retrograde peri implantitis

2/20/13 Retrograde peri-implantitis

www.ncbi.nlm.nih.gov/pmc/articles/PMC2933532/?report=printable 1/21

J Indian Soc Periodontol. 2010 Jan-Mar; 14(1): 57–65.

doi: 10.4103/0972-124X.65444

PMCID: PMC2933532

Retrograde peri-implantitis

Jumshad B. Mohamed, B. Shivakumar, Sabitha Sudarsan, K. V. Arun, and T. S. S. Kumar

Department of Periodontology and Oral Implantology, Sree Balaji Dental College and Hospital, Uthandi, Chennai, India

Department of Periodontics and Implant Dentistry, Ragas Dental College and Hospital, Uthandi, Chennai, India

Address for correspondence: Dr. B. Shivakumar, Department of Periodontics and Implant Dentistry, Ragas Dental College and Hospital,

Uthandi, Chennai, India. E-mail: shivabaskaran/at/rediffmail.com

Revised April 24, 2009; Accepted October 4, 2009.

Copyright © Journal of Indian Society of Periodontology

This is an open-access article distributed under the terms of the Creative Commons Attribution License, w hich permits unrestricted use,

distribution, and reproduction in any medium, provided the original w ork is properly cited.

Abstract

Retrograde peri-implantitis constitutes an important cause for implant failure. Retrograde peri-

implantitis may sometimes prove difficult to identify and hence institution of early treatment may not

be possible. This paper presents a report of four cases of (the implant placed developing to) retrograde

peri-implantitis. Three of these implants were successfully restored to their fully functional state while

one was lost due to extensive damage. The paper highlights the importance of recognizing the

etiopathogenic mechanisms, preoperative assessment, and a strong postoperative maintenance protocol

to avoid retrograde peri-implant inflammation.

Keywords: Implant, retrograde peri-implantitis, regeneration

INTRODUCTION

During the past decade, the use of osseointegrated implants has become an increasingly important

treatment modality for the replacement of missing teeth in fully and partially edentulous patients The

success of osseointegrated dental implants has revolutionized dentistry.[1] With more than three

decades of evidence to support the clinical use of osseointegrated dental implants, implant-related

prosthesis has become a predictable method of replacing missing teeth.[2,3]

The widespread use of these implants has in recent years, produced different types of complications.

Retrograde peri-implantitis, a lesion occurring at the periapical area of an osseointegrated implant, has

recently been described[4] as a possible cause for dental implant failure. The etiology of “implant

periapical lesion” (IPL) could be attributed to overheating of the bone;[5,6] overloading of the implant;

[7] presence of a pre-existing infection or of residual root particles and foreign bodies in the bone;[8,9]

implant contamination during production or during insertion[10] or placement of the implant.

The usual plaque related or occlusion related peri-implant failure is relatively easily identified when

compared to the retrograde peri-implant lesions. With the ever increasing esthetic demands of patients,

early loading of implants, especially in the anterior segment has become a necessity. As a number of

teeth in the anterior segment are lost due to trauma and other non-periodontal causes, the clinician

must be aware of the potential risk of developing retrograde peri-implantitis due to periapical pathology

in the existing socket/adjacent teeth. This paper presents four cases of retrograde peri-implantits (each

with different etiopathogenic mechanism), three of which were successfully managed and subsequently

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http://dx.doi.org/10.4103%2F0972-124X.65444

http://www.ncbi.nlm.nih.gov/pubmed/?term=Mohamed%20JB%5Bauth%5D

http://www.ncbi.nlm.nih.gov/pubmed/?term=Shivakumar%20B%5Bauth%5D

http://www.ncbi.nlm.nih.gov/pubmed/?term=Sudarsan%20S%5Bauth%5D

http://www.ncbi.nlm.nih.gov/pubmed/?term=Arun%20KV%5Bauth%5D

http://www.ncbi.nlm.nih.gov/pubmed/?term=Kumar%20TS%5Bauth%5D

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Discussion

Discussion

restored to function. The paper then discusses the possible etiopathogenic mechanism and suggests

guidelines for the early identification and management of peri-implantitis.

CASE SERIES

Case I [Figure 1a to 1j]

A 42-year-old female patient presented with a history of failed endodontics followed by extraction and

socket preservation in relation to #31 six months prior to reporting to the implant clinic. The adjacent

teeth #32 and #41 showed endodontic restorations. After clinical and radiological evaluation it was

decided to place a 3.0 × 12 mm single piece implant . Adequate primary stability was obtained at the

time of placement. When reviewed after six weeks, the site showed signs of abscess formation in the

alveolar mucosa in relation to implant #31. There was no evidence of probing depth around the

implant, but radiographs revealed peri-implant bone loss at the middle third region. The implant was

found to be stable with no mobility. Open flap debridement was done and the implant surface

decontaminated with universal implant deplaquer . The implant was subsequently followed up for a

period of one year with regular three-month clinical and radiological reviews.

The normal peri-implant sulcus depth and absence of other inflammatory signs in the peri-

implant mucosa suggests that anterograde peri-implantits was not the cause for bone loss observed in

this case. Even though endodontic therapy was performed in the adjacent teeth, placement of implant

might have triggered latent periapical pathology[11,12] from the adjacent teeth. Recent evidence

suggests the existence of an autoimmune response[13,14] in the periapical area in relation to an antigen

which may be microbial in origin. The host response that is triggered off, may affect the host tissues as a

result of similarity between the microbial and the host antigens, such as the heat shock proteins. In

such instances, even after thorough debridement of the root canal has resulted in elimination of the

microbial antigens, the host response may ensure continuation of an active inflammatory process.

The process of implant placement could result in activation of this latent response either due to

overheating or contamination or a combination of both. This activation could have resulted in the rapid

bone loss in a short period of time. The importance of periodic clinical and radiographic examination of

implants that are placed adjacent to endodontically treated teeth has to be emphasized and a shorter

recall program has to be instituted to identify and manage retrograde peri-implant bone loss in its early

stages.

Case II [Figure 2a to 2j]

An 18-year-old male presented with a history of trauma two weeks prior to presentation resulting in

avulsion of tooth #21. After clinical and radiological evaluation a 3.0 × 15 mm single piece implant

was placed with adequate primary stability. In two weeks’ time patient presented with signs of peri-

implant abscess formation and mobility of the implant in relation to tooth #21. Radiograph revealed

peri-implant bone loss at the apical third as well as the adjacent tooth #22. Open flap debridement was

done with universal implant deplaquer and the osseous defect was filled with calcium phosphate and

Hydrase . Tooth #22 was endodontically treated. The implant was subsequently followed up for a

period of one year with regular three-month clinical and radiological reviews.

In this case, the implant was placed in an avulsed site adjacent to tooth #22 that exhibited

signs of trauma (Ellis class II fracture). The tooth was tested for vitality using the EPT (electric pulp

tester), which revealed the presence of a vital pulp. Subsequently, the implant placement was

undertaken without endodontic therapy in tooth #22. This case illustrates the limitations of using the

EPT (which is actually an indicator of nerve stimulation) when testing the vitality of the tooth. The

undetected pericapical pathology flare following implant placement resulting in the retrograde peri-

implant lesion is identified in this case. The fractured tooth adjacent to an edentulous site must be

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Discussion

Discussion

critically evaluated for evidence of dormant periapical lesions[14] and the results obtained from EPT

may not be considered a gold standard for vitality of the pulp. In suspected cases where the fracture line

is close to the pulp, it may be prudent to consider intentional endodontic therapy prior to implant

placement regardless of the results obtained from the EPT.

Management of the peri-implantitis was performed as stated by Tözüm M et al,[9] and Peñarrocha

Diago M et al,[8] by treating the periapical implant pathology and the adjacent natural tooth without

the removal of the implant. The treatment procedure included root canal treatment followed by the

debridement of the apical bone lesion, and guided bone regeneration. Smaller peri-implant lesions heal

well even without a placement of bone replacement graft; however, in larger defects it may be prudent

to place these materials to enhance healing. The placement of the graft (calcium phosphate) allowed

greater chance for new bone formation as otherwise repopulation of the wound site by gingival cells,

could result in a fibrous rather than osseous healing.

Case III [Figure 3a to 3k]

A 38-year-old male presented with a history of treated chronic periodontitis and missing teeth #31 and

#41. Clinical and radiological examination revealed inadequate ridge width for implant placement;

hence block graft augmentation was performed with a ramus block graft at the site. After 6 months,

two 3.0 × 15 mm single piece implant was placed in relation to #31 and #41 with adequate primary

stability. At one-month review abscess formation was noticed around implant #31 with mobility.

Implant #41 was intact with no signs of peri-implantits. Radiographic examination revealed peri-

implant bone loss at the apical third as well as the adjacent tooth #32. A flap was raised and thorough

debridement was done with universal implant deplaquer followed by placement of bioceramic bone

graft and collagen membrane along with endodontic restoration of tooth #32 on the same day. The

implant was subsequently followed up for a period of one year with regular three-month clinical and

radiological reviews.

Existence of active periodontal inflammation in the adjacent teeth is one possible

etiopathogenic mechanism[15] responsible for periapical pathology and subsequent spread of infection

to involve peri-implant tissue in a retrograde manner. Existing periodontal disease must be scrutinized

carefully to ensure resolution of the active inflammatory lesion before implant placement is undertaken.

The usual clinical parameters of BOP, PD, and CAL have to be repeated serially after

surgical/nonsurgical periodontal therapy to ensure stability of the periodontium prior to implant

placement.

Case IV [Figure 4a to 4f]

A 25-year-old male patient presented with a history of failed endodontic therapy in relation to tooth #11

and subsequent extraction 6 months prior to presentation to implant clinic. Clinical and radiologic

examination revealed adequate hard and soft tissue dimensions for implant placement. A 3.0 × 15 mm

single piece implant was placed in relation to #11 with good primary stability. In two weeks’ time

patient presented with signs of peri-implant mucositis and mobility. The implant was removed the

subsequent week.

The existence of a periapical pathology necessitated extraction of the tooth after failure of

endodontic therapy. Although there was no radiographic evidence of any pathology in the periapical

region at the site of implant placement, the previous periapical pathology[16,17] had obviously not

resolved. These sites may be considered to be at greater risk for implant placement and underlies the

value of evaluation of the suspected sites with more sensitive investigative procedures such as CT scan.

Economic considerations may preclude the use of such procedure routinely, but the suspected sites have

to be evaluated with CT scan to avoid such retrograde implant failures.

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CONCLUSION

Retrograde peri-implantits constitutes an important source of implant failure. Careful preoperative

evaluation of the site, adjacent teeth, and postoperative assessment of the implant placed could reduce

the chances of development of retrograde peri-implantitis. Once diagnosed, the lesion has to be treated

aggressively rather than by observation and conservative management.

BioHorizons Maximus Single Piece Implant

Universal Implant Deplaquer (Straumann)

Regen Biocement and Hydrase (Steiner Laboratories)

Grabio Glascera

* Healiguide membrane

Footnotes

Source of Support: Nil

Conflict of Interest: None declared.

REFERENCES

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Figures and Tables

Figure 1a

Preoperative photograph

Figure 1b



Preoperative radiograph

Figure 1c



Six week photograph

Figure 1d



Six week radiograph

Figure 1e

Operative photograph

Figure 1f

Six month photograph

Figure 1g



Six month probing

Figure 1h

Six month radiograph

Figure 1i



One year photograph

Figure 1j



One year radiograph

Figure 2a

Preoperative photograph

Figure 2b




Figure 2c

Two week photograph

Figure 2d

Two week radiograph

Figure 2e




Figure 2f

Bone graft placed

Figure 2g




Figure 2h


Figure 2i

One year photograph

Figure 2j

One year radiograph

Figure 3a


Figure 3b

Radiograph showing block graft

Figure 3c



Four weeks photograph

Figure 3d



Four weeks radiograph

Figure 3e




Figure 3f

Bone graft placed

Figure 3g

Membrane placed

Figure 3h



Six month photograph

Figure 3i


Figure 3j



One year photograph

Figure 3k



One year radiograph

Figure 4a

Immediate postoperative photograph

Figure 4b

Immediate postoperative radiograph

Figure 4c

Two week photograph



Figure 4d

Two week radiograph

Figure 4e

Three week photograph

Figure 4f

Three week radiograph

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