J, Dent. 1991;
A. Milosevic Department
of Clinical Dental Sciences, School of Dentistry,
ABSTRACT This paper reviews the various calcium hydroxide preparations available for use in restorative dentistry and their constituents. The significance of individual constituents in relation to the properties of such materials and their mode of therapeutic action with respect to the dentine pulpal response and antibacterial activity is discussed. Applications of calcium hydroxide in restorative dentistry are also reviewed. KEY WORDS: Calcium hydroxide, Restorative dentistry, Review J. Dent. 1991;
19: 3-l 3 (Received 16 May 1990;
reviewed 10 July 1990;
accepted 10 September 1990)
Correspondence should be addressed to: Mr A. Milosevic, Department of Clinical Dental Sciences, School of Dentistry, University of Liverpool, Pembroke Place, PO Box 147, Liverpool L69 3BX, UK.
INTRODUCTION Calcium hydroxide preparations are used extensively in restorative dentistry as a therapeutic cavity liner, as an interim root canal dressing to induce hard tissue formation in various endodontic situations, and as the basis of permanent root canal sealers. This extensive usage, however, is not matched by clear understanding of how calcium hydroxide promotes osteodentine bridge formation nor its putative antibacterial activity, although hard tissue repair in pulp capping and in the periapical tissues after calcium hydroxide treatment has been widely reported (Glass and Zander, 1949; Berman and Massler, 1958; Stanley and Lundy, 1972; Schroder, 1973; Tronstad, 1974; Hendry et al., 1982; Holland and de Souza, 1985). The first part of this paper endeavours to review the tissue reactions and therapeutic activity of calcium hydroxide and aims to identify the areas of confusion that still exist. The applications of calcium hydroxide within restorative dentistry have widened with the great range of preparations now available. The second half of this paper discusses these applications. Indeed the long history and wide application are further surprising since this alkaline material is inherently non-biocompatible (Granath, 1982). Currently there is a wide range of commercially available products, but no specification for calcium hydroxide-based cements,. dressings or sealers. Some manufacturers utilize technical data relating to American Dental Association Specification No. 30 for zinc oxide @1991Butterworth-Heinemann Ltd. 0300-5712/91/010003-011
eugenol cements, but most do not specify the chemical constituents in the product literature and some change the constituents or their proportions without notice.
TISSUE REACTIONS AND THERAPEUTIC ACTIVITY OF CALCIUM HYDROXIDE Material constituents and effect on solubility The constituents and the proportions of commercially available calcium hydroxide cements vary from product to product. De Freitas (1982) and Prosser et al. (1982) have characterized calcium hydroxide preparations, and Table I is based upon their results. However, like all other dental cements, calcium hydroxide cements set by an acid-base reaction, the phenolic group in the alkyl salicylate ester acting as an acid (Prosser et al., 1979). Once set, therapeutic activity of the set material will depend upon the release of CaZ+ and OH- which can only occur if the cement is water soluble. It is the nature of the plasticizer that imparts this solubility. Currently, most cements set by some of the available Ca(OH), reacting with the salicylate ester chelating agent in the presence of a toluene sulphonamide plasticizer. The latter is hydrophilic and soluble. The set cement contains a matrix of calcium-a&y1 salicylate chelate, and excess unreacted calcium hydroxide. The fragility of the set cement suggests that the chelates are held together by weak secondary attractions rather than a
lsobutyl salicylate ester
Kerr, Sybron Corp, USA
MPC (withdrawn) Modified rosin
Modified rosin (abietic acid derivative)
Calcium hydroxide Barium sulphate Titanium dioxide
Paraffin oil Calcium hydroxide Barium sulphate Zinc oxide Titanium
lsobutyl salicylate ester
Kerr, Sybron Corp., Romulus, MI, USA
None Calcium hydroxide
Urethane dimethacrylate resin
De Trey Division, Dentsply Limited, Weybridge, UK
Titanium dioxide Barium sulphate Alumina
Kerr UK Limited, Peterborough, UK
polymer with calcium hydroxide and
Calcium hydroxide Zinc oxide
A liquid varnish presentation of methylethyl ketone/acrylic titanium dioxide. ? Other constituents
George Tau b Products, Jersey City, NJ, USA
Ortho and para N-ethyl toluene sulphonamide
Calcium hydroxide Zinc oxide
Titanium dioxide Calcium sulphate Calcium tungstate Alumina
Methyl salicylate ester
De Trey Division, Dentsply Limited, Weybridge, UK
Dycai Advanced Formula II
? A sulphonamide
? Calcium hydroxide
? Barium sulphate
? Salicylate ester
Ivoclar-Vivadent Ltd, Schann, Liechtenstein
? A sulphonamide
Basic paste Plasticizer components
Acid paste Inorganic Organic components
Espe, D-803 1, Seefeld/Oberbay, FRG
Tab/e 1. Some commercially available calcium hydroxide lining preparations and their constituents
stronger polymeric structure (Prosser et al., 1979). Most of the commonly used two-paste systems (Dycal, Life, and Alkaliner (Table I)) utilize this chemistry. However, Hydrex and MPC (Table I) had a hydrophobic paraffin oil plasticizer, and Hydroxyline (George Taub Products, Jersey City, NJ, USA) a methyl ethyl ketone solution of methyl methacrylate. Both Hydrex and MPC have been shown to be less relatively insoluble (Prosser et al., 1982) and have poor antibacterial propertiesin vitro (Fisher and McCabe, 1978; Fisher and Shortall, 1984) and have since been withdrawn from the market. Hydroxyline is marketed as resistant to acid-etch procedures, since it is highly insoluble and consequently the therapeutic potential is limited. Physical properties Compressive
The set calcium hydroxide lining materials are weak, brittle materials used in thin section in the deepest part of the cavity. Ray (1982) reported average 24 h compressive strengths for Dycal and Life of 7.8 N.mm-z and 8.2 N*mmM2respectively, concluding that these fully set cements were insufficient to withstand the average amalgam condensation pressure of 10.5 N*mme2 (Basker and Wilson, 1968). Contradicting these findings Draheim et al. (1988) found 24 h compressive strength for Dycal and Life to be of the order of 30 N.mmw2, and at 7 min approximately 10 Nemm-2 was attained. Nevertheless it would seem prudent to use a structural lining prior to amalgam placement. Acid dissolution Any lining inadvertently subjected to an acid etchant should be non-permeable and remain unaltered. McComb (1983) found Procal to be more susceptible to acid dissolution than Life. Burke and Watts (1986) reported Dycal lost a significantly greater percentage of its mass than Life, MPC or Procal. That MPC was least prone to acid attack was attributed to the paraffin oil plasticizer which also accounts for the resistance to aqueous dissolution (Prosser et al., 1982). Similar variation in behaviour between Dycal and Life is explained by the difference in plasticizer. Mode
Calcific bridge formation The mode of therapeutic activity of calcium hydroxide for either calcitic bridge formation or antibacterial activity is not clear despite extensive literature. The pulpal and periapical connective tissue responses to calcium hydroxide will not be the same since odontoblast precursors are unique to the pulp and inherently different preparations of calcium hydroxide are used in root canals compared to pulp capping agents. Calcific bridge
formation is a generic term describing repair by osteodentine bridge formation in pulpal exposure and cementum like material or cementoid formation in perapical or periodontal tissues. The pulpal response adjacent to calcium hydroxide has been documented but the actual sequence of histological changes varies and is dependent upon whether a proprietary hard setting cement or a laboratory made calcium hydroxide paste was used. Stanley and Lundy (1972) described in 35 teeth from 10 patients a Dycal-induced mummified layer which was phagocytosed and replaced by mineralizing granulation tissue. The hard tissue bridges, although of variable thickness, were present adjacent to the Dycal by 23 days in most specimens. Confirming this, Tronstad (1974) reported the juxtaposition of dentine bridges with Dycal by 30 days and Fitzgerald (1979) observed a l-3 cell thick layer of tibroblasts lying directly on Life, followed after 9 days by a lo-15 pm thick zone of osteodentine. However, a threelayered zone of necrosis l-l.5 mm thick was the consistent finding following calcium hydroxide paste application by Schroder and Granath (1971). Cellular organization and collagen production occurred along the border of necrosis after 4 days, followed by mineralization 3 days later. The greater dissociation and hence alkalinity of the paste may have accounted for the necrosis. Further histological evidence of bridging by Dycal and Life was shown by Pitt Ford (1985) in dogs and by Tagger and Tagger (1985) with Life but not with Reolit (Ivoclar Vivadent Ltd, Schann, Liechtenstein) in monkeys. The typical histological appearance from these studies is of a mineralized collagenous matrix with cellular and vascular inclusions. A comparison of Analar grade calcium hydroxide with zinc oxide/purified eugenol (Watts and Paterson, 1987) revealed dentine bridge formation after 28 days in seven out of 12 rat teeth and five out of 11 rat teeth respectively. However, further localized dystrophic calcification occurred in the pulp in the majority of teeth with both calcium hydroxide and zinc oxide/eugenol. Successful therapeutic activity is further evidenced by a reduction and eventual resolution of pulpal inflammation. Significantly reduced bridge formation and persistent coronal and radicular inflammation was observed in infected rat molars 28 days after a Dycal pulp cap when compared to germ-free controls (Paterson, 1976).However, all seven pulpal exposures that were left open for 24 h in monkeys and subsequently capped with Life had bridges and were inflammation free by 14 days (Cox and Bergenholtz, 1986). Interestingly, calcium hydroxide pretreatment of deep dentine reduced pulpal inflammation in teeth subsequently tilled with silicate cement (Warfvinge et al., 1987). Calcium ions and an alkaline pH have been proposed to act separately or synergistically in promoting calcitication. Early studies (Zander, 1939; Glass and Zander, 1949) suggested that the calcium in the osteodentine bridge was derived from the pulp capping material. Sciaky and Pisanti (1960) studied 42 teeth in two dogs having calcium
J. Dent. 1991;
19: No. 1
hydroxide containing calcium-45 placed over the pulps. After three or more weeks every tooth examined had a ‘new dentine roof, but radioactivity could not be demonstrated within any of the dentine bridges. In a second experiment (Pisanti and Sciaky, 1964) one dog had an exposed cavity cut in 16 teeth and was then perfused with 5 ml of radiolabelled calcium weekly over a 3 week period. Every ground section showed reparative dentine, although the exact number of sections assessed under the microscope and subsequently X-rayed and autoradiographed was not disclosed. The autoradiographs were superimposed upon the ground sections and the authors found radioactivity present in all dentine bridges, concluding that the bridge calcium was systemic in origin. Attalla and Noujaim (1969) confirmed this conclusion using a 45Calabelled paste, but the experimental method was fundamentally different since they cut deep cavities without pulpal exposures. The influence upon bridge formation of calcium hydroxide paste or cements in direct contact with pulpal connective tissue may be greater than when placed over a layer of intervening softened dentine, normal dentine or predentine. Contradicting the previous studies, Stark et al. (1964) found radioadrtive calcium transmitted from the pulp capping paste into the osteodentine bridge and scattered in the pulp in 25 per cent of their sections. Gordon et al. (1985) carried out an interesting in vitro study comparing the effects of calcium hydroxide of varying pH and molar concentration on bovine pulp enzyme activity. The enzymes investigated were lactic dehydrogenase and alkaline phosphatases, the latter having a long association with mineralization. Both alkaline phosphatase activity and lactic dehydrogenase activity were inhibited at a pH of 11.9-12.3 but significantly increased at pH 10.2; however at pH 7.2 a reduction in activity was noted. Changing the calcium ion concentration did not alter pulp enzyme activity. They concluded that the role of calcium was indirect, merely reducing the solubility of the hydroxide and thus the toxicity. Barium, ammonium and magnesium hydroxides have all caused greater inflammatory responses in the pulp which may be due in part to their greater dissociation producing too alkaline a local environment (Seltzer and Bender, 1958; Svejda, 1964; Rowe and Binnie, 1974). It would seem that there is a critical degree of alkalinity for dentinogenesis to take place, possibly around the optimum for alkaline phosphatases at pH 10.2. The periapical response to calcium hydroxide may depend on pre-existing periapical inflammation, either as a consequence of apically extending pulpal disease or resulting from poor endodontic technique. The latter situation may include pushing infected or necrotic material through the apical foramen or overinstrumentation leading to a ‘zipped’ apical constriction. Overfilling into the periapex with calcium hydroxide may promote an acute inflammatory reaction followed by phagocytosis and calcium hydroxide resorption with areas of ankylosis (Pitts etaI., 1984; Kawakami et al., 1987). The possible sequelae to calcium hydroxide overfilling
include connective tissue in-growth and cementogenesis along the root canal walls leading to partial or complete closure, osteoid bridging across the calcium hydroxide/ connective tissue interface or persistent mild to moderate chronic inflammation (Holland et al., 1979a, b). Contra,dicting these studies Dylewski (1971) observed in monkeys an uninflamed area of granulation tissue surrounding extruded calcium hydroxide paste. Antibacterial activity The antibacterial activity of calcium hydroxide is believed to be related to its alkalinity. An in viva study (Fisher, 1972) utilizing a calcium hydroxide/water paste rendered deep caries sterile in 10 occlusal cavities, although bacterial culture of the dentine was not performed. Subsequent work by Fisher (1977) compared Kalzinol, Hydrex and Dycal treated dentine by bacterial culture at treatment and 6 months afterward. Dycal rendered contaminated dentine sterile in all teeth, most of the Kalzinol tested teeth, but Hydrex in two out of nine only. This was attributed solely to the increased alkalinity of Dycal. Recent laboratory investigations on agar plates inoculated with oral microorganisms having various cut calcium hydroxide cement wells showed differing zones of bacterial inhibition (Fisher and Shortall, 1984; Barkhodar and Kempler, 1989). However, this technique is relatively insensitive depending upon inoculum size, incubation time, agar/cement contact and known difficulties in reproducibility of zones (Waterworth, 1971). Inhibition zone size may be influenced by molecular size and diffusion constant of the chemical agent employed. Dycal produced an average of 4.5 mm zone of inhibition after 48 h on blood agar plates inoculated with S. mutans NCTC 10449 in the Fisher and Shortall (1984) study but an average of 15.6 mm in the study by Barkhodar and Kempler (1989). From these studies S. mutans seems more susceptible to calcium hydroxide inhibition than S. sanguis or L. casei. Differences in application of the agar technique further complicate comparisons of the results. Lado and Stanley (1987) placed week-old set discs of calcium hydroxide cements into molten growth medium prior to microbial inoculation. They concluded that visible light cured Dycal was as effective as two-paste Dycal and Life as judged by diameter of inhibition zones, but pooled six different microorganisms in their results. Calcium hydroxide preparations for intracanal disinfection during root canal therapy have similarly been assessed for antibacterial activity. Stevens and Grossman (1983) reported poorer inhibition on agar plates and in cats ofS. faecalis by calcium hydroxide slurry or Pulpdent (Pulpdent Corporation, Watertown, MA, USA) than camphorated chlorophenol. DiFiore et al. (1983) placed cylinders ofcalcium hydroxide mixtures with camphorated para-chlorophenol, metacresyl acetate, a water paste or methyl cellulose (Pulpdent) onto set inoculated agar plates and reported inhibition of S. sanguis growth by the
Milosevic: Calcium hydroxide in restorative dentistry
Calcium hydroxide has been advocated for the relief of hypersensitive root dentine (Jorkjend and Tronstad, 1972; Levin et al., 1973; Green et al,, 1977). The proposed mechanisms for reducing dentine permeability include: (a) physical blockage of the tubule orifices, (b) production of precipitates or mineralizations, and (c) stimulation of secondary dentine. The influence of Ca++ in raising neuronal excitation thresholds has also been documented (Trowbridge et al., 1982). Pashley et al. (1986) reported a 75 pe; cent reduction in dentine permeability after a 2 min calcium hydroxide application and wash removal on acid etched dentine in vitro. Similar calcium hydroxide treatment of a smear layer further reduced dentine permeability by 52 per cent.
presents the basis for the indirect pulp cap technique. The subjective assessment of the hardness of this carious front may be difficult and inevitably some bacteria could be left in the deepest part of the cavity. Therefore the prime role for the placement of calcium hydroxide onto this deep softened dentine is to render it sterile through the antibacterial activity. This antibacterial activity if dependent on alkalinity may not be durable since the pH values of five pulp cap agents were neutralized within 5 min of mixing and placement on bovine dentine (Ida et al., 1989). The effect of calcium hydroxide on the remineralization of softened dentine is unclear. Kurosaki et al. (1977) stated that this inner layer contains recalcifiable collagen fibres and living odontoblastic processes adjacent to normal dentine. Remineralization of carious dentine by Dycal as measured by increased phosphorous concentration has been reported by Eidelman et al. (1965), but the mechanism for the remineralization or the influence of Dycal was not assessed. However, reduced odontoblast enzyme activity, particularly those enzymes involved in mineralization, was found in deep carious cavities by Karjalainen and Le Bell (1987). Brannstrom et al. (1976) reported an unpredictable and varying degree of tubule closure in tivo under Calasept and a calcium hydroxide/ calcium monofluorophosphate mixture over an 8 week period. As dentinal caries progresses one of two responses affecting the tubules may occur. Irregular secondary or reparative dentine produced by newly differentiated preodontoblasts from the cell-rich zone in the pulp may be deposited against a zone of atubular ‘interface dentine’, blocking off the empty tubules of the primary dentine which thus become dead tracts. Peritubular dentine, on the other hand, may thicken by progressive mineralization leading to partial or complete obturation of the tubule forming sclerosed dentine. Mechanisms of recalcification of the intertubular dentine and stimulation of intratubular mineralization by calcium hydroxide present further areas for study. The pulpal penetration of pulp cap agents has been observed in dogs but rarely in rats and is likely to vary with the animal model used (Watts and Paterson, 1982). The distinction between clinically exposed and unexposed deep cavities can be misleading as there may be a clinically undetected exposure present. In any event, the resolution of pulpal inflammation and associated symptoms will depend largely on cavity preparation under isolation and a good, durable cavity margin seal. Bacterial contamination from saliva during cavity preparation or subsequent microleakage will considerably reduce the successful outcome to both pulp cap techniques (Brannstrom and Nyborg, 1972, 1973, 1974; Paterson, 1976).
two former mixtures but not the water paste or Pulpdent. However, Bystrom et al. (1985) found a calcium hydroxide preparation (Calasept, Scania Dental AB, Knivsta, Sweden) rendered 34 of 35 canals sterile after 2-4 days yet and para-monochlorophenol camphorated phenol rendered only 20 of 30 canals sterile after 2 weeks. Interestingly, other investigators (Cotton, 1974; Paterson et al., 1981; Watts and Paterson, 1987) have found bacteria with a normal histological appearance, indicating possible viability, in intimate contact with calcium hydroxide. Surprisingly, Watts and Paterson (1987) believed antibacterial activity to be minimal since bacteria were present in the cavity and coronal pulp in the majority of calcium hydroxide treated rats. The possible species specificity of microbial sensitivity to calcium hydroxide complicates the testing of antibacterial activity.
THE APPLICATIONS HYDROXIDE
Calcium hydroxide has gained many applications in restorative dentistry since its introduction by Hermann in 1930 (Table Ir). Tab/e II. Applications of calcium hydroxide in restorative dentistry Dentine desensitizing agent Indirect pulp cap technique Direct pulp cap technique Endodontic intracanal dressing Hard tissue induction in root fractures, root perforations and root resorption Apexification Apical plug Root canal sealer Microleakage demonstrator
and direct pulp cap technique
Fusayamaetal, (1966) demonstrated that demineralization and staining preceded bacterial invasion of dentine. This
Calcium hydroxide has been advocated as a routine intracanal dressing (Safavi et al., 1985) or when exudate
J. Dent. 1991; 19: No. 1
persists or there is a long time interval between appointments (Stock, 1985). Matsumiya and Kitamura (1960) reported progressive bacterial reduction from infected dog root canals following intracanal application of calcium hydroxide. Calcium hydroxide B.P. can be mixed into a paste with sterile isotonic saline or local anaesthetic solution without vasoconstrictor and carefully spiralled into the canal (Webber et al., 1981). The antibacterial activity of intracanal calcium hydroxide dressings has been discussed previously. However, biomechanical preparation alone considerably cleanses the root canal system and any intracanal medicament should be minimally toxic yet maximally antiseptic and easy to remove (Engstrom and Frostell, 1964).A 1 per cent PCP solution on a squeezed, nearly dry, cotton wool pledget in the pulp chamber produces an antibacterial vapour over 14 days and is in common usage (Uchin and Parr-is, 1963; Harrison and Madonia, 1970; Cwikla, 1972; Ellerbruch and Murphy, 1977).
Hard tissue perforations
induction in root fractures, and root resorption
Root fracture Intra-alveolar root fractures occur relatively infrequently, accounting for less than 3 per cent of all dental trauma (Anehill et al., 1969; Zachrisson and Jacobsen, 1975). The fracture location influences the prognosis and treatment, and can be described as coronal, mid-root or apical third. Andreasen and Hjorting-Hansen (1967) categorized possible spontaneous repair into four types: 1. Healing by calcification across a narrow fracture line. 2. Healing with intervening fibrous connective tissue. 3. Healing with root end resorption and replacement by wide bony in-till. 4. Persistent granulation tissue. When a fracture occurs in the apical third treatment is often unnecessary since healing with calcified tissue interposed between the fragments is the usual sequela. Should periapical pathosis develop, endodontic treatment to the coronal segment and surgical removal of the fractured apical portion is usually successful. Cvek and Sundstrom (1974) advocated the use of calcium hydroxide between the two segments to induce a calcific barrier before obturating the coronal segment. However, this may take several months to occur. Root perforations Iatrogenic perforations can occur at the ‘elbow’ of a curved root canal during biomechanical preparation or during post hole preparation. A conservative technique to close the perforation with hard tissue induced by calcium hydroxide is possible if the defect is below the alveolar crest and is not in communication with the oral cavity
(Ingle and Abou-Rass, 1985). An alternative, surgical approach to obturate the perforation with amalgam is possible providing the defect is accessible. In any event, the conservative technique should be instigated immediately the root is perforated. Martin et al. (1982) advocated sealing a mixture of calcium hydroxide, barium sulphate and camphorated monochlorphenol in the canal for a few months. Once hard tissue formation had occurred the mixture was removed with endodontic hand instruments, the canal thoroughly irrigated, and finally filled with thermoplasticized gutta percha. This method is more likely to successfully fill the dentinal perforation against any hard tissue barrier according to Ingle and Abou-Rass (1985). The management of these lateral root perforations is less successful if the perforation occurs near to the gingival sulcus (Jew et al., 1982). According to Weine (1989) calcium hydroxide induced cementoid formation is less predictable in iatrogenic perforations than as an interim dressing in inflammatory resorption leading to perforation. A common problem is furcal perforation of the floor of the pulp chamber during endodontic access preparation. Care not to use rotary instrumentation indiscriminately will prevent this mishap. Harris (1976) reported the tissue response to calcium hydroxide was less predictable probably because of its poorer sealing albility, and Himel et al. (1985) found calcium hydroxide provoked significantly greater bone necrosis and inflammation than tricalcium phosphate or Teflon in iatrogenic perforations in dog furca. Root resorption Calcium hydroxide has been advanced for the management of both external and internal root resorption (Stock and Nehammer, 1985). Heithersay (1985) advocated the use of a commercially available temporary paste (Pulpdent, Pulpdent Corporation, Watertown, MG USA) in the conservative management of tooth and bone resorption. TempCanal, produced by the same manufacturer, is a similar calcium hydroxide in aqueous methylcellulose but modified to allow flow through 22,25 and 27 gauge needles. Internal root resorption that has not resulted in perforation is amenable to root tilling techniques, however should there be a perforation repeated calcium hydroxide dressings in a cleaned and prepared canal over several months can promote cementogenesis (Frank and Weine, 1973). External resorption of either the inflammatory or replacement type may be arrested with the aid of a calcium hydroxide intracanal dressing prior to root filling (Cvek, 1981). Hammarstrom et al. (1986) compared calcium hydroxide root treatment in infected and uninfected monkey root canals after cutting artificial root resorption defects. Limited necrosis and temporary ankylosis occurred initially followed by full coverage of the resorptive defects by reparative cementum at 8 weeks. Weine (1989) described the use of calcium hydroxide paste placed into canals 3 weeks after tooth replantation in order to reduce external root resorption. However, the
Milosevic: Calcium hydroxide in restorative dentistry
point is also made that if this is placed too soon, prior to periodontal ligament regeneration, resorption may be exacerbated. The basis for calcium hydroxide management of inflammatory root resorption relies on the pH change and neutralization of osteoclast produced acids, thus preventing mineral dissolution. An increased pH in circumpulpal dentine and on root surface dentine of calcium hydroxide filled pulp canals was reported by Tronstad et al. (1981) but not in similarly filled teeth immersed in water (Fuss et al., 1989). Apexification The upper central incisors are the teeth most commonly traumatized in children (Todd and Dodd, 1985).Immature roots with open apices may be managed with calcium hydroxide in either a pulpotomy procedure with calcium hydroxide placement over vital radicular pulp or as a temporary root filling material in cases of non-vital immature teeth with or without periapical pathology (Frank, 1966; Heithersay, 1970, 1975; Cvek et aI., 1976). The former situation may be regarded as true apexitication whereas the latter might best be regarded as induction of root end closure by hard barrier formation providing a stop for subsequent conventional endodontic filling techniques. The induction of root end closure is not confined to calcium hydroxide alone, although this material has the most widely reported success, with success rates ranging from 74 to 100 per cent having been reported (Hallett and Porteous, 1963; Cvek, 1978; Chawla, 1986; Ghose et al,, 1987). The histological appearance of the apical hard tissue barrier in human teeth has been described as comprising 1970) cementum, dentine and pulp (Heithersay, cementum like tissue with loose vital connective tissue inclusions (Cvek and Sundstrom, 1974) or cementum alone of both acellular and cellular types (Klein and Levy, 1974). However, both Heithersay (1970) and Klein and Levy (1974) described the histological appearance from only one tooth. Cvek and Sundstrom (1974) reported on 12 teeth that had all previously undergone successful calcium hydroxide treatment as judged radiographically but had subsequently substained root fractures (eight) or needed extraction for some other reason (four). They found new cementum like tissue and calcifications of wide ranging morphology on the root canal walls in many sections, but only three teeth with complete apical closure. Further evidence in monkeys for the heterogeneity of the hard tissue barrier has been reported (Dylewski, 1971; Ham et al., 1972; Torneck et al., 1973) and for incomplete apical closure (Steiner and Van Hassel, 1971). Torneck et al. (1973) found persistent periapical inflammation despite what appeared to be successful apical closure, relating this to the trapped and necrotic debris within the barrier and the root canal. Presumably the voids with necrotic material were in communication with vital periapical tissue or the barrier is permeable. They concluded that the presence of a calcitic barrier is
not by itself the criterion by which success should be measured. Although the experimenters of induction studies attempted to avoid extruding the calcium hydroxide into the periapical tissues, it cannot be assumed from these various studies that this had not occurred. As discussed in the previous section under ‘Mode of therapeutic action’, the tissue response to calcium hydroxide overfilling is unpredictable. Furthermore direct comparison of barrier induction results is difficult since different preparations of calcium hydroxide have been used; Pulpdent (Heithersay, 1970) calcium hydroxide with sterile saline (Cvek and Sundstrom, 1974), calcium hydroxide with CPCP (Torneck et al., 1973; Javelet et al., 1985) calcium hydroxide with CMCP (Steiner and Van Hassel, 1971) and calcium hydroxide with iodoform paste (Hollandet al., 1979a,b). Comparative studies have not tended to be carried out. Thus confusion arises in deciding which technique for root end induction is the most predictable and successful, and that current clinical criteria of success are relatively crude. Mackie et al. (1988) reported using Reogan Rapid (Ivoclar Vivadent Ltd, Schann, Liechtenstein) for a mean 5 month treatment period for root end closure in 11-15 year olds, but for twice as long in 6-8 and 9-10 year olds. Root apices that were < 2 mm in diameter took only 6.2 months to close as opposed to 11 months in apices > 2 mm. The clinical technique can be prolonged, involving monthly visits when the calcium hydroxide dressing is removed and a check for closure made either radiographically, or clinically by careful tapping with a paper point. Apical repair may be completed 6 months after calcium hydroxide insertion, but may take 2-3 years (Kennedy, 1986).It would seem that radiographic evidence of root enclosure alone should not lull the operator into a false sense of security and an open-ended follow-up policy would be prudent. Apical plug In situations where there is an open apex or indeed normal apical anatomy the dentine chip plug in the periapical tissue has been advocated as an artificial but biological apical stop against which to condense gutta percha (Tronstad, 1978; El Deeb et al., 1983). The intentional extrusion of calcium hydroxide powder to act as an apical stop itself, enabling condensation of gutta percha, has also been advocated with good clinical success rates (Coviello and Brilliant, 1979;Pitts et al., 1984). A slightly different technique of packing calcium hydroxide as a mechanical plug into the apical 2 mm of the tooth followed by laterally condensed gutta percha resulted in less dye penetration in vitro than gutta percha tilled apices without the plug (Weisenseel et al., 1987). Root canal sealer Calcium hydroxide has had such a long association with endodontics it is surprising that commercially available
J. Dent. 1991; 19: No. 1
calcium hydroxide root canal sealers were not developed sooner. Goldberg and Gurfinkel(1979) reported a 90 per cent success rate using Dycal as the root canal sealant in 77 teeth. Apical closure was observed more consistently using a calcium hydroxide paste of high alkalinity than a calcium chloride paste of pH 4.4 in monkeys (Javelet et al., 1985). Recently two commercially developed cilcium hydroxide products have appeared on the market; Calciobiotic Root Canal Sealer (CRCS, The Hygienic Corporation, Akron, OH, USA) and Sealapex (Kerr/ Sybron, Romulus, MI, USA). Cohenet al. (1985) compared the sealing ability of CRCS with Procosol (Star Dental Manufacturing Co., Conshohocken, PA, USA), a zinc oxide-eugenol sealer, and found similar clinically acceptable leakage patterns with both materials but that CRCS leakage decreased with time. Hovland and Dumsha (1985) reported acceptable and comparable leakage of Sealapex with Tubliseal and Procosol over 30 days. Jacobsen et al. (1987) found no significant leakage differences between CRCS, Sealapex and Roth Root Canal Cement (a zinc oxide-eugenol material). However, although Zmener (1987) reported increasing but not significant leakage differences between CRC& Sealapex and Tubliseal with time; he stated that this level of leakage was clinically unacceptable. Different root canal preparation techniques, obturation, and evaluation of results could account for these differing interpretations. Furthermore the long term durability of the apical seal is open to question. Whether these root canal sealers promote quicker healing or a more predictable tissue response than non-calcium hydroxide sealers has not been evaluated. Microleakage
A relatively novel application for calcium hydroxide, as a microleakage demonstrator, was proposed by Leinfelder et al. (1986). This was based on the solubility and OHrelease of these cements. Ice water (pH 7) was syringed onto Class V cavities in vitro that were filled with amalgam or Sevriton (De Trey Dentsply, Weybridge, UK) and lined with Dycal. Subsequent microleakage was detected by placing pH paper over the fillings and noting any colour change. They concluded that the method was simple, biocompatible, quick and could be used in viva. This was confirmed by an in viva. follow-up study (Isenberg et al., 1987). CONCLUSION The wide use of calcium hydroxide in restorative dentistry over many years has generated extensive research. Despite this, the actual mechanisms involved in calcium hydroxide induced hard tissue repair remain unclear, which could account for the unpredictable outcome when using this material in whatever form. Many other factors, both local and systemic, may influence osteodentine bridge and cementoid formation. For instance, the extent
of dentinal or periapical infection, the microbial species involved, the degree and nature of pulpal or apical inflammation could all modify the responses to calcium hydroxide. Age related tissue changes could further alter the healing reaction to calcium hydroxide. Furthermore, antibacterial activity implies a certain degree of cytotoxicity such that strong antibacterial activity is frequently associated with adverse reactions during and after treatment (Orstavik and Mjor, 1985). Orstavik (1988)’concluded with respect to endodontics that asepsis, interappointment disinfection, and relatively inert filling materials are superior to methods relying on antibacterial components. Whether calcium hydroxide is indeed antibacterial has been opened to question, and certainly varies with the preparation used. It would seem that investigation into the chemistry, biocompatibility, and antimicrobial activity of calcium hydroxide preparations is still necessary. Acknowledgements I am grateful to Mr J. Cunningham for constructive comments made in preparing this paper and Miss L. J. Jackson for typing the manuscript.
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Book Review Clinical Pharmacology in Dentistry, 5th edition. R. A. Cawson and Ft. G. Spector. Pp. 233. 1989. London, Churchill Livingstone. Softback, f 12.95. Ever since the first edition was published in 1975, this book has been regarded as essential reading for dental students. In essence, it distils the considerable clinical experience of one author (R.A.C.) in therapeutics with that of an acknowledged expert in applied pharmacology (R.G.S.). The format now A4, rather than A3, is otherwise similar to that of previous editions, 19 chapters with two appendices and an index. The authors rightly justify this new edition in their preface by documenting recent advances in clinical pharmacology which are of clinical relevance. Rather than jump straight into ‘receptor sites’, the authors have now elected to introduce the broader concept of pharmacokinetics and illustrate the significance of drug absorption and metabolism with dental examples. There is good advice on the legal aspects of writing of prescriptions for routine drugs and those controlled by the Misuse of Drugs Regulations (1973). In the management of infections, new information has been added on th reduced sideeffects of the newer tetracyclines and amoxycillin therapy in infective endocarditis. Details of the newer triazole antifungal agents should be included next time.
With regard to antiseptics, and other drugs used in routine dentistry, sensitization to rubber surgical gloves is a sufficiently serious hazard to warrant consideration. The discussion on the effects of centrally acting drugs on salivary function could be expanded as the list of those linked to xerostomia is ever increasing and it is a common clinical problem. Dihydrocodeine is noted as increasing postoperative dental pain, and why does pentazocine continue to be included in the Dental Practitioners Pormulary if it has nothing to offer such patients? I would disagree that remission from pemphigus vulgaris follows steroid and other immunosuppressive therapy: it is a lifelong disease irrespective of treatment. Although vitamins are viewed from a homeopathic viewpoint, recent evidence suggests they are important in some oral disorders, particularly burning mouth syndrome. Aetiological factors in some lichenoid reactions (e.g. ammoniated mercury from dental amalgams) or erythema multiforme (e.g. benzoic acid) merit inclusion (where dose clinical pharmacology end and oral medicine begins?). These are small reservations, however. This text continues to set a standard by which others are judged and it certainly represents extremely good value for money. P-J. Lamey