Calcium Hydroxide Paste as a Surface Detoxifying Agent for Infected Dental Implants: Two Case Reports

Dental implant treatment has been shown to be very successful. However, there are reports where an implant has become infected during or after osseointegration.1–12 Some types of bacteria or fungi may colonize the implant surface and produce localized bone loss or complete loss of bone around the fixture. To salvage an ailing or failing implant, tetracycline or citric acid has been typically used as an implant surface detoxifying agent.1,3,7,8 The apparent concept is to kill the colonizing bacteria and remove implant surface contaminants without defacing the surface. The surrounding bone should not be damaged to allow for continued or reinstated osseous healing. Many authors have published articles using tetracycline and citric acid as detoxifying agents with successful results.1,2,3 However, these agents have a pH range of 1–3 for citric acid, depending on concentration, and 1.8 for tetracycline HCl. The low pH may decalcify the osseous tissue around the implant and may inhibit healing. Another available detoxifying agent is calcium hydroxide (CH). CH is well known in dentistry. It has been used for decades as an endodontic intracanal medicament. It has a pH of slightly more than 12 that may not decalcify or confound bone healing, but it may be caustic to soft tissue. CH, in the dental pulp capping paste form, is US Food and Drug Administration (FDA) 510(k) approved for endodontic use and now is reported here as an implant surface detoxifying agent for infected implants.

CH paste as a surface detoxifier for apical (retrograde) implantitis has been previously reported.13 

A 44-year-old woman with failing endodontically treated maxillary central incisors presented for treatment (Figure 1). She had an unremarkable medical history. The teeth had been endodontically treated many years prior and had apical radiolucencies (Figure 2). After a discussion of options for treatment, extraction of the 2 teeth and implant placement for implant supported crowns were agreed upon. Both teeth were extracted and the facial cortices were found to be destroyed by the chronic infection. A facial barrier membrane (Biomend, Zimmer Dental, Carlsbad, Calif) was placed, and bone graft material was placed (Puros, Zimmer Dental) with rotated palatal pedicle grafts to attain primary closure (Figure 3). Additionally, the palatal pedicle grafts were used to increase the soft tissue thickness for appropriate gingival architecture around the definitive crowns. After 4 months of healing, 1 implant was placed in site #8 (3.7 × 13, Implant Direct, Ventura, Calif). Site #9 had poor bone quality for initial stabilization, therefore, the osteotomy was compressed with an osteotome and a larger implant was installed (4.7 × 13, Implant Direct) (Figure 4).The depth of the implant placement ensured an appropriate emergence profile for both proposed crowns despite the different diameters. At the eighth postoperative week, the patient presented with a small facial swelling at site #9. A drainage tract was seen and a radiograph was made with a #40 gutta percha point placed into the tract to act as an indicator to the source (Figure 5). The source of the infection was the mid body of the #9 implant. The site was locally anesthetized and surgically opened with a #15C scalpel to expose the infected implant body (Figure 6). The area was debrided with a periodontal curet, treated with calcium hydroxide paste (Pulpdent Corp, Watertown, Mass) for less than 30 seconds, and rinsed with sterile saline; an allograft material was then placed in the defect (Puros), and a barrier membrane was placed (Biomend) and was primarily closed with 4-0 polyglycolic acid suture (Vicryl) (Figures 6 through 9). The site healed uneventfully and 2 porcelain fused to metal crowns were subsequently made to complete the treatment (Figure 10). At all surgical visits the patient exhibited normal physiologic vital signs.

A 62-year-old woman presented for treatment of a failing, previously endodontically treated mandibular right lateral incisor. She had an insignificant medical history. Treatment options were discussed and extraction with implant treatment was decided upon. Tooth #26 was atraumatically removed and a 3.7 × 13 implant (Implant Direct) was installed. The implant was immediately nonfunctionally loaded with a provisional bis-acryl crown. After 4 months, the definitive porcelain fused to metal crown was fabricated and delivered. After 4 weeks, the patient presented with pain and slight swelling at the facial of #26. A radiograph taken with a gutta percha indicator revealed a radiolucency that indicated an infected mid body implant surface. The area was locally anesthetized and the fixture was surgically exposed. The bone defect was debrided, the implant surface was treated with calcium hydroxide paste for less than 30 seconds, and then rinsed with sterile saline. A bone allograft material was placed in the defect and primarily closed with polyglycolic acid suture (Vicryl). At all surgical visits the patient exhibited normal physiologic vital signs. The patient returned for follow-up appointments and healed uneventfully.

The root canal treatment paste product used in these cases was CH in aqueous methylcellulose with barium sulfate for radiopacity (TempCanal, Pulpdent Corp). The manufacturer claims the product is bacteriocidal and bacteriostatic. The CH is an alkali and packaged at a concentration of 5 mg/mm³. This is a very high concentration. It is not considered a carcinogen (Material Safety Data Sheet, TempCanal).

Bacterial implant infections can cause failures in healing and osseointegration. Many of these implant infections occur in failed endodontic sites. Both of the patients reported here had bouts of mid body implantitis after placement in sites where there were failed endodontically treated teeth. Both infected implant surfaces and the surrounding bone were successfully treated with CH. In both cases, the CH paste was left on the implant surface and bone defect for less than 30 seconds.

Empirically, the high pH of CH endodontic paste may be better tolerated by osseous tissue than a low decalcifying pH agent such as tetracycline or citric acid. However, both of these low pH agents have had successful treatment results reported.

Although CH paste is approved by the FDA for endodontic use, this treatment is an off-label use. This is where an agent is used for a treatment process not claimed by the manufacturer, but the clinician is allowed to use the product in a novel therapeutic way.

Enterococcus faecalis and Candida albicans are common species found in failed endodontic teeth.14 It may be that these and/or other species residually remain in the apical bone and vegetate until they are reactivated with implant surgery to colonize the implant surface.15–20,E faecalis in a vegetative or stationary phase resisted more than 10 minutes of exposure to CH or 0.05% chlorhexidine gluconate or 0.0001% sodium hypochlorite. However, the bacterial cells in a growth phase were completely killed at an exposure of 3 seconds to these materials.21 Additionally, at the higher concentration of 3.0%, sodium hypochlorite effectively killed E faecalis in both vegetative and growth phases.22 Sodium hypochlorite is corrosive and may not be safe for exposure to osseous and soft tissue and so may be inappropriate for in situ implant surface treatment.

CH is bacteriocidal on contact. It must be in direct contact with the bacteria to be lethal. CH has been shown to be active and not active against E faecalis and Pseudomonas aeruginosa.14,23 However, as with other antimicrobials, even though there is little effect at lower concentrations, there may be a bacteriocidal effect against E faecalis and other pathogens in high doses, 5 mg/mm³ of CH, that are applied topically as described here.

The literature has described a variation of inhibition of pathogens by CH. Asgary and Kamrani tested CH against Pseudomonas aeruginosa, E faecalis, Staphylococcus aureus, and Escherichia coli and found it to inhibit growth of these bacteria.24 Another study that tested serial dilution of CH against 6 endodontic pathogens found calcium hydroxide to be effective only at concentrations of about 50%.25 

Generally, planktonic microorganisms can be more susceptible to CH than when they are in a biofilm or adhering to dentin.26 These two factors increase bacterial resistance to the activity of CH.26 Conversely, Chai et al found that CH was able to completely eliminate E faecalis in a biofilm in a membrane filter with a 1-hour exposure.27 Balto in a review article found that CH was limited in its effectiveness in killing E faecalis when the testing was done by culturing techniques.28 

Apparently, CH is effective at higher concentrations against many pathogens and dependent upon the surface onto which the pathogen is adhering. Although not studied, a titanium surface may make the bacteria more susceptible than a dentin surface.

One interesting research article by Baik and co-workers found that CH was able to detoxify lipoteichoic acid. This toxin is an important virulence factor for gram-positive bacteria, such as E faecalis. The toxin, when inactivated by CH, did not stimulate the release of tumor necrosis factor in a sheep macrophage cell line.29 

There was no attempt to culture and identify the pathogen in the infected lesions in the cases presented here due to the unreliability of clinical culturing in these areas.

CH also is a source of calcium ions. Thus, any small residual material inadvertently left in the site may be of benefit for osteogenesis. However, this author does not recommend leaving any visually apparent material in the surgical site. Material with a pH value this high may not be well tolerated by soft tissue and produce a tissue reaction. The site should be lavaged of all visible calcium hydroxide. Severe sequelae have been reported with calcium hydroxide paste extruded beyond the tooth root foramen.30 

Many anaerobic infections are caused by a mixture of organisms. Bacteroides spp can be inhabitants of tooth periapical lesions.16 These bacteria are generally susceptible to metronidazole,31 cefoxitin,32 chloramphenicol,33 and clindamycin.34,Bacteroides spp also encapsulates itself in a polysaccharide that probably promotes its virulence, survival, and importance in mixed infections.18,35,Bacteroides forsythus has been shown to persist in asymptomatic periradicular endodontic lesions and may survive in bone in an encapsulated form after an extraction and subsequently infect an implant.36,37 At 10% concentration, calcium hydroxide was effective against Bacteroides fragilis.38 

Interestingly, as much as 50% of an endodontic infection is caused by bacteria that have not yet been cultivated.39 These bacteria may be left intraosseously after an extraction and subsequently colonize an implant surface.

Chlorhexidine gluconate is active against E faecalis and other endodontic pathogens.14 It may not be as effective against C albicans as calcium hydroxide.14 While the 2 cases reported here were successful with 1 calcium hydroxide direct topical treatment, a subsequent lavage with 0.2% chlorhexidine may be of value in recalcitrant infections or infections where virulent pathogens are suspected.

A sequential treatment of calcium hydroxide paste and 0.2% chlorhexidine gluconate may provide a broad range of antimicrobial action for detoxifying an infected dental implant.40,41 Because these implant infections uncommonly occur, appropriate long-term studies may be difficult.

Calcium hydroxide endodontic paste may be an appropriate direct surface detoxifying agent for infected dental implants when administered in very high concentrations. A subsequent topical treatment of 0.2% chlorhexidine gluconate may provide a broad range of antimicrobial action for detoxifying an infected dental implant. Calcium hydroxide should not be left in the surgical site to prevent a severe tissue reaction.