' teeth. Journal of Endodontics, 3,411^17, FISHER, F.J. (1972) Tbe effect of calcium hydroxide/water paste on micrct-organisms in carious dentine. British Dental Journal, 133,19-21. FISHER, F.J. (1977) The effect of three proprietary lining materials on micro-oi^anisms in carious dentine: an in vivo investigation. British Dental Journal, 143,231-235. FISHER, F.J. & MCCABE, J . F . (1978) Calcium

hydroxide base materials. An investigation into the relationship between chemical structure and antibacteriai properties. British Dental Journal, 144, 341-344. FISHER, F.J. & SHORTALL, A . C . (1984) Setting

calcium hydroxide base tnaterials. Studies on the antibacterial effects in vitro. British Dental Journal, 157,13J-t35. FLEISCH, H . & BiSAZ, S. (1962) Mechanism of calcification: inhibitory role of pyrophosphate. Nature, 195,911. Fc«EMAN, P.C. & SoAMES, J.V. (1988) Structure and composition of tubular and non-tubular deposits in root canal systems of human penna-

nent teeth. International Endodontic Journal, 21, 27-36. FRANK, A . L . (1966) Therapy for the divergent puipless tootb by continued apical formation. Journal of the American Dental Association, 72, 87-93. FREITAS, J.F. DE (1982) Characterization and aqueous extraction of calcium bydroxide materials. Australian Dental Journal, 27, 352-356 Fuss, Z., SzAjKis, S. & TAGGER, M . (1989) Tubular permeability to calcium hydroxide and to bleaching agents. Journal of Endodontics, 15, 362-364. GORDON, T.M. & ALEXANDER, J.B. (1986) In-

fluence on pH level of two calcium hydroxide root canal sealers in vitro. Oral Surgery, Oral Medicine and Oral Pathology, 6t, 624-628. GORDON, T.M., RANLY, D M . & BOYAN, B . D .

(1985) The effects of calcium hydroxide on bovine pulp tissue: variations in pH and calcium concentrations. Journal of Endodonttcs, It, 156— 160. GRANATH, L - E . (1959) Nagra synpunkter pa behandiingenavtraumatiseradeincisiverpabarn. Odontologisk Revy, 10,272. Guo, M.K. & MESSER, H.H. (1976) Properties of Ca^* Mg^* activated adenosine triphosphate from rat iticisor pulp. Archives of Oral Biology, 21, 637-640. HANNAH, D . R . & ROWE, A . H . R . (1971) Vital pulp-

otomy of deciduous molars using Nj and other materials. British Dental Journal, 130,99-170. HASSELGREN, G . , KEREKES, K, & NELLESTAM, P.

(1982) pH changes in calcium hydroxide-covered ientin. Journal of Endodontics, 8,502-505. HASSELGREN, G . , OLSSON, B . & CVEK, ,M. (1988)

Effects of calcium hydroxide and sodium hypochlorite on the dissolution of necrotic porcine muscle tissue. Journal of Endodontics, 14, 125127. HAUSCHKA, P.V. & REID, M X . (1978) Vitamin D

dependence of a calcium-binding protein conaining gamma-carboxygiutamic acid in chicken bone. Journal of Biological Chemistry, 253, 9063-9068. HEIDE, S. & KEREKES, K . (1987) Delayed direct puip capping in permanent incisors of monkeys. International Endodontic Journal, 20,65-74. HEITHERSAY, G . S . (1975) Calcium hydroxide in the treatment of pulpless teeth witb associated pathology. Journal of the British Endodontic Society, 8,74-93. HEYS, D.R., Cox, C,F., HEYS, R . J . & AVERY, j . K .

(1981) Histological considerations of direct pulp cappitig agents. Journal of Dental Research, 60, 1371-1379.

A review of calcium hydroxide HIMEL, V.T., BRADY, J. & WEIR, J. (1985) Evalu-

ation of repair of mechanical perforatiotis of the pulp chamber floor using biodegradable tricalcium phosphate or calcium hydroxide. JourBa/ of Endodontics, 11,161-165. HOLLAND, R . , NERY, M.J., DE MELLO, W . , DE SOUZA, V., BERNABE, P . F . E . & OTOBONI FILHO,

J.,'\. (1979) Root canal treatment with calcium hydroxide :1. Effect of overfilling and refilling. Oral Surgery, Oral Medicine and Oral Pathology, 47,87-92. HOLLAND, R. & DE SOUZA, V. (1985) Ability of a

new calcium hydroxide root catial filling material to induce hard tissue formation. Journal of Endodontics, 11,535-543.



MELFI, R . C . & DRISKELL, T . D . (1975) Induced

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GRON,NI.NGSAETER, A . G . (1989) A clinical and roentgenological study of 55 cases of root perforation. International Endodontic Journal, 22, 75-84. LANGELAND, K . , DOWDEN, W.E., TRONSTAD, L .

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HOVLAND, E.J. & DUMSHA, T.C. (1985) Leakage

LIM, M . Y . L . & MCCABE, J.F. (1982) Lining

evaluation in vitro of tbe root canal sealer cement Sealapex. International Endodontic Journal, 18, 179-182. HUGO, W.B. (1971) Inhibition and Destruction ofthe Microhial Cell. Academic Press, London, 277 pp.

materials for amalgam restorations. British Dental Journal, 152,313-315. MAGNUSSON, B.O. (1980) Pulpotomy in primary molars: long-term clinical and histological evaiuation. International Endodontic Journal, 13,143155. MARKS, S.C. (1983) The origin of osteociasts: evidence, clinical implications and investigative challenges of an extra-skeletai source. Journal of Oral Patholog}', 12,226-256. MASSLER, M . (1967) Preventive endodontics: \ital pulp therapy. Dental Clinics of North .America, 11,663-673!


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Review of calcium hydroxide.

Calcium hydroxide is a material which has been used for a variety of purposes since its introduction into dentistry in the early part of the twentieth...
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