Effects of Materials Used in Pediatric Dentistry on the Pulp: A Review of the Literature

This paper reviews a selection of materials used in treating children's teeth. Often, the success of the material is determined by its effect on the underlying pulp tissue, either by virtue of its direct effect or in its ability to prevent ingress of contaminants. The materials reviewed will include some of those used for cavity liners, bases, restorations, pulp capping, and pulpotomies.

A variety of materials have been used in the treatment of children’s teeth. Many were adopted for use in primary teeth because of their successful use with permanent teeth. Other materials seem to empirically perform better in either primary or permanent teeth, but not in both. Some materials that appeared to be promising when introduced did not fulfill the manufacturers’ claims when used clinically. A large number of studies related to the biocompatibility of materials cited in the literature involve research on permanent teeth. In many instances, similar information is missing for primary teeth. Extrapolation of these results for use in primary teeth, in many cases, is based on clinical experience alone. This paper will review a selection of materials used in treating children’s teeth. Often, the success of the material is determined by its effect on the underlying pulp tissue, either by virtue of its direct effect on the pulp or in its ability to prevent ingress of contaminants to the pulp. The materials reviewed will include some of those used for cavity liners, bases, restorations, pulp capping, and pulpotomies.

Cox and colleagues ³ studied pulp capping with calcium hydroxide with a one- and two-year observation period. They found that nine out of 29 teeth with nonexposed pulps demonstrated a moderate grade 2 chronic inflammation. Reparative dentin at one year equaled 149 F m and at two years equaled 162 F m. In the exposed pulps, 45 of 91 demonstrated pulpal healing; nine of 91 were totally necrotic; 25 of 91 had acute inflammatory lesions; and 12 of 91 demonstrated a chronic inflammatory response.

Since calcium hydroxide does produce bridging (mineralization), will this act as a barrier and protect the pulp? Goldberg and colleagues¹¹ evaluated bridging in intact human premolars. Three to eight months following treatment, the teeth were examined histologically; and the coronal surface of the bridge showed crystals of different shapes, sizes, and dispositions. The pulpal surface of the bridge was formed by the coalescence of calcospherites and a great number of holes. The holes were oval with diameters of from 20 to 250 F m, and leakage analysis showed passage of methylene blue dye through the holes.

Cox and colleagues¹² studied tunnel defects in dentin bridges in monkeys. Pulp tissue in 235 teeth were exposed and capped with calcium hydroxide. Hard-tissue dentin bridges were observed in 192 teeth. Multiple tunnel defects with subjacent pulp tissue inflammation were noted in 172 teeth, with some showing necrosis. The defects were patent and filled with capillaries and inflammatory cells.

Liners and bases placed on nonexposed and exposed dentin need to seal the dentin and be biocompatible with the pulp. Calcium hydroxide, though initially bactericidal to bacteriostatic, does not adhere to dentinal tubules, dissolves after one year, does not adhere to composite resin systems, and degrades upon tooth flexure.⁶ There is a necrotic zone in the pulp tissue at the interface of the calcium hydroxide with the pulp.⁹ This produces a chronic inflammatory response and prevents pulpal healing.

Calcium hydroxide does stimulate mineralization and form a dentin bridge. This hard tissue dentin bridge does not act as a protective barrier because it has many tunnel defects and holes.^11,12 Using calcium hydroxide as a liner does not satisfy the need for a liner that seals the dentin and is biocompatible with the pulp.

Clinically, calcium hydroxide should probably be used for apexification, root end closure, and possibly in the Cvek technique when one treats a complicated crown fracture in the immature permanent tooth. Its use in primary teeth is questionable.

Eugenol and related compounds have a long history of use in dentistry as an obtundant, base, and temporary filling. Eugenol is found in clove oil and is related to phenol, a weakly acidic alcohol. When eugenol is mixed with zinc-oxide, a chelation reaction occurs, and zinc-eugenolate is formed. When ZOE is exposed to an aqueous medium such as saliva or dentinal fluid, a hydrolysis occurs yielding eugenol and zinc hydroxide.¹³

Trowbridge and colleagues¹⁴ found that eugenol liquid and ZOE paste blocks intradental nerve activity. This may explain why it is able to allay tooth pain. The effects of eugenol on tissue appear to be highly dependent on tissue concentration of eugenol. Direct application of eugenol to the pulp tissue (high dose) is toxic and induces cell death and vascular changes and inhibits cell growth and respiration. ZOE placed on dentin releases eugenol from ZOE through dentinal tubules to the pulp (low dose) and inhibits prostaglandin synthesis, nerve activity, and white cell chemotaxis, which is beneficial for reducing inflammation. ¹³

Hume,¹⁵ in describing the pharmacology and toxicology of ZOE, stated that the bioavailability of eugenol when placed on dentin peaks after one day. Ten days after placement of ZOE, 50 percent of the one-day release is still present. He also notes that ZOE on dentin acts as a seal by excluding inward diffusion of dietary substrate from cariogenic bacteria, as well as bacterial toxic end products.

Watts and colleagues¹⁶ placed ZOE on small exposures in germ-free rat teeth and after 28 days found chronic inflammation and/or necrosis in every tooth where there was direct contact of ZOE with the pulp. This negates the use of ZOE as a liner in deep carious lesions.

Attempts at using ZOE as a pulpotomy medicament also have generally been unsuccessful. In a histologic study on teeth in dogs, pulps treated with a plain reinforced ZOE all demonstrated a moderate to severe chronic inflammatory response in the coronal one-third of the canal. If the pulps were first treated with formocresol, the inflammation under the ZOE was milder.¹⁷

Since ZOE is an excellent dentin sealer, its use as a base material may still be indicated beneath amalgam restorations and the cementation of stainless steel crowns, but it is not indicated as a base beneath composite restorations because it may interfere with the polymerization of composite resins. ZOE is the material of choice to fill root canals in primary teeth following a formocresol pulpotomy or pulpectomy because it is resorbed¹⁸ along with the primary roots at the time of exfoliation.

When using ZOE to fill root canals in primary teeth, one must not use reinforced ZOE or the filler material will not resorb. This may produce delayed and/or ectopic eruption of the succedaneous permanent tooth.

Pulpotomy Medicaments

Exposure of pulpal tissue in primary teeth due to dental caries is common. Therefore pulpotomy and pulpectomy therapy in primary teeth is an integral part of pediatric dentistry. The problem is in determining what medication to place in the pulp chamber and/or root canals to ensure successful treatment.

The pulp can heal itself if no bacteria or bacterial products are present. Kakehashi and colleagues performed pulpotomies on gnotobiotic rats in a germ-free environment.¹⁹ Even when food debris was present in the pulpotomy site, a dentinal bridge was laid down and the pulps healed. Cariously exposed pulps treated clinically have bacteria and/or bacterial products present in the pulp chambers, therefore bactericidal medicaments must be used to ensure a successful pulpotomy treatment. If one could place a medicament in the pulp that would kill the bacteria and seal the tooth from the oral environment, one could conceivably allow the tooth to heal. Many medicaments have been tried with varying success.^20-25

The medicament of choice for many years has been formocresol. Formocresol is bactericidal in a concentration of 1.5 percent when applied for two minutes to bacteria and yeast forms.²⁶ Berger²⁰ performed pulpotomies in primary molars using formocresol as a pulpotomy dressing. At three weeks, he found superficial debris below the amputation site, then a compressed layer with good cellular detail. In the middle third of the root canal, he found early coagulation necrosis, and the apical portion of the canal had late coagulation necrosis to the foramen. At seven weeks, the coronal and middle third of the canal were the same as at three weeks, but the apical third showed an ingrowth of granulation tissue from the apical foramen. Specimens examined from a later period showed the same results except that the granulation tissue appeared in the middle and coronal portions of the canal. Magnusson²¹ performed formocresol pulpotomies in 110 roots in 56 primary molars. Between six and 30 months following the pulpotomies, histologically none of the roots showed healed pulps; 16 roots (15 percent) were necrotic; 89 roots (81 percent) had internal resorption with or without repair; and 13 roots (12 percent) showed slight infiltration of inflammatory cells. In addition, formocresol may be found systemically following pulpotomy treatment. Formocresol has been found in blood, urine, and lung, liver, and kidney tissue.^27,28

Because of these findings, other medicaments have been substituted for formocresol with varying success. Glutaraldehyde histologically had a similar pulp reaction and residual effect as formocresol.^22,29 Ferric sulfate has also been used in pulpotomies with good clinical success.^24,30 However, the degree of inflammation present in the root canals was similar to the formocresol group.^23,24 Added to this list of medicaments for use in pulpotomies are calcium hydroxide and ZOE, which were discussed previously. Neither calcium hydroxide^1,10 nor ZOE has been successful for pulpotomies in primary teeth.

Formocresol is still considered the medicament of choice for pulpotomy treatment in primary teeth. Clinically the success rate is more than 90 percent,^31,32 although histologically the results are less and variable.³³ It is recommended that it be used in the diluted form (4 percent formaldehyde) to reduce the amount of possible systemic absorption.³⁴ Further studies need to be done to verify if a 1.5 percent or 2 percent solution of formaldehyde will be successful in pulpotomy treatment in primary teeth. Diluting the formocresol to this level might reduce the possibility of systemic absorption.

Adhesive Liners

With the introduction of adhesive dentistry, many of the materials tested in permanent teeth are now being used in both primary and permanent teeth in children. The results in primary teeth are often similar to those found in permanent teeth. Many studies have indicated that composite materials are compatible with pulp tissue.^6,35-37

The success of adhesive dentistry is dependent on etching the enamel and dentin of the tooth requiring a restoration. When phosphoric acid was used as an etching agent, even in teeth with pulp exposures, it did not produce inflammation and/or necrosis.^29,38-40 Brannstrom³⁸ inadvertently etched teeth with small pulp exposures. He reported that when infection was avoided, there was no damage or inflammation to the pulp. Pashley³⁹ delineated some variables regulating the type of pulpal response to acid etching. They are the type of acid, pKa and pH, applied concentrations, the time of etching (acid challenge = time x concentration), remaining dentin thickness, and the ability of subsequently placed restorative materials to seal the dentin. The use of phosphoric acid to remove the smear layer and allow cohesive hybridization is not detrimental to the pulp.

Various adhesive liners have been tested with good results. Horsten-Bindslev⁴¹ placed Gluma Dentin Bond (glutaraldehyde, water, and hydroxyethylmetacrylate) in deep cavities in monkeys. At eight days, 19 of 23 had slight or no inflammation, and 20 of 23 had no bacterial penetration. At 90 days, 20 of 20 had slight or no inflammation, and 20 of 20 had no bacterial penetration.

Pashley and colleagues⁴² tested the dentin permeability to various liners after etching with phosphoric acid. They etched 0.7 mm dentin discs (all having an artificial smear layer) with 37 percent phosphoric acid for two minutes. The authors found that:

* The phosphoric acid allowed 100 percent penetration.

* Barrier (a polyamide liner) with one coat allowed 44.2 percent leakage.

* Copalite (a copal varnish) allowed 49.4 percent leakage.

* Scotchdond (an adhesive resin) with one coat light-cured allowed 7.7 percent leakage.

* Hydroxyline (a calcium hydroxide liner) with one coat allowed 11.8 percent leakage, and

* A calcium oxalate liner allowed 2.5 percent leakage.

Usami and colleagues³⁵ tested the pulpal response of a light-activated fluoride-releasing adhesive liner in dogs. All cavity preps were within 1 mm of the pulp. At three, 30, and 90 days, there was none to slight inflammatory response; and no bacterial penetration found on either the dentin or in the dentinal tubules.

Cox and colleagues ⁶ studied four composite lining materials using HEMA as a primer (which is hydrophilic) and both light activated and autopolymerizing bonding agents (which are hydrophobic). They found that there was cohesive hybridization and that the hybrid layer penetrated the dentin 5-7 F m. The only restorations that produced a pulpal response were those that allowed bacteria and bacterial products into the dentinal tubules with subsequent inflammation and/or necrosis.

Tsuneda and colleagues³⁶ tested four adhesive liners placed directly on exposed pulp tissue in Wistar rat molars. At three days, the inflammatory infiltrate was similar in all materials; but, in the seven-day specimens, only one showed none to slight inflammatory response. In the evaluation of microleakage, the one with none to slight inflammation at seven days demonstrated no microleakage. The other three liners all had microleakage with bacterial penetration.

Kitasako and colleagues³⁷ performed direct pulp caps on exposed monkey teeth using four adhesive resin systems. The diameter of the exposures ranged from 0.3 mm to 1.3 mm. The materials tested were All-Bond 2, Bond Well LC, Liner Bond II, and Superbond C&B. The specimens were examined at seven, 14 and 60 days. There was no bacterial penetration along the cavity walls, and no moderate or severe inflammatory reaction was found in any of the specimens. Kopel⁴³ has advocated the use of adhesive liners for pulp capping procedures in primary teeth, however, there have been no scientific studies to date that support this procedure.

The results of the studies cited above are important to consider when choosing an adhesive liner. Equally important is the technique utilized in placing these materials, whether in the primary or permanent tooth. The ability of the liners to seal the dentin and prevent bacteria and bacterial products from contaminating the pulp are critical to ensure pulpal healing.

There are some minor problems with the use of the resin-based systems. There is a release of formaldehyde from composite restorations. Oysaed and colleagues tested nine composites and found a continuous release of formaldehyde during the first 10 days. Formaldehyde release was still detectable 115 days after polymerization.⁴⁴ In addition, Olea and colleagues found bisphenol A and dimethacralate in saliva samples following placement of sealants in humans.⁴⁵ Both of these compounds display estrogenic activity (xenoestrogens). Hamid and Hume examined the chemical release from seven light-cured pit and fissure sealants available in the United States and could not detect any bisphenol-A release.²⁵ Solderholm and colleagues reviewed the literature on the synthesis of BIS-GMA and its biological effects in cell culture and animals. They concluded that based on existing research, it must be accepted that certain impurities may be present in some BIS-GMA resin; and these impurities, when released from restorations, are potentially estrogenic. Under extreme conditions, these impurities are capable of inducing weak estrogenic effects on target tissues. However, the amounts of bisphenol A that may be present as an impurity or produced as a degradation product from dental restorations are quite small and far below doses needed to affect the reproductive tract.⁴⁶

In addition, even with cohesive hybridization, nanoleakage of adhesive bonding systems does occur.⁴⁷ This could be due to marginal gaps between the resin and the dentin of the cavity preparations. Arbabzadeh and colleagues compared the bond strength and marginal discrepancies of five adhesive systems.⁴⁸ They measured the gap widths at five sites and found that the best adhesive system, All Bond 2, had gap widths of 1.6 to 4.7 F m. The other four materials had even greater marginal discrepancies.

Research is needed to provide better adhesive systems without polymerization shrinkage in order to eliminate marginal gaps and seal the pulp from bacteria and bacterial products so it can heal. Research is also needed to create materials free of impurities and degradation products.

Restorative Materials

The restorative materials used in pediatric dentistry (e.g., amalgam, composite resins, glass ionomer cement, resin-modified glass ionomer cement, and stainless steel crowns cemented with zinc-phosphate or polycarboxylate cement) will not produce inflammatory responses in the pulp as long as a seal can be achieved to prevent microleakage to the pulp tissue.^49,50

Yakushiji and colleagues⁵¹ studied the effects of glass ionomer as a base in human teeth with an average of 1.68 mm of dentin overlying the pulp. The restorative materials placed over the glass ionomer bases were amalgam and composite resin. Histologic sections were done between two and 219 days following placement of the restorations. The authors found "no to slight" inflammation at all periods when both the amalgam and composite restorations covered the glass ionomer bases.

Gaintantzopoulou and colleagues⁵² evaluated pulpal reactions to light-cured glass ionomer cements. They prepared deep Class V preparations in 96 teeth from three young beagles. The animals were sacrificed at one, four, and 12 weeks following the operative procedure. No etching was done prior to the placement of the glass ionomer cement. Ninety-one of the specimens had intact cavity floors and 89 of the pulps had a mild reaction with two having a moderate response. Eighty-two of the specimens were bacteria-free. The authors concluded that light-cured glass ionomer cements do not impair pulpal healing.

Pulpal response to a resin modified glass-ionomer material was studied by Tarim and colleagues⁵³ on both nonexposed and exposed monkey pulps. Tissues were collected at six to seven, 21 to 27, and 90 to 97 days. Except for one resin-modified glass-ionomer-treated pulp at six days in the nonexposed group, the inflammatory response was mild. In eight of 36 teeth in which resin modified glass ionomers were placed over pulpal exposures, the pulps showed various grades of inflammatory response, all associated with stained bacteria. Bacterial staining data in the nonexposed pulps indicated that the resin-modified glass ionomer provided a complete seal against microleakage in 17 cavities at 21 and 97 days.

Some of the advantages of the glass-ionomer cements, according to the manufacturers, are that etching is not needed prior to their placement, fluoride is released, and they adhere to dentin. Even with these advantages, their biggest disadvantage is their inability to seal and prevent bacterial ingress to the pulp tissue. As previously discussed, this variable is critical to the success of any material.

Cox and colleagues⁴⁹ tested amalgam, zinc-phosphate cement, composite resin, and silicate cement on exposed pulps in monkeys. One half of the cavities were surface sealed with ZOE, and the other half were restored to the cavosurface margin with the test materials. Sixty-five percent of the unsealed amalgam restorations showed moderate to severe inflammation and had bacteria present on the cavity walls. Twelve percent of the sealed amalgam restorations showed slight inflammation, and 12 percent had bacterial staining on the cavity walls. All of the unsealed composite restorations showed severe inflammation and necrosis and had bacterial staining, while 40 percent of the sealed restorations had slight inflammation, and 50 percent showed bacterial staining.

Fuks and colleagues⁵⁰ surface sealed composite restorations in baboon teeth. At 90 days, 11 teeth had no inflammation, and one tooth had a slight inflammatory response.

The materials used to restore teeth in children will not produce inflammatory responses in the pulp as long as the tooth is sealed. One of the possible reasons for the lack of sealing in primary teeth is the fact that primary enamel is not as mineralized as permanent enamel and therefore does not etch in the same manner as permanent teeth. Wilson and colleagues⁵⁴ found when primary incisors and canines where compared with their homologous successors overall mineralization levels were lower in the primary dentition and when primary molars were compared to premolars, the primary molars were also relatively less mineralized. There are other shortcomings to these restorative materials. Silver amalgam still has the mercury controversy,^55-57 and the composite resins have the problems discussed earlier.

Conclusions

This paper has reviewed some of the materials used in the treatment of primary teeth and their effect on the pulp tissue. Admittedly, the current paper is an attempt to present some key points from a large body of information. Most of the previous literature has been limited to studying the effects of materials on permanent teeth. (For an excellent review of this subject, the reader is referred to a paper by Schuster and colleagues. ⁵⁸) This review has attempted to present some of the problem areas that must still be addressed with the materials used in the treatment of children.

The best-case scenario for treatment is still prevention so as to avoid the use of any materials for the restoration of teeth. When one must do a pulpotomy or restore a primary tooth, one must choose and use the available materials carefully, basing the decision on scientific data and successful clinical outcomes. Additional clinical and histologic studies need to be done on primary teeth to demonstrate which materials will give the best long-term results. It is hoped that there soon will be other classes of materials -- such as mineral trioxide aggregate, freeze dried bone, and cloned enamel -- that might better satisfy the need to seal the dentin and restore teeth in both the primary and permanent dentitions. The ideal restorative material would be tooth-colored, be easily placed in a cavity preparation, have adhesive qualities, and prevent the ingress of bacteria and bacterial products from the oral cavity.

Author/

David L. Good, DDS, is a clinical professor in the Department of Pediatric Dentistry at University of Southern California School of Dentistry.

References

1. Schroder U, Szpringer-Nodzak M, et al, A one year follow-up of partial pulpotomy and calcium hydroxide capping in primary molars. Endod Dent Traumatol 3:304-6, 1987.

2. Warfvinge J, Rozell B, Hedstrom K-G, Effect of calcium hydroxide treated dentine on pulpal responses. Int Endod J 20:183-93, 1987.

3. Cox C, Bergenholtz G, et al, Pulp capping of dental pulp mechanically exposed to oral microflora: a 1-2 year observation of wound healing in the monkey. J Oral Pathol 14:156-68, 1985.

4. Foreman PC, Barnes IE, A review of calcium hydroxide. Int Endo J 23:283-97, 1990.

5. Matsuzaki K, Fujii H, Machida Y, Experimental study of pulpotomy with calcium hydroxide-iodoform paste in dogs’ immature permanent teeth. Bull Tokyo Dent Coll 31:9-15, 1990.

6. Cox CF, Suzuki S, Re-evaluating pulp protection: calcium hydroxide liners vs. cohesive hybridization. J Am Dent Assoc 125:823-31, 1994.

7. Kontakiotis E, Nakou M, Georgopoulou M, In vitro study of the indirect action of calcium hydroxide on the anaerobic flora of the root canal. Int Endod J 28:285-9, 1995.

8. Qin M, Zhang S, et al, Calcium hydroxide compound pulpotomies for primary teeth: A clinical study of two-year follow-up. Ped Dent J 8:25-30, 1998.

9. Schroder U, Effects of calcium-hydroxide-containing pulp-capping agents on pulp cell migration, proliferation and differentiation. J Dent Res 64:541-8, 1985.

10. Heys RJ, Heys DR, et al, The response of four calcium hydroxides on monkey pulps. J Oral Pathol 9:372-9, 1980.

11. Goldberg F, Massone EJ, Spielberg C, Evaluation of the dentinal bridge after pulpotomy and calcium hydroxide dressing. J Endod 10:318-20, 1984.

12. Cox CF, Subay RK, et al, Tunnel defects in dentin bridges: their formation following direct pulp capping, Oper Dent 21:4-11, 1996.

13. Markowitz K, Moynihan M, et al, Biologic properties of eugenol and zinc-oxide eugenol. Oral Surg Oral Med Oral Pathol 73:729-37, 1992.

14. Trowbridge H, Edwall L, Panopoulos P, Effect of ZOE and Ca(OH)₂ on intradental nerve activity. J Endod 8:403-6, 1982.

15. Hume WR, The pharmacologic and toxicological properties of zinc oxide-eugenol. J Am Dent Assoc 113:789-91, 1986.

16. Watts A, Patterson RC, Pulpal response to a zinc oxide-eugenol cement. Int Endod J 20:82-6, 1987.

17. Garcia-Godoy F, A comparison between zinc-oxide eugenol and polycarboxalate cement on formocresol pulpotomies. J Pedod 6:203-17, 1982.

18. Augsburger RA, Peters DD, Radiographic evaluation of extruded obturation materials. J Endod 16:492-7, 1990.

19. Kakehashi S, Stanley HR, Fitzgerald RJ, The effects of surgical exposure of dentin pulps in germ-free and conventional rats. Oral Surg Oral Med Oral Pathol 20:340-9, 1965.

20. Berger JE, Pulp tissue reaction to formocresol and ZOE. J Dent Child 32:13-28, 1965.

21. Magnusson BO, Therapeutic pulpotomies in primary molars with the formocresol technique. ACTA Odontol Scand 36:157-65, 1978.

22. Fuks AB, Bimstein E, Michaeli Y, Glutaraldehyde as a pulp dressing after pulpotomy in primary teeth of baboon monkeys. Pediatric Dent 8:32-6, 1986.

23. Cotes O, Boj J, et al, Pulpal tissue reaction to formocresol vs. ferric sulfate in pulpotomized rat teeth. J Clin Pediatr Dent 21:247-54, 1997.

24. Fuks AB, Eidelman E, et al, Pulp response to ferric sulfate, diluted formocresol and IRM in pulpotomized primary baboon teeth. J Dent Child 64:254-9, 1997.

25. Hamid A, Hume WR, A study of component release from resin pit and fissure sealants in vitro. Dent Mater 13:103-10, 1997.

26. Hill SD, Berry CW, et al, Comparison of antimicrobial and cytotoxic effects of glutaraldehyde and formocresol. Oral Surg Oral Med Oral Pathol 71:89-95, 1991.

27. Ketley CE, Goodman JR, Formocresol toxicity: Is there a suitable alternative for pulpotomy of primary molars. Int J Paed Dent 2:67-72, 1991.

28. Araki K, Isaaka H, et al, Excretion of ¹⁴C-formaldehyde distributed systemically through root canal following pulpectomy. Endod Dent Traumatol 9:196-9, 1993.

29. White KC, Cox CF, et al, Pulpal response to adhesive resin systems applied to acid-etched vital dentin: damp versus dry primer application. Quintessence Int 25:259-68, 1994.

30. Fey A, Udin R, Johnson R, A clinical study of ferric sulfate as a pulpotomy agent in primary teeth. Pedatr Dent 13:327-32, 1991.

31. Law DB, Lewis TM, Formocresol pulpotomy in deciduous teeth. J Am Dent Assoc 69:601-7, 1964.

32. Redig DF, A comparison and evaluation of two formocresol pulpotomy techniques utilizing "Buckley’s" formocresol. J Dent Child 35:22-30, 1968.

33. Rolling I, Lambjerg-Hansen H, Pulp condition of successfully formocresol-treated primary molars. Scand J Dent Res 86:267-72, 1978.

34. Morawa AP, Straffon LH, et al, Clinical evaluation of pulpotomies using dilute formocresol. J Dent Child 42:360-3, 1975.

35. Usami Y, Okamoto A, et al, Pulpal response to a new light-activated fluoride releasing liner. Dent Mater 9:344-349, 1993.

36. Tsuneda Y, Hayakawa T, et al, A histopathological study of direct pulp capping with adhesive resins. Oper Dent 20:223-9, 1995.

37. Kitasako Y, Inokoshi S, et al, Short-term reaction of exposed monkey pulp beneath adhesive resins. Oper Dent 23:308-17, 1998.

38. Brannstrom M, Communication between the oral cavity and the dental pulp associated with restorative treatment. Oper Dentistry 9:57-68, 1984.

39. Pashley DH, The effects of acid etching on the pulpodentin complex, Oper Dent 17:229-42, 1992.

40. Gilpatrick RO, Johnson W, et al, Pulpal responses to dentin etched with 10% phosphoric acid. Am J Dent 9:125-9, 1996.

41. Horsten-Bindslev P, Monkey pulp reactions to cavities treated with gluma dentin bond and restored with a microfilled composite. Scand J Dent Res. 95:347-55, 1987.

42. Pashley EL, Galloway SE, Pashley DH, Protective effects of cavity liners on dentin. Oper Dent 15:10-7, 1990.

43. Kopel HM, The pulp capping procedure in primary teeth "revisited." J Dent Child 64:327-33, 1997.

44. Oysaed H, Ruyter IE, Sjovik Kleven IJ, Release of formaldehyde from dental composites. J Dent Res 67:1289-94, 1988.

45. Olea N, Pulgar R, et al, Estrogenicity of resin-based composites and sealants used in dentistry. Environ Health Perspect 104:298-305, 1996.

46. Soderholm K, Phil M, Mariotti A, BIS-GMA based resins in dentistry: Are they safe? J Am Dent Assoc 130:201-9, 1999.

47. Sano H, Yoshiyama M, et al, Comparative SEM and TEM observations of nanoleakage within the hybrid layer. Oper Dent 20:160-7, 1995.

48. Arbabzadeh F, Gage JP, et al, Gap measurements and bond strength of five selected adhesive systems bonded to tooth structure. Australian Dent J 43:175-80, 1998.

49. Cox CF, Keall HJ, et al, Biocompatability of surface-sealed dental materials against exposed pulps. J Prosth Dent 57:1-8, 1987.

50. Fuks AB, Funnell B, Cleaton-Jones P, Pulp response to a composite resin inserted in deep cavities with and without a surface seal. J Prosthet Dent 63:129-34, 1990.

51. Yakushiji M, Kinumatsu T, et al, Effects of glass ionomer cement on the dental pulp and its efficiency as a base material. Bull Tokyo Dent Coll 20:46-59, 1979.

52. Gaintantzopoulou MD, Willis GP, Kafrawy A, Pulp reactions to light-cured glass ionomer cements. Am J Dent 7:39-42, 1994.

53. Tarim B, Hafez A, Cox C, Pulpal response to a resin-modified glass-ionomer material on non-exposed and exposed monkey pulps. Quintessence Int 29:535-42, 1998.

54. Wilson PR, Beynon AD, Mineralization differences between human deciduous and permanent enamel measured by quantitative microradiography. Arch Oral Biol 34:85-8, 1989.

55. Mandel ID, Occupational risks in dentistry: comforts and concerns. J Am Dent Assoc 124:41-9, 1993.

56. Dilley DC, Bawden JW, Mercury exposure due to environmental factors and amalgam restorations in a sample of North Carolina children. Pediatr Dent 21:114-7, 1999.

57. Mackert JR, Dental amalgam and mercury. J Am Dent Assoc 122:54-61, 1991.

58. Schuster GS, Lefebvre CA, et al, Biocompatibility of posterior restorative materials. J Calif Dent Assoc 24:17-31, 1996.

To request a printed copy of this article, please contact/David L. Good, DDS, Department of Pediatric Dentistry, USC School of Dentistry, 925 W. 34th St., Los Angeles, CA 90089-0641.