Perigraftitis, an independent biologic complication associated with implants placed in grafted bone

Abstract

Background

Perigraftitis is a recently introduced concept describing biologic complications specifically associated with implants placed in grafted bone. It is characterized by inflammation resulting from bacterial colonization of grafted bone and/or residual graft particulates. Reported cases have been managed by removal of the implant, grafted bone, and surrounding inflammatory tissue, and therefore have not definitively established perigraftitis as an independent disease entity. This report describes a histologically confirmed case of perigraftitis treated successfully without implant removal, supporting its recognition as a distinct pathologic condition.

Methods

A 63‐year‐old healthy, nonsmoking Asian male presented with discomfort, and a foul taste around implant #31, placed in a site previously grafted with deproteinized bovine bone mineral. Examination revealed infection and bone loss that centered on the grafted bone, and the site was diagnosed with perigraftitis. The implant crown was removed, and surgical access was obtained using a laser. Three hard tissue specimens were removed and submitted for histology, revealing numerous graft particulates surrounded by mature necrotic host bone with bacterial aggregates within intertrabecular spaces of all three specimens. The site was thoroughly debrided and allowed to heal without the use of any biomaterials.

Results

Three weeks post‐treatment, symptoms had resolved. At 13.5 months post‐treatment, crestal bone regeneration up to the implant collar was observed. Vertical implant soft tissue augmentation with a subperiosteal circumferential connective tissue graft was then performed, and the implant crown was reseated following soft tissue healing.

Conclusions

The histologic findings and clinical outcome of this case support the recognition of perigraftitis as an independent disease entity. Further controlled studies are warranted to elucidate the etiopathogenesis, risk factors, and prevalence of perigraftitis, and to optimize its prevention and treatment.

Key points

• Perigraftitis may be considered an independent disease entity, distinct from peri‐implant mucositis and peri‐implantitis.

• Perigraftitis is an inflammatory response induced by bacterial colonization of grafted bone and/or residual graft particulates, with the implant fixture and its transmucosal components likely providing the pathway for oral bacteria to access and infect the grafted bone.

• Perigraftitis may be successfully resolved through the removal of the infected grafted bone and associated inflammatory tissue without the need for implant removal.

Plain language summary

A patient had discomfort, foul taste, and bone loss around an implant on the lower right jaw that had been placed into grafted bone. The site was diagnosed with perigraftitis, defined as inflammation resulting from infection of the grafted bone. The implant crown was removed, and a laser was used to obtain surgical access. Three hard tissue masses were removed and submitted for biopsy. The site was thoroughly cleaned and allowed to heal naturally. After 3 weeks, the patient reported discomfort and foul taste had resolved. Thirteen and a half months after treatment, bone had regenerated around the implant. Vertical implant soft tissue augmentation was then performed. The implant crown was reseated after soft tissue healing. The tissue biopsy confirmed infection of the grafted bone and the diagnosis of perigraftitis. The treatment outcome supports perigraftitis as an independent disease entity, distinct from peri‐implant mucositis and peri‐implantitis.

INTRODUCTION

Perigraftitis is an emerging concept introduced ¹ and refined over three publications ² , ³ , ⁴ to explain biologic complications specifically associated with implants placed in grafted bone. In two of the cases reported, ² , ³ , ⁴ implants were placed in sites that had undergone alveolar ridge preservation (ARP).

In the first case, ² the extraction socket of tooth #18 was grafted with an unknown synthetic material in the 1980s. The site remained asymptomatic for three decades while the grafted bone was submerged. An implant (SP, Ø 4.8 mm WN, SLActive 10 mm, Roxolid REF 033.612S, Straumann USA) was placed at site #18 and restored with a screw‐retained crown in 2016. It was removed in 2017 due to pain and mobility; the implant explantation site was not grafted. A second implant (BLT, Ø 4.8 mm RC, SLActive 10 mm, Roxolid REF 021.7310, Straumann USA) was placed in 2018 and restored with a screw‐retained crown in 2019. It was removed in 2020 by flapless implant reversal due to infection and bone loss. Infection persisted 4 months post‐implant removal until a flap was reflected and the grafted bone from the 1980s and associated granulation tissue were removed. The grafted bone specimen exhibited multiple parallel indentations consistent with implant threads. Microscopy of the specimen revealed numerous graft particulates surrounded by mature host bone, and in the coronal periphery, graft particulates surrounded by an inflammatory infiltrate characterized by numerous neutrophils, lymphocytes, and plasma cells.

In the second case, ⁴ the extraction socket of tooth #19 was grafted with a bovine bone xenograft (Osteograf N‐700, Dentsply Implants Manufacturing GmbH) and a non‐resorbable dense polytetrafluoroethylene (dPTFE) membrane (Cytoplast Regentex, Osteogenics Biomedical, Inc.) in 2008. The site remained asymptomatic for 9.5 years while the grafted bone was submerged. An implant (RePlant Implant, SBM 4.3 mm D × 11.5 mm L, 4.3 mm D Platform, REF 604311, Implant Direct Sybron Manufacturing LLC) was placed and restored with a screw‐retained crown in 2018. It was removed in 2021 due to pain and mobility. A second implant (Neo CMI Implant, Ø 5.0 × 8.5 mm, REF BIS5008A, NeoBiotech USA) was placed in the implant explantation site. However, it was removed 6 months later, in 2022, due to persistent infection. The site was then grafted with a bone allograft (VeraGraft Mineralized Cort/Can Bone Particulate 250‒1000 µm, Product Code 5V25100, Avtec Surgical, LLC) and a composite graft of biphasic calcium sulfate and synthetic hydroxyapatite granules (Bond Apatite REF HA‐BB‐Pack1, Augma Biomaterials), and a resorbable collagen foam (Resorbable Collagen Foam 3 mm × 2 cm × 4 cm, REF 5092000, ACE Surgical Supply Co., Inc.). Infection persisted until a flap was elevated and all grafted bone and inflammatory tissue were removed in 2023. Microscopy revealed the hard tissue specimen, which exhibited multiple parallel indentations consistent with implant threads, consisted of multiple graft particulates surrounded by mature host bone, while the soft tissue specimen contained a dense inflammatory infiltrate dominated by lymphocytes and plasma cells, and isolated bacterial colonies surrounded by neutrophils.

In both cases, a third implant was successfully placed and restored. ³ , ⁴

It was hypothesized that, in both cases, the nidus of the infection was the grafted bone, and that the implant fixture and its transmucosal components provided a pathway for oral bacteria to access and colonize the grafted bone, as the implant fixture was in direct contact with the grafted bone. Bacterial colonization of the grafted bone elicited an inflammatory response in the surrounding tissue, leading to bone loss. Perigraftitis was, therefore, proposed as inflammation induced by bacterial colonization of grafted bone and/or residual graft particulates, ¹ , ² , ³ , ⁴ distinct from peri‐implant mucositis and peri‐implantitis, which are caused by bacterial colonization of the implant fixture and its transmucosal components. ⁵

While the two previously reported cases achieved resolution of infection following removal of the grafted bone and surrounding inflammatory tissue, the affected implants were also removed. Consequently, those cases did not definitively establish perigraftitis as an independent disease entity. The purpose of this report is therefore to demonstrate that perigraftitis is a distinct and independent pathologic condition by presenting a histologically confirmed case of perigraftitis successfully treated without removal of the affected implant.

MATERIALS AND METHODS

This case report follows the CARE guideline. ⁶

A 63‐year‐old healthy, nonsmoking, Asian male presented to a periodontist (J.H.D.) in San Diego, California, USA, for evaluation of implant #31 on June 20, 2024. The patient reported localized discomfort and a foul taste around the implant.

Dental history

A determination of the dental history (Figure 1) revealed the following:

FIGURE 1.

History of site #31. (A) Pre‐extraction of tooth #31 on March 28, 2013. (B) Post‐extraction of tooth #31 with alveolar ridge preservation and placement of implant #30 on April 15, 2013. (C) Restoration of implant #30 on February 11, 2014. (D) Placement of implant #31 on September 11, 2018. (E) Osseointegration check of implant #31 on December 5, 2018. (F) Restoration of implant #31 on January 29, 2019. (G and H) Clinical and (I) radiographic presentation of implant #31 on January 18, 2020.

Tooth #31 served as the distal abutment of a 29‐x‐31 fixed dental prosthesis. Tooth #30 had been missing for over three decades, and the extraction socket had healed naturally without ARP. Tooth #31 was extracted on April 15, 2013, by an oral surgeon due to severe periodontitis (Figure 1A). At the time of extraction, the socket was grafted with deproteinized bovine bone mineral (Bio‐Oss, Geistlich Pharma AG) (DBBM) and covered with a non‐resorbable dPTFE membrane (Cytoplast, Osteogenics Biomedical, Inc.). Concurrently, an implant (SP, Ø 4.8 mm WN, SLActive 10 mm, Ti, REF 033.652S, Straumann USA) was placed at the edentulous site #30 (Figure 1B). Impression was taken on January 23, 2014, and implant #30 was restored with a cement‐retained crown (Figure 1C) on February 11, 2014, by a general dentist. Implant #31 (BLT, Ø 4.8 mm RC, SLActive 10 mm, Roxolid, REF 021.7310, Straumann USA) was placed on September 11, 2018 (Figure 1D) and cleared for restoration on December 5, 2018 (Figure 1E), by the same oral surgeon who performed tooth #31 extraction and ARP in 2013. The implant was restored on January 29, 2019, with a screw‐retained restoration (Figure 1F) by a different general dentist.

The patient was first examined by the periodontist (J.H.D.) on January 18, 2020, for evaluation of implant #18, which was diagnosed with peri‐implantitis and concomitant perigraftitis. ² At that visit, implant #31 was asymptomatic, with probing depths of 3 mm and no bleeding on probing (BOP). The peri‐implant mucosa appeared pink and firm, and well‐adhered to the implant (Figure 1G,H). A periapical radiograph (Figure 1I) demonstrated mesial and distal crestal bone were located at the implant shoulder, with a narrow radiolucency between the implant collar and the mesial crestal bone. The distal coronal half of the implant was in contact with dense grafted bone, while the remaining bone surrounding the implant exhibited normal trabeculation.

Cross‐sectional imaging on April 1, 2021 (Figure 2A–C) showed a radiopacity on the distobuccal aspect adjacent to the implant collar, circumscribed by a thin radiolucency. Cross‐sectional imaging on June 17, 2024 (Figure 2D‒F) revealed persistence of the radiopacity with a marked increase in the surrounding radiolucency, extending approximately 5 mm distal to the implant.

FIGURE 2.

Cross‐sectional imaging of implant #31. (A‒C) April 1, 2021, and (D‒F) June 17, 2024. A radiopacity (arrow) is present on the distobuccal aspect of the implant, demarcated from the surrounding bone by a radiolucent border.

Clinical presentation

At the clinical examination on June 20, 2024, mild to moderate erythema and edema were observed around and distal to implant #31 (Figure 3A,B). Palpation elicited discomfort and expressed exudate from the mucosal margin of implant #31. No mobility was detected. Buccal probing depths at implant #31 measured 4 mm (mesial), 5 mm (midbuccal), and 6 mm (distal), all with BOP and suppuration. Lingual probing depths measured 3 mm (mesial), 3 mm with BOP (midlingual), and 9 mm with BOP and suppuration (distal).

FIGURE 3.

(A and B) Clinical and (C) radiographic presentation of implant #31 on June 20, 2024.

A periapical radiograph (Figure 3C) demonstrated a narrow radiolucency extending from the mesial alveolar crest to the second thread, and a broad radiolucency extending approximately 5 mm distal to the implant fixture, from the alveolar crest down to the sixth thread. Within the radiolucency, adjacent to the distal implant surface, was a radiopacity consistent with grafted bone. These findings corroborate with the radiographic changes observed on the cross‐sectional imaging (Figure 2D‒F).

The periodontist rendered a diagnosis of perigraftitis, and treatment planned for implant crown removal and laser‐assisted surgical access for debridement. The implant crown would be reseated after 6‒12 months of healing should the procedure be successful.

Case management

For all surgical procedures, written informed consent was obtained, and the patient was prescribed ibuprofen 800 mg, q8h, acetaminophen 500 mg × 2, q8h, in between the ibuprofen as needed, and triazolam 0.25 mg, sublingual 30 min before surgery for anxiolysis.

Implant #31 was surgically accessed on June 28, 2024 (Figure 4). Following local anesthesia, the implant abutment screw was accessed and removed. Implant crown removal revealed inflamed mucosa, and mucosal dehiscence with bone exposure adjacent to the distal implant platform (Figure 4B). A neodymium‐doped yttrium aluminum garnet (Nd:YAG) laser (PerioLase MVP‐7, Millennium Dental Technologies, Inc.) equipped with a 360‐µm fiber was used at 3.9 W, 100 µs pulse duration, and 20 Hz to obtain surgical access. The laser fiber was inserted from the mucosal margin to the base of the defect parallel to the implant fixture and withdrawn in a J‐shape motion circumferentially to ablate the inflamed epithelium. The implant and the defect were meticulously debrided and degranulated under illumination and magnification (Zeiss OPMI pico, Carl Zeiss Meditec) using a piezo ultrasonic instrument (Piezon 250, E.M.S. Electro Medical Systems S.A.) with the ball (LANAP Ball Tip, Millennium Dental Technologies, Inc.) and PS (Piezon PS [Perio Slim] Instrument, E.M.S. Electro Medical Systems S.A.) tips under copious distilled water irrigation, and a curette (4R/4L Columbia University Curette, SC4R/4L9E2, Hu‐Friedy). Three tissue specimens were removed and placed in formalin: specimen 1 (Figure 4C) from the distobuccal aspect, specimen 2 (Figure 4D) from the distolingual aspect, and specimen 3 (Figure 4E,F) from the base of the defect distal to the implant. After thorough debridement, the Nd:YAG laser was applied at 3.9 W, 550 µs pulse duration, and 20 Hz for hemostasis (Figure 4G). A healing abutment (RC Healing abutment, Ø 6 mm, H 4 mm, REF 024.0004S, Straumann USA) was attached to the implant fixture (Figure 4H,I). No postoperative antibiotics or antimicrobial rinses were prescribed. The patient was instructed to maintain normal home care with an extra‐soft manual toothbrush and to avoid mastication on the right side.

FIGURE 4.

Surgical access and management of implant #31 on June 28, 2024. (A) Pretreatment. (B) Removal of the implant crown revealed mucosal dehiscence with bone exposure adjacent to the distal implant platform (arrow). (C) Specimen 1, removed from the distobuccal aspect of the implant. (D) Specimen 2, removed from the distolingual aspect of the implant. (E) Radiograph indicating the location (arrow) of (F) specimen 3. (G) Clinical presentation following through debridement of the implant and defect, and (H) placement of the healing abutment. (I) Post‐treatment radiograph.

All three tissue specimens were submitted to an oral pathology service. Microscopic examination of the decalcified specimens (Figures 5, 6, 7) revealed numerous DBBM particulates surrounded by mature necrotic host bone, with bacterial aggregates on the periphery and within intertrabecular spaces of all three specimens. Formation of host bone within graft particulates was observed in specimen 1 (Figure 5) and specimen 3 (Figure 7). Specimen 2 exhibited a piece of capillary‐rich granulation tissue that contained numerous lymphocytes, macrophages, neutrophils, and plasma cells (Figure 6).

FIGURE 5.

(A) Specimen 1 in hematoxylin and eosin stain (4× objective). (B) Specimen consisted of deproteinized bovine bone mineral (DBBM) particulates (*) surrounded by mature necrotic host bone with bacterial aggregates (◊) (10× objective). (C) Higher magnification showing reversal lines (black arrows), empty lacunae (white arrows), and bone formation (#) within a DBBM particulate (*) (20× objective). (D) Bacterial aggregate (◊), surrounded by necrotic host bone, displaying a mixture of cocci and filamentous microbes (100× oil immersion objective).

FIGURE 6.

(A) Specimen 2 in hematoxylin and eosin stain (4× objective). (B) Specimen consisted of deproteinized bovine bone mineral (DBBM) particulates (*) surrounded by mature necrotic host bone, capillary‐rich granulation tissue (§), and bacterial aggregates (◊) (10× objective). (C) A DBBM particulate (*) surrounded by host bone (#) and bacteria (◊); capillaries (arrows) are visible in the granulation tissue (20× objective). (D) Bacterial aggregate (◊) containing a mixture of rods and cocci; granulation tissue exhibiting numerous lymphocytes (yellow arrow), macrophages (blue arrows), neutrophils (black arrows), and plasma cells (green arrows) (100× oil immersion objective).

FIGURE 7.

(A) Specimen 3 in hematoxylin and eosin stain (4× objective). (B) Specimen consisted of deproteinized bovine bone mineral (DBBM) particulates (*) surrounded by mature necrotic host bone with bacterial aggregates (◊) (20× objective). (C) Bacterial aggregate (◊) adjacent to host bone (#) containing cocci, and medium‐to‐long rods, with scattered degenerating inflammatory cells (arrows) (100× oil immersion objective). (D) Host bone formation (#) within a DBBM particulate (*) (100× oil immersion objective).

RESULTS

Healing was uneventful.

At 3 weeks post‐treatment on July 19, 2024, the patient reported complete resolution of pain and foul taste. Palpation no longer produced exudate. The debridement and subsequent reduction in inflammation resulted in significant tissue shrinkage (Figure 8A), leading to partial exposure of the distal surface of the implant fixture. A periapical radiograph demonstrated increased mesial and distal radiolucency (Figure 8B).

FIGURE 8.

Post‐treatment healing. (A and B) Three weeks post‐treatment on July 19, 2024. (C‒E) Fifteen weeks post‐treatment on October 11, 2024. (F‒H) Six months post‐treatment on December 20, 2024. (I‒K) Eleven months post‐treatment on May 28, 2025. (L‒N) Thirteen and a half months post‐treatment on August 14, 2025. Note: partial exposure of the implant platform (C) 15 weeks and (F) 6 months post‐treatment, and complete submergence of the implant fixture (I and J) 11 months and (L and M) 13.5 months post‐treatment, as well as gradual improvement in bone level and increase in mesial and distal bone density over time.

At 15 weeks post‐treatment on October 11, 2024, the site remained asymptomatic. Tissue had filled in the distal defect, although part of the implant platform remained exposed (Figure 8C,D). A periapical radiograph (Figure 8F) demonstrated increased radiopacity, and distal bone fill to the second thread of the implant.

At 6 months post‐treatment on December 20, 2024, soft tissue had begun to cover the previously exposed distal implant platform (Figure 8F,G). A periapical radiograph (Figure 8H) showed increased distal bone density and narrowing of the mesial radiolucency.

At 11 months post‐treatment on May 28, 2025, the peri‐implant mucosa had completely submerged the implant fixture (Figure 8I,J). A periapical radiograph (Figure 8K) showed increased distal bone density and distal bone fill to the bottom of the first thread, and mesial bone fill to the implant collar. The implant remained asymptomatic, with negative findings on palpation and percussion.

At 13.5 months post‐treatment on August 14, 2025, the implant fixture remained fully submerged (Figure 8L,M), and the crestal bone exhibited continued maturation (Figure 8N). To enhance the peri‐implant mucosal phenotype, vertical implant soft tissue augmentation (VISTA) with a subperiosteal circumferential connective tissue graft (SC CTG) was performed at implant #31 through a buccal vestibular incision (Figure 9). The patient began azithromycin 250 mg (Zithromax Z‐Pak, Pfizer) 1 day prior to surgery.

FIGURE 9.

Vertical implant soft tissue augmentation (VISTA) with a subperiosteal circumferential connective tissue graft (SC CTG) at implant #31. (A) Pretreatment on August 14, 2025. (B) Healing abutment removal showing the implant platform fully submerged. (C) SC CTG with a perforation created using a punch to allow passage of the healing abutment. (D‒F) SC CTG positioned within the subperiosteal tunnel over the implant platform and stabilized with a new healing abutment (RC Healing abutment, Ø 6 mm, H 4 mm, REF 024.0004S, Straumann USA). (G‒I) Three weeks post‐treatment on September 5, 2025.

At 15.5 months post‐treatment on October 8, 2025, 8 weeks following VISTA, removal of the healing abutment revealed improved peri‐implant mucosal thickness (Figure 10). The previously removed implant crown was recontoured to reduce the restorative emergence angle and distal cantilever, polished, and reseated with a new abutment screw.

FIGURE 10.

Implant #31 crown reseating on October 8, 2025. (A) Removal of the healing abutment revealed thickened peri‐implant mucosa. (B) Previously removed crown was (C) recontoured and polished. (D) Radiographic and (E, F) clinical presentation after crown seat.

DISCUSSION

The presence of mature host bone surrounding DBBM particulates (Figures 5, 6, 7) indicates that the 2013 ARP was successful and that the DBBM served as a scaffold for bone formation. The observation of host bone within DBBM particulates (Figures 5C and 7D) demonstrates that DBBM can undergo resorption by the host. However, the persistence of multiple DBBM particulates in all three specimens confirms its low resorption and substitution rates, consistent with previous histologic studies. ⁷ , ⁸ Consequently, the grafted bone represents “composite repaired tissue” ⁹ rather than true regenerated bone. There is no evidence that repaired bone containing residual graft particulates exhibits the same metabolism, homeostasis, and response to mechanical stress and inflammation as natural host bone.

The distinct radiopacity demarcated from the surrounding bone at the distobuccal aspect of the implant (Figure 2), which was identified as specimen 1 (Figures 4 and 5), suggests that grafted bone does not respond to stimuli—such as trauma or heat from implant osteotomy preparation, pressure from implant placement, or bacterial challenge—and resorb as natural host bone. It is also possible that grafted bone is more susceptible to necrosis than natural bone, although it remains unknown whether necrosis predisposes the site to bacterial colonization or vice versa. The radiopacity exhibited features consistent with a sequestrum, a finding typically associated with chronic osteomyelitis. ¹⁰ Although analogous, important distinctions exist between osteomyelitis and perigraftitis. Osteomyelitis represents inflammation arising from infection of native bone, ¹⁰ whereas perigraftitis denotes inflammation resulting from infection of grafted bone. Osteomyelitis of the jaw is often predisposed by local and systemic factors—such as radiotherapy, antiresorptive medications, malignancy, and immunosuppression—that compromise bone vascularity, alter host defenses, and impair healing. ¹⁰ , ¹¹ Management of chronic osteomyelitis frequently requires marginal or segmental resection combined with intensive antibiotic therapy. ¹⁰ In contrast, perigraftitis is predisposed by compromised vascularity and impaired healing of the grafted bone itself, and treatment is directed toward removal of the infected grafted bone and associated inflammatory tissue, typically without the need for systemic antibiotics. ² , ³ , ⁴

The presence of bacterial aggregates along the periphery and within intertrabecular spaces of all three specimens (Figures 5, 6, 7) confirms that oral bacteria can access and colonize the grafted bone, likely via the implant fixture and its transmucosal components. The presence of inflammatory cells adjacent to bacterial aggregates within the granulation tissue attached to specimen 2 (Figure 6), and within intertrabecular spaces of all three specimens supports the hypothesis that perigraftitis represents an inflammatory response induced by bacterial colonization of the grafted bone. The subsequent resolution of inflammation and bone fill (Figure 8) following removal of the infected grafted bone further supports the concept of perigraftitis as a distinct disease entity, separate from peri‐implant mucositis and peri‐implantitis.

A laser was employed for surgical access rather than a flap to maximize clot and wound stability—both essential for tissue regeneration—and to minimize bone loss, as elevation of either split‐thickness or full‐thickness flaps has been shown to induce crestal bone loss (Figures 8N and 10D). ¹² , ¹³ The access achieved (Figure 4) was similar to an extraction socket orifice and provided adequate visualization and access for instrumentation under a surgical microscope. This procedure should not be equated with the laser‐assisted peri‐implantitis procedure (LAPIP Protocol, Millennium Dental Technologies, Inc.), ¹⁴ as all granulation and granulomatous tissue, as well as grafted bone within the inflammatory zone, were completely removed to eliminate infection and facilitate resolution—analogous to thorough debridement of an extraction socket prior to ARP. Although it is possible the laser energy contributed to implant surface decontamination, thereby contributing to the healing process, such benefit should be viewed as inadvertent as the laser was not directed toward the implant surface for the purpose of disinfection.

The defect was intentionally left to heal naturally without the use of any bone substitute to attain true bone regeneration, and to avoid any potential of complications associated with graft materials. The contained portion of the defect was anticipated to undergo bone fill, analogous to healing of an extraction socket of a mandibular third molar impacted against the second molar, provided the root surfaces of the second molar are free of calculus. Since the buccal and lingual bone peaks were positioned apical to the implant shoulder (Figure 2E), bone fill coronal to these peaks was not anticipated, as the clot in this area lacked sufficient stability. While the expected bone fill did not reach the implant shoulder, peri‐implant tissue health can exist even with reduced bone support. ⁵ Thus, no attempt was made to augment bone to the implant shoulder.

VISTA (Figure 9) with a SC CTG was performed through a vestibular incision to enhance the peri‐implant mucosal phenotype and to establish a dense circumferential connective tissue seal (Figure 10) around the implant's transmucosal component. The subperiosteal tunnel maintained intact marginal tissue and fully submerged the graft, which optimized wound stability and vascular perfusion to the graft. ¹⁵ The SC CTG, which featured a perforation created with a punch to permit passage of the healing abutment, ¹⁶ enabled the graft to be stabilized solely by the abutment, and allowed circumferential enhancement of the peri‐implant mucosal phenotype in a single, sutureless procedure.

The patient described in this report is the same individual previously reported ² , ³ to have concomitant peri‐implantitis and perigraftitis at site #18. This patient has implants at sites #18, #30, and #31. Implant #30 is tissue level, and implant #31 is bone level. The first implant at site #18 was the same tissue‐level design placed at site #30; the second implant at site #18 was the same bone‐level design placed at site #31; the third implant at site #18 was the identical bone‐level design but 2 mm shorter. Notably, the extraction socket of tooth #30 healed naturally without ARP, whereas the extraction socket of tooth #18 was grafted with an unknown synthetic graft material, and the extraction socket of tooth #31 was grafted with DBBM. Implant #30—the first placed (Figure 11), and the only one surrounded by native bone—remains free of bone loss and biologic complications. It is unlikely that this correlation is coincidental.

FIGURE 11.

Panoramic radiograph (December 15, 2015). Implant #30 is visible, along with dense grafted bone at sites #18 and #31.

The narrow radiolucency observed between the implant collar and mesial crestal bone (Figure 1E) indicates crestal bone resorption on implant #31 occurred within the 3 months after placement (Figure 1D), despite the platform‐switched implant having been placed with its shoulder level to the mesial and distal crestal bone. A comparative clinical study ¹⁷ by Linkevicius et al. concluded that “platform switching does not prevent crestal bone loss if, at the time of implant placement, mucosal tissue is thin.” Thus, two potential risk factors for perigraftitis are insufficient mucosal thickness and inadequate implant placement depth, both of which necessitate crestal bone resorption for establishment of the supracrestal tissue attachment (STA). ¹⁷ , ¹⁸ If the grafted bone cannot resorb while the surrounding natural host bone resorbs to establish the STA, the grafted bone may protrude into the STA and become vulnerable to colonization by bacteria that inhabit the peri‐implant sulcus.

Conversely, increasing mucosal tissue thickness and/or subcrestal placement of a platform‐switched implant may provide sufficient vertical dimension for STA formation when soft tissue thickness is inadequate. ¹⁷ When implants are placed subcrestal, crestal bone profiling is essential to provide adequate space for soft tissue and optimal prosthetic emergence profile. ¹⁹ Thus, sufficient mucosal tissue thickness, proper implant placement depth and appropriate crestal bone profiling appear to be three key parameters for stabilizing crestal bone, ¹⁷ , ¹⁹ and preventing perigraftitis when implants must be placed in grafted bone.

It is possible that sites undergoing simultaneous bone augmentation and implant placement in a single‐stage protocol have a lower risk of perigraftitis than sites where implants are placed in mature grafted bone. With simultaneous bone augmentation and implant placement in a single‐stage protocol, the STA forms before the grafted bone matures, thereby preventing mature grafted bone from protruding into the STA and becoming vulnerable to bacterial colonization. However, non‐resorbing graft particulates embedded in the peri‐implant mucosa may still become exposed and colonized by oral bacteria. ¹ Therefore, decisions regarding whether, when, how, and with what material to graft should be made with careful consideration to minimize the risk of perigraftitis.

CONCLUSIONS

The clinical, radiographic, and histologic findings, together with the treatment outcome of this case support the following hypotheses:

• Oral bacteria can access and colonize submucosal grafted bone, with the implant and its transmucosal components likely providing the pathway.

• Bacterial infection of the grafted bone can induce in an inflammatory response in the surrounding soft and hard tissues.

• This inflammatory response may be successfully resolved through the removal of the infected grafted bone and associated surrounding inflammatory tissue without the need for implant removal.

Within the limitations of this case report, perigraftitis may therefore be considered an independent disease entity, distinct from peri‐implant mucositis and peri‐implantitis. Further controlled studies are warranted to elucidate the etiopathogenesis, risk factors, and prevalence of perigraftitis, and to optimize its prevention and treatment.

AUTHOR CONTRIBUTIONS

Conceptualization, investigation, visualization, writing—original draft preparation, and writing—review and editing: Jonathan H. Do. Conceptualization, visualization, and writing—review and editing: Charles M. Cobb. Conceptualization and writing—review and editing: John T. Shen.

CONFLICT OF INTEREST STATEMENT

The authors declare they have no conflicts of interest.