Implant Periapical Lesions: Etiology and Treatment Options

Implant Periapical Lesions: Etiology andTreatment OptionsGeorgios E. Romanos, DDS, Dr med dent, PhD1*Stuart Froum, DDS, MS2

Silvia Costa-Martins, DDS2

Sean Meitner, DDS, MS1

Dennis P. Tarnow, DDS2

Implant failures due to apical pathology are conditions that have not been extensively

studied nor reported in the literature. The implant periapical lesion (IPAL) has different

symptoms, and several etiologies have been proposed in the literature. This article

reviews cases of IPAL reported in peer-reviewed journals and presents possible treatment

options. Analysis of the data collected was performed based on diagnosis, cause of

extraction of the natural tooth, location, period of implant placement, implant surface,

and treatment approach. Even the data presented in this review are based on few

reported cases the etiology of these lesions seems to be multifactorial or with an

unknown origin. Contamination of the implant surface, bone overheating during surgery,

excessive torquing of the implant, poor bone quality, perforation or thinning of the

cortical bone, premature or excessive load over the fixture, fracture of the bone inside

the hollow portion of the hollow implant, and an implant placement in an infected

maxillary sinus have been discussed. In general, areas around endodontically

compromised teeth should be carefully analyzed prior to implant placement to prevent

implant failures.

Key Words: endodontic lesion, implant periapical lesions

INTRODUCTION

Endosseous oral implants, have

demonstrated high survival rates

with different treatment proto-

cols,1–5 implant surfaces,6,7 im-

plant design geometries, and

diameters.8 When failures have been docu-

mented, possible causes have been pro-

posed.9–12

Implant failures are typically character-

ized by clinical and radiographic signs such

as pain, paresthesia, mobility, peri-implant

radiolucency, and excessive loss of alveolar

bone.13 Such failures are traditionally cate-

gorized as failures due to infection (ie, peri-

implantitis or retrograde peri-implantitis) or

failures due to trauma (ie, excessive over-

loading or implant fracture).14 When mobility

is present, the implant is considered a failure.

However, when mobility is absent and there

are signs of periapical pathology, such as

bleeding, suppuration, deep probing depths,

and evidence of osseous loss, the implant

may be classified as ailing.15 Many different

strategies are described in the literature to

treat ailing implants.15 Most of these thera-

1 Division of Periodontology, Eastman Institute for OralHealth, University of Rochester, Rochester, NY.2 Department of Periodontology and Implant Dentistry,New York University, College of Dentistry, New York,NY.* Corresponding author, e-mail: [email protected]: 10.1563/AAID-JOI-D-09-00067

LITERATURE REVIEW

Journal of Oral Implantology 53

peutic procedures are performed on im-

plants with crestal (marginal) bone loss and

crestal radiolucency. However, apical implant

pathology is also a condition that may be

indicative of a failing or ailing implant.

Although implant periapical radiolucen-

cies have been reported, there is little

information as to why such lesions occur

and what the best treatment option is.

The implant periapical lesion (IPAL), also

referred to as ‘‘abscess formation around the

apex of an implant’’16,17 or as ‘‘retrograde

peri-implantitis’’18–21 was first described in

1992 by McAllister et al.22 Since then, IPAL has

been defined as an infection located at the

apex of an implant.23 In 1995 the prevalence

of such lesions was estimated to be approx-

imately 0.26%.23 A more recent review article

reported a 1.86% incidence with machined

and textured surface implants.21

Implant periapical lesions can either be

inactive or active. They are considered as

inactive when the radiographic findings are

not associated with clinical symptoms (Fig-

ure 1). A periapical scar of dense collagen is

usually seen when the drilling depth during

osteotomy preparation exceeded the length

of the implant placed22 or when the apex of

the implant is placed near an existing scar23

(Figure 2). These situations should be peri-

odically reevaluated. If they remain stable, no

therapy is needed.22 In contrast, an IPAL can

be categorized as active when there is an

increase in radiolucent size, usually accom-

panied by symptoms22 (Figure 1). Although

IPALs are often found around the apex of an

implant, they may spread coronally and/or

laterally (Figures 2 through 8). Therefore,

an aggressive therapy is usually ad-

vised.16,19,20,22 Even with the diagnostic aids

available today, it is still not possible to

determine whether these apical lesions are

healthy scar tissue, new tissue destruction, or

a reactivation of preexisting pathology.24,25

The symptoms reported and radiographic

evaluation are the main tools available for

IPAL detection. Several etiologies have been

proposed in the literature. Today, the etiol-

ogy of these lesions is considered multifac-

eted.26

The purpose of this article was to review

all of the cases of IPAL reported in peer-

reviewed journals up to December 2007 and

to present possible treatment options.

MATERIALS AND METHODS

Medline was searched on the words ‘‘peri-

apical,’’ ‘‘dental implant,’’ and ‘‘lesion’’ alone

and in combination within articles published

between April 1990 and December 2007.

Forty-eight articles were found.

Articles consisting of case reports, retro-

spective studies, and literature reviews were

included in the present paper. Reports of

IPALs directly associated with endodontic

pathology that included an apical ‘‘implanti-

tis’’ as an extension of a periradicular lesion

on an adjacent tooth, or that resulted from

the insertion of the implant, which resulted

in adjacent tooth devitalization26–29 were

considered as endo-implant or implant-

endodontic infections and were excluded

from the present analysis. Cases that in-

volved root canal therapy or apicoectomy on

the adjacent teeth30,31 do not require a

surgical approach on the implant site.

Therefore, only reported IPALs in which

there were no evidenced periapical pathol-

ogy at the time of implant placement, the

adjacent teeth were vital or asymptomatic,

and there was no invasion of the adjacent

tooth periodontal ligament space, were

included in this review.

Twelve case reports were found in the

literature, in which the etiology of the IPAL

was multifactorial, thus fitting the previous

criteria, and therefore were included in this

review (Table).

Data were analyzed and included cause

of extraction of the natural tooth, location,

healing time, type of implant surface, diag-

Implants and Endo Lesions; Complications

54 Vol. XXXVII/No. One/2011

nostic sign or symptom present, treatment

approach, available histologic evaluation,

and implant survival and failure rates.

RESULTS

Analysis of the data collected (Table) is

summarized below.

Diagnostic

Radiographic evidence of IPAL was found in

all cases.

The signs/symptoms encountered were:

fistulous tract (21/32, 65.6%), pain (14/32,

43.8%), and swelling (11/32, 34.4%).

The signs/symptoms of IPAL started

from 6 days after implant placement up to

FIGURES 1–5. FIGURE 1. Schematic transversal view of an implant periapical lesion (IPAL). FIGURE 2. Four-month postoperative radiograph of an implant apicoectomy (#4) in order to treat an IPAL. FIGURE 3.Preoperative radiograph of implant sites adjacent to endodontically treated tooth. FIGURE 4.Postoperative radiograph taken several months after the implants have been restored. Patientpresented with swelling at the apex of the implant in the # 4 site. The infection did not respond toantibiotic and was removed. FIGURE 5. Postoperative radiograph taken after adjacent tooth wasremoved. The lesion at the apex of the endodontically treated tooth has spread to the apex of theimplant as indicated with a gutta percha point inserted into the fistula.

Romanos et al


18 months after loading. Twenty-three of

the 32 cases were detected before the

stage II procedure (71.9%), 6 before or at

implant loading (18.8%), and 3 post loading

(9.4%).

Cause of Extraction of the Natural Tooth

Twenty-two of the 32 cases (68.8%) were on

previous endodontically involved areas, and

only 3 cases were related to advanced

periodontal disease. For 4 of the implants

the cause of extraction was not specified.

Location

Twenty-five of the 32 IPALs (78%) were

found associated with maxillary implants.

Of the IPALs included in this literature

review, one (3.1%) was a lower second molar,

4 (12.5%) were canines, 9 (28.13%) were

incisors, and 16 of the 32 IPALs (50%) were

found in the premolar areas.

Period of Implant Placement

Healing time from tooth extraction to

implant placement varied considerably, from

time of immediate placement until years

after extraction.

Implant Surface

Implant surfaces studied were mainly ma-

chined (21/32). One implant had a HA-

coated surface,22 2 implants had acid-etched

surfaces (Osseotite, 3i, Palm Beach Garden,

Fla),32,33 and 7 implants had anoxidized

titanium surfaces (TiUnite, Nobel Biocare,

Yorba Linda, Calif ).21

Treatment Approach

In none of the cases reported was antimi-

crobial therapy alone considered an effective

method of treating the IPALs.

All cases were accessed surgically with a

mucoperiosteal flap elevation. A crestal

incision was the preferred flap design (22/

32, 68.8%),18,19,21,22,33,34 followed by the

semilunar incision (6/32, 18.8%).19,20,32 One

case report utilized an extraoral incision.16

Complete debridement of the lesion was

attempted in 25 of the 32 cases with only 2

of these reporting implant failure21,34 (2/25,

8%). In one case20 there was no debridement

of the implant surface, although the bony

FIGURES 6–8. FIGURE 6. Clinical view of a fistularemaining after the adjacent tooth was removed.FIGURE 7. Clinical view after the implant wasremoved showing bone defect remaining afterthe implant was removed. FIGURE 8. Apical half ofthe implant body had little or no apical boneremaining. Because of the extent of the involve-ment, an apicoectomy was not recommended asthe treatment of choice.



defect was addressed. The implant was still

present 11 months following this therapy. In

2 cases no debridement21 was performed

because the explorative flaps did not reveal

perforation of the cortical bone. Survival of

these implants was reported, but the follow-

up duration was not specified. In the

remaining cases without debridement (4),

the implants were removed during the

explorative opening.23,25,33,35

In 3 cases apicoectomy (Figure 2) of the

implant was performed to gain access to the

defect walls and allow a complete debride-

ment.16,32,34 One failure was reported after

implant apicoectomy. This approach was

also recommended in other articles,18,19,33

although the procedure was not performed

in the cases cited by those authors.

Surface detoxification was attempted on

11 implants (34.4%) using tetracycline (8),

chlorhexidine (1), povidone-iodine (1), citric

acid (1), or calcium hydroxide (1). Only 1

failure was reported after the use of tetracy-

cline.34 No failures were reported with the

other implant surface conditioners.

Guided bone regeneration (GBR) was

performed in 13 of the 32 cases. In 6 cases

demineralized freeze-dried bone allograft

(DFDBA) was used, 5 cases were treated

using particulate bovine bone (Bio-Oss); in 1

case demineralized bone matrix (DynaGraft)

was used and in another bioactive glass

(PerioGlas). When particulate bone substi-

tutes were used, 7 of the 11 cases were not

covered with an occlusive membrane. No

implant failures were reported with any of

the GBR technique treated cases.

Exclusive guided tissue regeneration

(GTR) was performed in 2 cases.

The use of GBR or GTR techniques for the

treatment of IPALs was not recommended in

one report.19

Histologic Evaluation

In a total of 32 reported implants retrieved

and histologically evaluated, bacteria were

detected in 1 study, while 3 other studies

showed aseptic bone necrosis. No other

histologic data were available in the litera-

ture.

Implant Survival and Failure

Twenty-four of the 32 implants (75%) diag-

nosed with an IPAL survived after treatment

with follow-up times varying from 4 months

to 7 years.

In a total of the 32 implants diagnosed

with IPAL were lost (21.9%) but only one

failed after therapy. Therefore, the survival

after IPAL diagnosis and treatment was

96.2% (25 out of 26).

It should be noted that in one of the case

reports included in the present review,22 five

implants with IPALs were described in a

single patient but 4 of them were in close

proximity to each other. This finding may be

considered as a cluster effect.

DISCUSSION

The data presented in this review should be

evaluated in light of the few reported cases.

Statistics of survival rates might vary if the

number of reported cases was larger.

The articles found in the literature show

that factors can cause IPALs. The etiology of

these lesions has been referred to as a

multifactorial26 or with an unknown or

inconclusive origin.32 The etiology, which

has been described in the literature, included

the following:

Contamination of the implant surface.

Contamination can be caused by the

manufacturer or contamination of the fix-

ture by the clinician,24,32,33,36 adjacent tooth

endodontic infection,18,24,27,28,31,32 invasion

of the adjacent tooth periodontal ligament

during implant placement causing adjacent

tooth endodontic infection, and subsequent

IPAL28,31 and residual periapical lesion of the

extracted natural teeth (granulomas, residual

cysts, root remnants, and foreign body reac-

Romanos et al


tions).18–20,22,24,32 Most of the cases reported

occurred in previous endodontically compro-

mised areas. Although a microbial component

is highly probable, only one of the implants

analyzed histologically reported the presence

of bacteria on the IPAL area. Therefore, an

exclusive microbiologic etiology cannot be

accepted as the only reason for such pathology.

Bone overheating during surgery.37,38 This

could result in necrosis of the surrounding

bone, and a subsequent sequestrum forma-

tion around the apex of the implant might

occur.18,23–25,32,35

Excessive torquing of the implant. Trauma

during surgery with excessive in-depth

placement of the implant causing compres-

sion of the bone fragments could cause

ischemia, necrosis, and bone sequestra-

tion.20,23,35 Several histologic studies39,40 re-

veal trabecular microfractures with circulation

impairment in compressed areas with subse-

quent necrosis. One of the articles reviewed32

rejected this hypothesis citing success found

in osteotome procedures, in which bone

compression is deliberately achieved with

successful results.3

Poor bone quality. This occurs where

there is a lack of sufficient osteoprogenitor

cells to colonize the apical area.23,25,35 Most

of the IPALs reported were in maxillary

locations, where the bone quality tends to

be poor.

Perforation or thinning of the cortical

bone. A small cortical surgically undetected

perforation or excessive thinning from the

medullary side of the cortex on the apical

TABLE

Studies on implant and endodontic lesions�

Article

No. of

Patients

No. of

Implants

Cause of

Extraction

Tooth

No.

Healing

Before

Stage I

Implant

Type

Diagnosis

of IPAL

Signs or

Symptoms

Pre-op

Medication

Success

McAllister22 2 4 Endo-perio 6–11 0 M 3 mo (SI) F (3/4), X No1 Perio 10, 11 7 mo HA 7 mo (SI) F, X *

Balshi16 1 1 * 26 * M 8 mo (SII) F, S, P, X *Piattelli34 1 1 Caries (endo) 5 10 y M 2 mo (SI) F, S, P, X NoBretz18 1 1 Endo 10 3 y M 6 mo (SI) F, X *Piattelli25 1 1 * 29 * M 5 mo (SI) F, P, X NoPiattelli35 1 1 Caries (endo) 5 2 mo M (+GBR) 8 mo (SI) F, X NoScarano24 1 1 * 28 * M 6 mo (SI) P, X *Ayangco19 3 1 Endo 12 9 wk M (GTR) 18 mo (L) F, S, X No

1 Endo 13 4 mo M 9 mo (L) S, X *1 Endo 6 Previous M 1 mo (SI) P, X *

Jalbout32 4 1 Caries (endo) 5 * M 14 mo (SI) F, S, P, X No1 Fracture

(endo)9 1 y M 1 mo (SII) F, S, P, X *

1 Fracture(endo)

8 8 mo postGBR

Osseotite 4 mo (SII) P, X *

1 * 5 * M 3 mo (L) F, X *Flanagan20 1 1 Endo 12 3 mo Osseotite 10 wk (SI) F, P, X NoQuirynen33 4 1 Endo 5 9 mo M 3 mo (SI) F, P, X No

1 Endo 12 6 mo M 3 wk (SI) P, X No1 Endo 28 5 mo M 2 wk (SI) F, S, P, X *1 Endo-perio 12 9 mo M 6 d (SI) S, X No

Quirynen21 9 1 Impacted 10 Years TiU 0 (L) X *1 Endo 5 10 mo M 3 mo (SI) F, X *1 Endo 9 12 mo TiU 1 mo (SI) S, P, X *1 Perio 9 18 mo TiU 3 mo (SI) F, X *1 Endo 5 7 mo TiU 3 mo (SI) F, X *1 Endo 12 29 mo TiU 1 mo (SI) F, S, P, X *1 Endo 20 7 mo TiU 0 (L) X *1 Endo 20 8 mo M 0 (L) X *1 Endo 18 6 mo TiU 2 wk (SI) F, S, X *

*Not mentioned.�M indicates; HA, hydroxyapatite; and TiU, TiUnite; IPAL, impact periapical lesion; SI, Stage I; SII,

Stage II; L, after load; F, fistula; P, pain; S, suppuration; X, X-ray radiolucency; GBR, guided boneregeneration; GTR, guided tissue regeneration; CLHX, chlorhexidine digluconate; DFBA, demineralizedfreeze dried bone allograft; FDDMA, freeze-dried demineralized allograft.



area of the osteotomy could serve as a path

of least resistance to infection progres-

sion.20,35 According to Scarano et al,24 if

the cortical bone becomes thinner than

0.5 mm, natural bone resorption could cause

a dehiscence leading to infection of the soft

tissues.

Premature or excessive load over the

fixture. This would result in bone micro-

fractures around the implant.16,18,24 This

etiology may be considered either when

the IPALs appear after implant loading (small

number of cases reported in the literature) or

when the patient is supporting a removable

prosthesis, which could cause a traumatic

lesion.41 This hypothesis, however, does not

explain the apical location of these lesions,

since occlusal overloading is described in the

literature as a situation that leads to crestal

bone loss and bone microfractures at and

near the bone-implant interface.42 Based on

the literature, most of the IPALs were found

before stage II procedures. Therefore, exces-

sive loading probably may not be a primary

risk factor.

Fracture of the bone inside the hollow

portion of hollow implants. The rationale for

this hypothesis is that the bone fracture

would cause a vascular impairment and

consequent aseptic bone necrosis in the

hollow part of this type of implant.25 Since

this type of implant is not routinely used any

longer, this hypothesis will not be further

discussed in the present paper.

Other etiologic factors proposed in the

articles reviewed include: implant placement

in an infected maxillary sinus, which could

cause a spread of the maxillary sinus

infection onto the implant surface,24 absence

of primary stability,26 and reduced healing

ability of the host.26 None of these etiologies

were reviewed because no data were avail-

able in the literature to allow an adequate

analysis of these possible factors.

Surgical Approach of the IPALINo.

Lost

No.

Survived

Follow-up

TimeDebridement Tetracycline Anti-septic Citric Acid CaOH GBR GTR

Yes Yes No No No DFDBA No 0 5 4 moYes No No Yes No DFDBA Vicryl

mesh?

Yes (+A) No Povidone No No No No 0 1 3 yYes (+A) Yes No No No No FDDMA 1 0 BacteriaYes No CLHX No No DFDBA CollaCote 0 1 17 moNo No No No No No No 1 0 BANNo No No No No No No 1 0 BANNo No No No No No No 1 0 BANYes Yes (rinsed) No No No No No 0 3 8 moYes Yes (rinsed) No No No No No 1 yYes Yes (rinsed) No No No No No 8 yYes (+A) No No No No Bio-Oss Bio-Gide 0 4 22 moYes No No No No Bio-Oss Resolut

XP24 mo

Yes No No No No DynaGraft No 4 mo

Yes No No No No PerioGlas No 7 yYes (not implt) No No No Yes No No 0 1 11 moYes No No No No No No 2 2 1 yYes No No No No No No 3 yNo No No No No No NoNo No No No No No NoYes No No No No Bio-Oss No 1 7 14 moYes No No No No No No 18 moYes No No No No Bio-Oss No 2 moYes No No No No No Yes* 15 moYes No No No No Bio-Oss No 6 moYes No No No No No No 6 moNo No No No No No No *Yes No No No No No NoNo No No No No No No *

TABLE

Extended

Romanos et al


According to the articles reviewed in the

present report, the postextraction healing

time appeared to be irrelevant in terms of

preventing IPALs. However, several articles

proposed a postponed implant placement

after an endodontic failure that leads to

extraction of the natural tooth in order to

allow a more predictable bone healing.31

In most of the cases, IPALs were associ-

ated with machined surface implants. One

case reviewed was associated with one HA-

coated implant,22 which was treated suc-

cessfully and one reported an IPAL around

TiUnite surfaced implants.22 The authors22

concluded that although the textured im-

plant surface (specifically the TiUnite) was

more sensitive to infection and bacterial

invasion, the treatment of the IPAL was

predictable.

All cases reported in the current review

presented with periapical implant radiolu-

cencies, which were accompanied by fistu-

lous tract formation, pain, or swelling as the

most frequent clinical findings. Therefore, a

fistula formation in the apical part of the

implant should be considered an important

sign for the diagnosis of an IPAL.22,24

Several therapeutic alternatives were pre-

sented in the literature. Most authors recom-

mended the exposure of the implant apex,

degranulation of the defect, detoxification of

the implant surface, and regeneration of the

lost bone.22 However, no consensus could be

found concerning the treatment of such cases

except that they should be approached

surgically. Several methods were proposed

to detoxify the implant surface. However, a

distinction has to be made between HA-

coated implants and machined titanium

surfaces. For HA-coated implants, research

supports the use of citric acid for 30–60

seconds.22,26 If the hydroxylapatite looks

pitted, blotchy or resorbed, it should be

removed down to the underlying titanium

and then it should be treated as a pure

titanium surface.22,26 For implants with ma-

chined titanium surfaces, surface treatment

with tetracycline paste,19,22,34 10% povidone-

iodine solution,16 0.12% chlorhexidine diglu-

conate (CLHX),18 and calcium hydroxide

paste20 were proposed. Simple saline solution

irrigation was also used in some cases,21,22,32–34

not with the intention of detoxifying, but

simply rinsing the surgical area after debride-

ment. Other solutions described in the peri-

implantitis literature for implant surface decon-

tamination were stannous fluoride, hydrogen

peroxide, polymyxin B, and chloramine-T and

also included the ultrasonic or air-powder

abrasives (with the risk of emboli formation)

and laser irradiation.26,43–45 From the cases

reviewed, no treatment could be considered as

the most predictable, although the tetracycline

application was the most frequently used.

GBR procedures appeared in the litera-

ture as a method of regenerating tissue and/

or bone lost after control of the infection.

However, it cannot be determined in the

data found in the reviewed articles if

regeneration was achieved or only repair,

because there is no histologic information

from successfully treated IPALs.

The cases treated with bone substitute

materials with or without membrane were

successful in terms of survival of the

implants. The cases treated with a mem-

brane only (Vicryl mesh, freeze-demineral-

ized dura mater membrane, or collagen

membrane) were also successful in terms of

implant survival, except for one report with

freeze-dried demineralized allograft (FDDMA),

where the implant failed after treatment. One

study compared the use of particulate bone

xenograft without membrane vs no-GBR and

found no differences on the implant survival

rate after several months.21 However, there

were no histologic data to support this

isolated trial. From a biologic point of view,

fibro-integration is a more plausible healing

response at the apical area of an implant

treated for IPAL when no GBR is utilized. If the

main goal is to achieve bone regeneration



around the implant surface, detoxification of

the contaminated fixture surface should be

attempted to not compromise that and allow

fibroblast migration and attachment.46 But

this hypothesis remains opened to discussion

since no histologic evaluation of the wound

healing was attempted in any study of IPALs

to date. In the present literature review, only 2

implants were lost when debridement of the

defect was performed in immobile implants

with IPALs.21,34

More documented cases including histo-

logic data from successfully treated cases

and clinical studies comparing different

protocols and their outcomes to determine

an effective treatment protocol for implants

with IPALs are necessary.

CONCLUSIONS

From the literature reviewed in this report,

areas with endodontically compromised

teeth might interfere with implant success;

therefore, a careful analysis should be made

prior to the implant placement regardless of

the healing time after the extraction of the

natural tooth. The IPALs were mainly found

around implants in the maxilla and have a

higher prevalence in the premolar area.

When radiographic evidence of periapical

lesions accompanied by symptoms such as

pain, swelling, and fistula formation are

present, these cases should be treated

aggressively.

Lacking a consensus, the etiology of these

lesions are preexisting bone pathology, con-

tamination of the fixture before placement,

surgical trauma with thinning, or perforation

of the cortical bone during stage I surgery and

a poor bone quality. Most of the articles in the

literature suggest a microbial involvement,

but an exclusive antimicrobial therapy was

not considered in any article as effective

treatment for the IPAL.

Surgical approach should include the

exposure of the defect as conservatively as

possible but with adequate access, debride-

ment of the defect, detoxification of the

implant surface, and a GBR if re-osseointe-

gration is the goal of the surgery and not

only arrest of the infection.

Although the high survival rate after

therapy was reported in the articles re-

viewed, it should be stressed that there have

been a small number of cases reported in the

literature. Moreover, many variables existed

in the studies cited including the type of

implant surface, size, and chronicity of the

defect, which might have influenced the

results following treatment. More standard-

ized studies and data are needed to more

predictably prevent and treat implants with

IPALs.

ABBREVIATIONS

CLXH: chlorhexidine digluconate

DFDBA: demineralized freeze-dried bone

allograft

FDDMA: freeze-dried demineralized allograft

GBR: guided bone regeneration

GTR: guided tissue regeneration

HA: hydroxyapatite

IPAL: impact periapical lesion

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Implant Periapical Lesions: Etiology and Treatment Options