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Official journal of the SocietĂ Italiana Specializzati in Chirurgia Odontostomatologica ed Orale Vol. 4 issue 2 September 2013 ISSN 2037-7525

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European journal of oral surgery Official journal of the SocietĂ Italiana Specializzati in Chirurgia Odontostomatologica ed Orale

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• References: References should be limited to those specifically referred to in the text, cited numerically, in order of appearance in the text and listed according to the following style (Vancouver style): Journals: 1. Del Fabbro M, Testori T, Francetti L, Taschieri S, Weinstein R. Systematic review of survival rates for immediately loaded dental implants. Int J Periodontics Restorative Dent 2006;26:249–264.

Books: 1. Tarnow DP, Cho S-C, Wallace SS, Froum SJ. Effect of surface morphology on implant survival in the grafted maxillary sinus. In: Jensen OT (ed). Bone Graft, ed 2. Chicago: Quintessence; 2006. p.223– 227.

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Vol. 4 issue 2 SEPTEMBER 2013

page 29

The development of the alveolar bone by static osteogenesis: microanatomy and clinical implications

page 38

Peri-implant Peripheral Giant Cell Granuloma (PGCG) with a 6-year follow-up: a case report with implant preservation

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European journal of oral surgery Official journal of the Società Italiana Specializzati in Chirurgia Odontostomatologica ed Orale

Editorial

Dr. Federico Mandelli Editorial manager

Dear colleagues, The Fall has come and the 4-5th October Congress has came along with it. Together with Camlog, SISCOO’s efforts were aimed at building up a scientific program focused not only on dental implants, but also on other aspects of our discipline. Our wish is to underline, especially to students, that implantology is just a technique subservient to a correct treatment planning.

Let me remind you that last June, the SISCOO’s course with Silvio Taschieri was a success: in these years literature has been reporting new worrying data on peri-implantitis and I am not the only one who is quite confident that many articles will be published in the near future on this topic. Well aware of this, Taschieri gave the audience an exhaustive overview on what endodontic surgery state of the art is: state of the art is: save a tooth and postpone the placement of an implant can often be a good treatment option. The real problem is that our literature is packed with articles based upon a poor methodology and a super-short follow-up, that report astounding success rates up to 100%.

In this issue we went “back to basics”. We asked Tonino Traini to write about bone biology; he already published many papers on this topic and he pleased us with new insights about bone formation. This is an interesting subject for every clinician who approaches bone surgery, since the better he knows the development patterns and healing processes, the better he makes clinical decisions.

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Monograph

The development of the alveolar bone by static osteogenesis: microanatomy and clinical implications Tonino Traini Scientific Consultant, Department of Dentistry, Vita Salute University, San Raffaele Hospital, Milan, Italy Assistant Professor, Department of Medical, Oral and Biotechnological Sciences, University of Chieti-Pescara, Chieti, Italy

Aim

Materials and methods

Regeneration of alveolar bone is essential for immediate implant placement after tooth extraction, while the bone formation is still uncertain. To clarify the mechanism of alveolar bone healing we evaluated and compared the bone formation of the jaws during both ontogenesis and bone healing after dental extraction. In addition, peri-implant bone remodelling was also evaluated.

Three hamster fetuses of 24-days post-conception, ten bone cores retrieved during implant placement after three (5 samples) and four (5 samples) weeks of healing and two fractured implants retrieved after five years of loading were used in the present study. The investigation was carried out by means of a bright field microscope and a scanning electron microscope (SEM).

Results

In Hamster fetuses alveolar bone formation was related to static osteogenesis (SO), whereas the basal bone facing the Meckel’s cartilage was formed by dynamic osteogenesis (DO). In human alveolar sockets, after 3 weeks, the healing appeared to follow the SO mechanism, while after 4 weeks the bone increases by a DO mechanism. Around peri-implant bone the remodelling process was characterized by a DO mechanism.

Conclusion

These results demonstrate that static bone formation (SBF) is a process not only related to skeletal development but it also occurs during the early phase of bone healing as a rapid mechanism with a great ability of spacefilling. Later on, the primary bone trabeculae are adapted by dynamic bone formation (DBF). Around dental implant, the remodelling process was governed by a DBF mechanism.

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Key words: Alveolar bone regeneration; Dental follicle; Dynamic osteogenesis; Intramembranous ossification; Meckel’s cartilage; Static osteogenesis.

Traini T.

Introduction In order to improve our knowledge on the mechanisms involved in alveolar bone sockets healing after tooth extraction, it is imperative to understand the alveolar bone tissue development during odontogenesis. Moreover, this aspect is of fundamental importance to shed light on biologic reactions occurring around dental implants placed immediately after teeth extractions.

Teeth ontogenesis is a complex process derived from the oral epithelium in the embryonic oral cavity. Primitive mesenchymal tissue condenses in the future central region of the tooth, in what will become the pulp cavity. Inside this region odontoblasts begin the process of making dentin, by laying down a matrix material and then calcifying it. As they do so, they move backwards towards the centre of the pulp cavity, remaining active throughout life. On the outside surface of the tooth a similar process takes place.

A population of ameloblasts differentiates,as a row of nicely columnar cells facing the odontoblasts. They lay down an uncalcified matrix first, and then harden it, backing away as the enamel layer is built up.

Odontoblasts and ameloblasts have some similarities; both cell types are tall and columnar in shape. In the course of tooth formation, differential deposition of dentin and enamel creates the proper shape of the tooth by several inductive and exquisitely coordinated processes.

Independent genetic pathways are responsible for developing of different teeth. Dlx-5 and Dlx-6 are two gene clusters (homeobox) linked to molar development, while Msx-1 and Msx-2 are responsible for incisor development (13). The tooth shape is locally programmed by mesenchymal genes and by timing expression of BMPs molecules.

Root formation is similarly controlled by intercellular signalling that switches on and off as needed; and by selective timed losses of cell populations and subpopulations. Once the tooth erupts, the cells of the stellate reticulum as well as ameloblasts cells die.

Unlike bones of the trunk, which develop because of a pre-existing cartilage model (endochondral ossification), alveolar bone develops directly from mesenchymal cells (4) (intramembranous, or desmal ossification).

In the jaw bone, Meckel’s cartilage gradually regresses while the bone ossifies by both membranous ossification and endochondral ossification (symphyseal region) (5,6).

Two mechanisms of bone formation were recently reported for intramembranous ossification (7-9) as dynamic osteogenesis (DO), which involves osteoblast movement, to distinguish from static osteogenesis (SO) a disregarded type of bone deposition occurring at the onset of ossification. SO is performed by immobile stationary osteoblasts that transform into osteocytes at the same site where they differentiate. The stationary osteoblasts are arranged irregularly in cords of 2-3 layers of cells, polarized in different directions with different osteogenic surfaces.

In contrast, movable osteoblasts form monostratified laminae which are polarized in the same direction with the same osteogenic surface. The differences between the two types of osteoblasts regard their arrangement and polarization. This means that in SO osteoblasts become osteocytes by a mechanism of “self-burial”, whereas in DO the osteoblasts selected to transform into osteocytes are embedded within the bone by the secretory activity of the

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adjacent movable osteoblasts (7).

The objectives of the present study were to histologically investigate bone formation mechanism during ontogenesis of the jaws, during bone healing of alveolar sockets as well as during peri-implant bone remodelling, in order to asses if different bone formation modality were present.

Materials and methods The study was performed in accordance with both the provisions of the Declaration of Helsinki 1995 (as revised in Edinburgh 2000) and the principles of laboratory animal care (NIH publication 85-23, 1985), included the national laws on animal use.

Hamster fetuses of 24-days post-conception (3 samples) were used to evaluate intramembranous ossification around dental follicles (10). Ten human bone cores were retrieved from post-extraction alveolar sockets after three (5 samples) and four (5 samples) weeks of healing. The specimens were collected during implant placement by means of a trephine of 3 mm in diameter to be used to evaluate the bone-healing formation inside post-extraction sites. Fractured implants (2 samples) retrieved after five years of loading were used to investigate the mechanism of peri-implant bone remodelling.

Light microscopic analysis All specimens were fixed in a10% buffered formalin, washed in sodium phosphate at pH 7.2, dehydrated in graded alcohols and embedded in resin (LR White, London Resin, Berkshire, UK). Undecalcified cut sections of 50 μm were prepared by using the TT System (TMA2, Grottammare, Italy) and ground down to about 30 μm using the EXAKT grinding system (EXAKT Vertriebs, Norderstedt, Germany). The sections were double stained with acid fuchsine and Azure II. The investigation was carried out by means of a bright field light microscope (Axiolab, Carl Zeiss, Jena, Germany). The optical system was connected to a high-resolution CCD-IRIS digital camera (Sony DXC107-A, Tokyo, Japan) and the images were captured using an image processing software (Image-Pro Plus 6.0, Media Cybernetics Inc., Bethesda, MD, USA).

Scanning electron microscope analysis The specimens were fixed in a 10% buffered formalin, washed in sodium phosphate at pH 7.2, dehydrated in graded alcohol solutions and embedded in resin (Technovit 7200 VLC, Kulzer, Wehrheim, Germany). The specimens were cut into two halves using the TT System and accurately polished with 0.5 lm alumina to an optical finish, lightly etched with 0.1 N of HCl solution for 10 seconds, treated with trypsin (80 U/ml) at pH of 7.2 for 1 minute at 37°C and finally sputter-coated with gold (Emitech K 550, Emitech Ltd, Ashford, Kent, UK).

The samples were placed on the storage of a SEM with LaB6 (Zeiss EVO 50 XVP, Carl Zeiss SMY Ltd, Cambridge, UK), equipped with tetra solid-state BSE detector. SEM operating conditions included 30 kV accelerating voltage, 10 mm working distance and a 870 pA probe current. The images were captured with 20 scans using a line average technique.

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Monograph

Results

the basal bone facing the Meckel’s cartilage was formed by dynamic osteogenesis (DO) (Fig. 9, 10).

In human alveolar sockets, after 3 weeks, healing appeared to follow the SO mechanism (Fig. 11, 12), while after 4 weeks the bone increases by a DO mechanism (Fig. 13, 14, 15).

In the Hamster fetuses (Fig. 1) alveolar bone formation was related to static osteogenesis (SO) (Fig. 2-8), while

fig. 1 Image at 12 x of Hamster fetus of 24-days post-conception.

Longitudinal medial section of the head.

Acid fuchsine and azure II stain.

fig. 2 Image at 100 x of first molar of Hamster fetus. Alveolar bone formation at late bell stage.

D: dentin E: enamel PD: dental papilla RS: stellate reticulum EAI: inner enamel epithelium EAE: outer enamel epithelium CM: Meckel cartilage AB: alveolar bone.

Undecalcified section, acid fuchsine and azure II stain.

fig. 3 Image at 100 x of Hamster fetus.

Alveolar bone formation early bell stage of a maxillary incisor.

DP dental papilla DS dental sac AB alveolar bone SR stellate reticulum CM Meckel cartilage D dentin IEE inner enamel epithelium OEE outer enamel epithelium EO enamel organ Undecalcified section, PAS stain.

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Traini T. fig. 4 Image at 100 x of Hamster fetus. Alveolar bone formation early bell stage of a maxillary incisor.

PD: dental papilla SD: dental sac AB: alveolar bone AC: cervical loop Q Meckel cartilage Undecalcified section, acid fuchsine and azure II stain.

fig. 5 200 x magnification of figure 4. The alveolar bone (AB) appears to be formed by cords of stationary osteoblasts (SBF mechanism). Small blood vessels (*) can be noted at about 30 Âľ from osteoblasts.

DP: dental papilla D: dentin Od: odontoblasts Ab: ameloblasts Undecalcified section, acid fuchsine and azure II stain.

fig. 6 400 x magnification of figure 4.

There is a close relationship between the alveolar bone (AB) and the dental sac (DS).

D: dentin E: enamel DP: dental papilla Od: odontoblasts Ab: ameloblasts Undecalcified section, acid fuchsine and azure II stain.

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Monograph fig. 7 400 x magnification of figure 4.

There is a close relationship between the alveolar bone (AB) and the dental sac (DS).

D: dentin E: enamel DP: dental papilla Od: odontoblasts Ab: ameloblasts.

Undecalcified section, acid fuchsine and azure II stain.

fig. 8 Image at 1000 x of alveolar bone formation with SBF mechanism in Hamster fetus. The cords of stationary osteoblasts, visible inside the circle (a), show the direction of bone growth, that is from right to left. Black arrows show mineralized bone around a self-buried osteocyte (*).

B: mineralized bone Bc: blood vessel.

Undecalcified section, acid fuchsine and azure II stain.

fig. 9 Image at 400 x of alveolar bone growth with DBF mechanism in Hamster fetus. The bone trabeculae laid down by static osteogenesis and basal bone appear to be carpeted by movable osteoblastic laminae (with arrows).

Undecalcified section, acid fuchsine and azure II stain.

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Traini T.

fig. 10 Image at 1000 x of alveolar bone growth with DBF mechanism in Hamster fetus. The surface of mineralized bone trabeculae (B) is carpeted by movable osteoblastic laminae (black arrows). Osteoblasts (mOb) appear polarized on the same direction of the bone growth from left to right. Undecalcified section, acid fuchsine and azure II stain.

fig. 11 Image at 200 x of alveolar bone socket regeneration in human, after three weeks of healing. An overlapping of proliferative and maturation phases of wound healing can be noted. Inside this nidus of granulation tissue several mineralized bone nodules (*) can be seen. The bone nodules appeared associated to cords of osteoblasts (white arrows) resembling those of SBF reported during embryonic bone development (Fig. 7). Undecalcified section, acid fuchsine and azure II stain.

fig. 12 Image at 200 x of alveolar bone socket regeneration in human, after three weeks of healing. The mineralized bone nodule (*) appears organized to form bone trabeculae laid down by static osteogenesis. Plump osteocytes are embedded inside mineralized bone matrix. Undecalcified section, acid fuchsine and azure II stain.

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Monograph fig. 13 Image at 200 x of alveolar bone socket regeneration in humans, after four weeks of healing. While bone trabeculae (B) appeared to be in an advanced phase of mineralization, the thickening process of the trabeculae is associated to movable osteoblastic laminae (white arrows). After four weeks in some wound healing areas the initial SBF mechanism appears to be substituted by DBF mechanism.

Undecalcified section, acid fuchsine and azure II stain.

fig. 14 SEM image at 874 x of alveolar bone socket regeneration in humans, after four weeks of healing. Newly formed trabecular bone (B) appeared to be well mineralized and embedded by several plump osteocytes (circles).

The surfaces of the bone trabeculae are covered in some area by an osteoid rim associated to movable osteoblastic laminae (white arrows).

fig. 15 Image at 400 x of alveolar bone socket regeneration in humans, after four weeks of healing. The underlined area (A) shows an SBF mechanism with a high number of embedded plump osteocytes.

On the surface of the bone trabeculae, an area of lamellar bone (*) with few spindle-shaped osteocytes is noted.

Black arrows indicate rim of osteoblasts as reported for a DBF mechanism.

Undecalcified section, polychromic silver stain.

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Traini T. fig. 16 Image at 200 x of human periimplant bone near an osseointegrated implant after five years of loading.

Lamellar bone (B) with several spindleshaped osteocytes embedded inside mineralized bone matrix (circles) can be noted. The osteoid rim (*) appears to be carpeted by typical movable osteoblastic laminae (black arrows).

A DBF mechanism is responsible for bone modelling/remodelling. (I) Implant.

Undecalcified section, azure II stain.

fig. 17 Image at 200 x of human periimplant bone near an osseointegrated implant after five years of loading.

The peri-implant bone (B) shows a remodelling secondary osteon (black arrows). Several spindle-shaped osteocytes embedded inside mineralized bone matrix (circles) can be noted. (Hc) Havers canal; (I) implant. Undecalcified section, acid fuchsine and azure II stain.

Around peri-implant bone the remodelling process was characterized by a DO mechanism in either osteonic and trabecular bone (Fig. 16,17).

The results show a close relation between embryonic alveolar bone formation mechanism and alveolar bone wound healing mechanism in adult humans. Around dental implants after several years from osseointegration, the remodelling process follows the DO mechanism.

Discussion The present results provide, for the first time, evidence that the SBF occurs also during the early phase of alveolar wound healing, and that later on SBF follows the DBF mechanism. Due to the impact of bone exposure, the healing process includes a number of responses.

Different areas of the socket wall may experience different responses, depending on the trauma of the extraction, the bone health of the patient, and to what degree the blood clot is retained. The apex of the extraction site quickly

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undergoes regeneration by reincorporating and covering the necrotic bone with new bone. More coronal on the alveolar wall, bone may be undermined and sloughed into the extraction socket. In some instances, the socket wall may be completely resorbed. Independent of what is happening to the alveolar wall, if normal healing occurs, the fibrin clot will convert into granulation tissue and organize into a collagen plug during the first month. This collagen plug will increase in density forming a nidus for new bone growth, to be gradually replaced from the apex and periphery by bone deposition.

In human post-extraction alveolar sockets after three weeks of healing several areas of SO were visible, while after four weeks DO was in action to increase the bone thickness of the trabeculae. Around dental implants after five years of function only area with DBF mechanism were present. The bone remodelling process appeared to be governed by DBF mechanism, while the modelling process in wide bone defects seemed to be governed by a double mechanism. In the early phase, SBF creates a trabecular bone framework of woven bone in a fast way, later on the DBF mechanism increase the size of the trabeculae with lamellar bone. The mechanism appeared to resemble the intramembranous ossification showed for alveolar bone

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Monograph formation around bell stage. It is necessary to make further research to establish if the SBF is a mechanism to fill large bone defects or if it is related to cell lineage.

Conclusion

What can we learn from embryonic development?

Knowledge of how a tooth normally forms may aid to understand the healing process around dental implants immediately placed in alveolar sockets, where it is essential to apply an adequate clinical protocol. The dental follicle appears as a transient structure able to originate cementum, bone and periodontal ligament (4). Cells from the condensing mesenchyme around the epithelial tooth bud end up forming also alveolar bone at the bell stage.

The main mechanisms occurring during intramembranous ossification are SBF and DBF. SBF is characterized by pluristratified cords of stationary osteoblasts, at a mean distance of 28 ± 0.4 μm from blood capillary, polarized in different directions. All the osteoblasts become osteocytes. DBF is formed by a movable osteoblastic lamina with all osteoblasts polarized in the same direction.

Only selected osteoblasts become osteocytes (8, 9). The former process is performed by stationary osteoblasts and allows the formation of a trabecular bone framework, which is subsequently expanded by typical movable osteoblasts.

In both embryonic formation and alveolar wound healing bone modelling seems to follow the same mechanism. This observation led us to better understand clinical situations in which dental implants placed in fresh extraction sockets with a critical discrepancy of 3 mm and an adequate primary stability can be successfully osseointegrated.

Nevertheless, it will be necessary to investigate in depth if the SBF is exclusively related to the presence of the alveolar bone wall (which derives from mesenchymal cells of the dental sac) or if it is a mechanism retained in atrophic bone crestal ridges (basal bone).

The results demonstrate that SBF is a process not only related to skeletal development but it occurs also during the early phase of bone healing as a rapid mechanism with a great ability of space-filling. Later on, primary bone trabeculae are adapted by DBF. Around dental implants, the remodelling process is governed by a DBF mechanism for both osteonic and trabecular bone.

References 1. Thomas BL, Tucker AS, Qui M, Ferguson CA, Hardcastle Z, Rubenstein JL, Sharpe P. Role of Dlx-1 and Dlx-2 genes in patterning of the murine dentition. Development 1997; 124:4811-4818.

2. Bei M, Maas R. FGFs and BMP4 induce both Msx1-independent and Msx1-dependent signaling pathways in early tooth development. Development 1998;125: 4325-4333.

3. Hardcastle Z, Mo R, Hui C-C, Sharpe P. The Shh signalling pathway in tooth development: defects in Gli2 and Gli3 mutants. Development 1998; 125: 2803-2811.

4. Diep L, Matalova E, Mitsiadis TA, Tucker AS. Contribution of the tooth bud mesenchyme to alveolar bone. J Exp Zool B Mol Dev Evol 2009; 312B(5):510-7.

5. Radlanski RJ, Renz H, Klarkowski MC. Prenatal development of the human mandible. 3D reconstructions, morphometry and bone remodelling pattern, sizes 12-117 mm CRL. Anat Embryol 2003; 207(3): 221-32.

6. Radlanski RJ, Renz H. Genes, forces, and forms: mechanical aspects of prenatal craniofacial development. Dev Dyn. 2006; 235(5): 1219-29.

7. Marotti G, Ferretti M, Muglia MA. Palumbo C, Palazzini S. A quantitative evaluation of osteoblastosteocyte relationships on growing endosteal surface of rabbit tibiae. Bone 1992; 13: 363-368.

8. Marotti G. Static and dynamic osteogenesis. Ital J Anat Embryol 2010;115(1-2):123-6.

9. Ferretti M, Palumbo C, Contri M, Marotti G. Static and dynamic osteogenesis: two different types of bone formation. Anat Embryol 2002; 206: 21-29.

10. Hamster. Encyclopædia Britannica. Standard Edition. Chicago: Encyclopædia Britannica, 2007.

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Case report

Peri-implant Peripheral Giant Cell Granuloma (PGCG) with a 6-year follow-up: a case report with implant preservation Giuseppe Basile Paolo Ronchi Department of Maxillofacial Surgery, S. Anna Hospital, Como (Italy)

Background

Case report

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Peripheral giant cell granuloma (PGCG) is the most common oral giant cell lesion which occurs on the gingiva or alveolar mucosa and probably does not represent a true neoplasm but rather it could be based on a reactive inflammatory process. To date have been reported in literature only 12 cases of PGCG associated with dental implants.

This work describes an additional case with clinical and histological analysis, surgical treatment and six year follow up.

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Key words: Dental implant, Exophytic growth, Implant preservation, Peri-implant reactive lesion, Peripheral giant cell granuloma.

Case report

Introduction The Peripheral Giant Cell Granuloma (PGCG) is a reactive exophytic lesion of gingiva and alveolar ridge which originates from the periosteum or periodontal ligament (1). It is a polypoid or nodular lesion, primarily of bluish red color with a smooth shiny or ulcerated surface, a stalky or sessile base, small and well demarcated.

PGCG are variable in size, although they rarely exceed 2 cm in diameter.

The lesion can develop at any age, though it is more common between the fifth and sixth decades of life, and shows a slight female predilection (2, 3). This lesion is probably not a true neoplasm, but rather of a reactive nature. The starting stimulus has been believed to be due to local irritation or trauma, but the cause is not clearly known.

The treatment of this type of lesion includes surgical resection and elimination of the underlying etiologic factors with complete removal of the entire base of the lesion. If the resection of the lesion is too superficial or incomplete then the lesion may recur (4).

The PGCG is a soft tissue lesion that infrequently affects the underlying bone, although sometimes the latter may undergo superficial erosion, detectable by radiographic exams.

Malignant transformations have never been described (5).

Histological features of PGCG reveal a non-capsulated mass of tissue containing a large number of young connective tissue cells and multinucleated giant cells in a background of mononuclear stromal cells. Often extravasated red blood cells (which lead to hemosiderin

deposits) are detectable, inflammatory cells, and newly formed bone or calcified material may also be seen throughout the cellular connective tissue (6).

The PGCG bears a close microscopic resemblance to the central giant cell granuloma (CGCG), and some pathologists believe that it may represent a soft tissue counterpart of the central bony lesion which was first described by Jaffe in 1953 (7). The true nature of CGCG is still unknown: it could be a reactive lesion, a developmental anomaly or a benign neoplasm. Chuong et al in 1986 and Ficarra et al in 1987 suggested categorizing CGCG into aggressive and non-aggressive types based on their clinical and radiographic characteristics, since there are no histologic parameters able to predict their clinical behavior (8, 9).

The last WHO Classification of Head and Neck Tumours (2005) includes CGCG in bone related lesions defining it as fibrotic tissue with hemosiderin deposits, osteoclast-like giant cells and reactive bone formation.

PGCG associated with dental implants is rare; to the best of the authors’ knowledge only 12 cases have been reported in the literature to date and none has a follow up longer than 4 years (10). In one case the dental implant was removed contextually to the lesion’s excision (4), while in other 4 reported cases the explantation was performed after the excision of PGCG because of frequent recurrences (5, 6).

PGCG is more common in the lower jaw than in the upper jaw and generally develops in the gingival tissue or alveolar processes of the incisor and canine region (11). According to other authors the preferential zone is the

fig. 1 Exophytic mass near the free margin of removable partial prosthesis.

premolar and molar zone (12).

The present study assesses the etiologic potential of PGCG on implant failure and peri-implant bone loss, although it is not always necessary to remove the implant as we demonstrate.

Case report

A 65 year-old non smoking woman presented in February 2007 to our attention with an exophytic lesion located at the mucosa around a dental implant in the left lower first premolar region. The patient had began to feel the presence of the mass two months previously and it grew rapidly causing bleeding during toothbrushing and difficulty while eating.

The patient’s past medical history was unremarkable and she was taking no medications. No drugs allergies were reported.

The patient underwent the positioning of two dental implants in an edentulous area of left and right inferior mandible four years previously, with a removable prosthetic rehabilitation. At that time, according to what the patient reported, the peri-implant tissues showed no symptoms of inflammation.

Intraoral examination revealed a rounded nodular lesion of 1 cm in diameter, located near the free margin of the removable partial prosthesis close to 3.4 region (Fig. 1, 2). The exophytic mass appeared with a pedunculated base, nonulcerated, smooth surface, blue-colored and with a soft elastic consistency.

X-rays showed severe bone loss in the form of an irregular and concave depression involving the adjacent tooth root and inducing the exposure of the implant neck, which was not mobile (Fig. 3).

fig. 2 Clinical appearance of the lesion close to the implant without dental involvement.

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fig. 3 X-ray image shows a partial bony resorption and an erosion of dental root.

fig. 5 Histological aspect of the excised mass.

fig. 7 Bioptic specimen.

Because of the bone resorption an incisional biopsy of the nodular lesion was performed (Fig. 4) and the obtained specimen, fixed in a 10% formalin solution, underwenthistologic evaluation.

Each block of paraffin-embedded tissues was cut in sections of 5 Âľ, which were stained with hematoxylin and eosin. The lesion contained numerous giant cells in a well-vascularized

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fig. 4 Lesion’s aspect after incisional biopsy.

fig. 6 Clinical aspect during surgery

fig. 8 Postoperative appearance with absorbable suture.

connective tissue stroma of ovoid and spindle-shaped mesenchymal cells (Fig. 5). The lesion was identified as a peripheral giant cell granuloma.

After infiltration anesthesia with 2% mepivacaine, a complete excision of the nodular mass, which inclued the tooth with wide margins of resection, was performed. The resection of the underlying alveolar bone was also achieved. Moreover, because of

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prosthodontic indications, the two near teeth were also extracted. The neck of the implant was smoothed, carefully cleaned and polished with diamond burs and rubbers in order to preserve it (Fig. 6, 7).

After an accurate hemostasis the site was sutured with absorbable suture 4.0 (Fig. 8).

The patient was instructed to avoid both brushing tissues and wearing the

Case report

fig. 9 Clinical aspect at the follow-up of one year.

fig. 10 Clinical aspect at the follow-up of six years.

fig. 11 Radiographic aspect at the follow-up of six years.

prosthesis, and to rinse her mouth with 0.2% chlorhexidine. We set antibiotic therapy with amoxicillin and clavulanic acid (1 gr twice in a day for six days).

The new specimens were sent to a new histological examination that confirmed the previous diagnosis of PGCG. Ten days after surgery we proceeded to prosthetic rehabilitation. There were no postoperative complications.

The clinical and radigraphic followup revealed no lesion recurrence at 6 years (Fig. 9 -10 -11).

Discussion Peripheral giant cell granuloma (PGCG) is a common pseudotumoral reactive lesion rarely associated with dental implants. Only 12 cases have been reported in the international literature and, to the best of the authors’ knowledge, this is the first with a so long follow-up to date.

The incidence of this lesion is higher between the fifth and sixth decades of life and the females are more often affected.

The etiology and incidence of PGCG associated with dental implants has not yet been determined because of the scarce number of reported cases (13). The diagnosis relies only on histopathology and, as such, is dependent on the clinician’s ability of submitting for examination all surgically excised peri-implant tissues.

Therefore, the data from the literature could not reflect the accurate incidence of PGCG in peri-implant tissue.

Different local causal factors have been associated to PGCG, including inadequate chewing forces, entrapment of food debris, ill-fitting dental appliances or other iatrogenic factors.

The gingival mucosa is an area of the oral cavity that is exposed to constant irritation; gingival tissues can react to these irritant factors by developing a lesion commonly known as epulis.

This term has been used to describe a number of lesions with a wide range of histological patterns. The main reactive lesions of the gingival include: piogenous granuloma, peripheral gingival fibroma, peripheral ossifying fibroma and peripheral giant cell granuloma. Moreover, since PGCG induces sometimes a superficial

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resorption of the underlying alveolar bone crest, it may be difficult to determine whether the mass is a peripheral lesion or a central giant cell granuloma eroding through the cortical plate into the gingival soft tissue (14).

In any case, the histological study of the resected tissues establishes the definitive diagnosis.

Histologically a PGCG consists of a non-encapsulated mass of reticular and fibrillar connective tissue containing ovoid or fusiform connective cells and multinucleated giant cells.

These last are assumed to arise from the syncytial fusion of mononuclear preosteoclasts originating in the bone marrow. The lesion typically contains vessels especially in the more peripheral zones with hemorrhagic foci and hemosiderin pigment deposits.

The radiological features are very important to determine whether the lesion is of gingival origin or arises centrally spreading towards the surface.

In our case, because of the X-ray images, which showed a partial bone resorption and dental root erosion, we preferred to perform an incisional (not excisional) biopsy just to initially exclude a malignant origin of the lesion (15).

Only after histological diagnosis of PGCG we proceeded to the “en bloc” removal of the reactive mass and the involved tooth with wide margins of resection, followed by smoothing and polishing of the neck of the dental implant and by extracting the two residual teeth because of the prosthetic indication.

Our surgical approach with preservation of the dental implant has proven to be indicated since the 6 years follow-up does not show, to date, any kind of complication or recurrence of the lesion. Our choice of a vol. 4 n. 2 2013

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conservative treatment was supported by the firmness of the dental implant and by the limited involvement of the peri-implant bone. Moreover the literature, even though with a shorter follow up, reports of only 5 implants removed while the other 7 ones were preserved after a careful curettage of the exposed implant near the lesion that was completely excised with wide margins. Of course early detection and treatment are important for implant survival.

Conclusion Our surgical approach with preservation of the dental implant has proven to be indicated since the follow-up to 6 years does not show, to date, any kind of complication or recurrence of the lesion. Our choose of a conservative treatment was supported by the firmness of dental implant and by the limited involvement of the peri-implant bone. Moreover the literature, even with a shorter follow up than our, reports that only 5 implants were removed while the other 7 ones were preserved after a carefull

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curettage of the exposed implant near the lesion that was completely excised with wide margins. Of course early detection and treatment are important for implant survival.

Obviously it would be useful to have more case studies similar to this one in order to confirm our therapeutic indication.

7.

8.

9.

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