Introduction
Dental osseointegrated implants are made of titanium, which is a tissue-friendly and osseointegratable material; the implants have been widely used in preprosthetic surgery. Dental plaque, inadequate oral hygiene, traumatic occlusion, and anatomic drawbacks can cause complications associated with dental implants resulting in peri-implantitis and implant failure.1 However, gingival reactive lesions like Pyogenic granuloma (PG) or peripheral giant cell granuloma (PGCG) are thought of as common lesions in the natural dentition while such lesions in association with dental implants are uncommon.
Pyogenic granuloma is a common, inflammatory hyperplasia of the oral cavity. Although the term “pyogenic” is used, PG is not an infectious lesion.2 PG usually occurs as a response to different stimulating factors such as local trauma or irritation, iatrogenic and hormonal factors.1–2 Because of the female hormone factor it has very high incidence in young females, principally in the second decade of life. Clinically, PG presents as a painless, smooth, or lobulated shape. It is classed as a hemorrhagic lesion because of its vascular structure and its color ranges from pink to dark red. In addition, it bleeds very easily when touched. Sometimes its surface may be covered by a pseudo-membrane due to secondary ulcerations.3
There are only two case reports in the literature that describe PG associated with dental implants. The aim of this paper is to present the case of a patient with PG in association with dental implant, which had been inserted after bone splitting.
Case Report
A 55-year-old female patient was referred to our clinic for preprosthetic management of a partially edentulous mandible. After clinical and radiologic examination we decided to insert endosteal implants to the right first molar, premolars and canine regions of the mandible. Under local anesthesia (Maxicaine, Vem Drugs, Istanbul, Turkey) crestal horizontal and vertical releasing incisions were made and a full thickness mucoperiostal flap was elevated. Alveolar bone splitting was performed with piezosurgery along the right mandible due to inadequate bucco-lingual width. Implant sockets were prepared by implant drills and 4 dental implants (3i Dental Implant System, BIOMET, Inc. Warsaw, IN, USA) were inserted manually to the regions of the second incisor (26) (3.25 mm × 13 mm), canine (27) (3.25 mm ×11.5 mm), first (28) (3.25 mm × 10 mm), and second (29) (3.25 mm × 8.5 mm) bicuspids in the right mandible and the osteotomy line was filled with a 1 cc xenograft. (BioOss, Geistlich Pharma AG, Wolhusen, Switzerland).The implants were then sealed with cover screws. Autologous blood was taken (30 cc) and then centrifuged at 10 min/3000 rpm to obtain platelet rich fibrin (PRF). PRF membranes were put over the implants and the mucoperiostal flap was closed primarily with 3/0 silk suture. After surgery, antibiotics, analgesics, and mouthwash with clorhexidine were prescribed. The healing period was uneventful, but 1 month after surgery the patient came back to the clinic suffering from pain and “gingival hyperplasia” in the her right posterior region of the mandible (Figure 1). The intraoral clinical examination showed a hyperplastic lesion 0.7 cm × 1 cm × 1 cm in size, which was a reddish color and bled on touch. We noticed that the lesion was related to the most posterior implant but had no radiographic appearance (Figure 2). Under local anesthesia the lesion was totally excised and a mucoperiostal full thickness flap was elevated to perform a debridement and it was found that the most posterior implant had not osseointegrate. The failed implant was removed. The empty socket and other implant areas were curetted. PRF membranes were put over the implants and the socket and flap was closed with 3/0 silk suture. The patient was prescribed antibiotics, analgesics and mouthwash with clorhexidine. After 1 week, a healthy, pink colored mucosa was observed. The histopathologic analysis revealed an intense vascular proliferation with extensive areas of ulceration, mixed inflammatory infiltrate and abundant macrophages. The histopathologic diagnosis was pyogenic granuloma (Figure 3). Three months after the second surgery the patient was referred for prosthetic management (Figure 4).
Figure 1. Clinical view of PG 1 month after surgery. Figure 2. Peri-apical radiograph of affected site. Figure 3. In the upper left side of the section the surface epithelium shows regenerative changes. Other sides of the epithelium are ulcerative. Leak connective tissue with edema, proliferative capillary vessels, aggregation of active-chronic inflammatory cells can be seen at bottom line of ulceration and in the subepithelial side. (hematoxylin and eosin; original magnification 100×). Figure 4. 3 months after the second surgery, at the time of prosthetic management.
Figure 1. Clinical view of PG 1 month after surgery. Figure 2. Peri-apical radiograph of affected site. Figure 3. In the upper left side of the section the surface epithelium shows regenerative changes. Other sides of the epithelium are ulcerative. Leak connective tissue with edema, proliferative capillary vessels, aggregation of active-chronic inflammatory cells can be seen at bottom line of ulceration and in the subepithelial side. (hematoxylin and eosin; original magnification 100×). Figure 4. 3 months after the second surgery, at the time of prosthetic management.
Discussion
The oral soft tissues play an important role for the long-term success of dental implants. Some complications of peri-implant mucosa are fistula, mucositis, dehiscence, hyperplastic gingival inflammation and peri-implantitis. These complications are usually related with poor oral hygiene or low grade-long term irritants.
According to Dojcinovic et al, gingivitis and gingival hyperplasia are the most common soft tissue complications. They are found in 1% and 30% of all cases.4Al-Khateeb reported that oral PG was found in 148 (18%) of 818 patients who had benign oral masses5 and also reported that PG can be seen from as young as 10 to the age of 70. Willies-Jacobo reported a very rare case of PG seen in a male infant6 and Gonçales et al reported PG occurrence on the upper lip and defined this situation as an unusual location.7 Shivaswamy et al showed that PG exists in the oral cavity as the most common location. They reported the very first case in the literature in 2011 about generalized PG in the oral cavity.8
The etiology of PG is unclear; however trauma, poor oral hygiene, low-grade irritants, and dental plaque can cause PG and it regresses when the causes are removed.4 PG-like lesions can occur during pregnancy due to hormonal changes in female patients. Johnson et al reported a case of PG that occurred in a postmenopausal woman undergoing hormone replacement therapy.9 Due to this kind of clinical situation, the terms “pregnancy tumors” and “granuloma gravidarum” are used.4
As the popularity of dental implants increases, various soft tissue complications may occur. Implant related hyperplasic tissue response is uncommon. To our knowledge, there are 2 published cases in the literature about the relation between dental implants and PG. One of these cases was reported by Olmedo et al1 and the other was reported by Dojcinovic et al.4 To our knowledge and a survey of the literature we believed that the present case is only the third case to be reported.
Dojcinovic et al reported that about 30% to 50% of patients with PG have a history of local trauma and mentioned that the occurrence of implant related PG in their report was associated with inappropriate healing caps of implants.4 In addition Olmedo et al reported two cases of reactive lesions related with implants. One of their cases was diagnosed as PG while the histological feature of the second case was found to be consistent with peripheral giant cell granuloma (PGCG).1
Maestre-Rodríguez et al reported a lesion in a 52-year-old male patient at a previous site in the superior maxilla. They recognized this quick growing oral lesion as PG clinically but biopsy showed that the lesion was actually metastasis of a renal clear-cell carcinoma to the oral mucosa.10 Oral lesions such as PG must be very carefully examined, especially in older patients, and the final diagnosis must be supported by biopsy findings.
In the present case, the possible reason for PG development may have been due to the gap between the alveolar bone and implant surface, which was probably caused by bone splitting. Although bone splitting was performed atraumatically with piezosurgery and the gap between the lingual and buccal cortical bone was filled with graft material and covered with a membrane, possible trauma from upper the dentition and lack of adequate keratinized mucosa resulting in soft tissue invasion between the most posterior implant and alveolar bone may have been responsible for PG development.
There are several treatment options for PG such as surgical excision, cryotherapy, electro- cauterization, laser applications and steroid injections.4 However, providing adequate keratinized soft tissue should be the first step to prevent such lesions for reactive lesions related with dental implants. In addition, management should include the detection and elimination of the possible local irritant factor, such as abnormal superstructure and healing cap-implant relationship or unfavorable implant-bone relationship.
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