Peripheral giant cell granuloma: This enormity is a rarity

Abstract

Peripheral giant cell granuloma (PGCG) is an infrequent exophytic lesion of the oral cavity, also known as giant cell epulis, osteoclastoma, giant cell reparative granuloma, or giant cell hyperplasia. Lesions vary in appearance from smooth, regularly outlined masses to irregularly shaped, multilobulated protuberances with surface indentations. Ulcerations of the margin are occasionally seen. The lesions are painless, vary in size, and may cover several teeth. It normally presents as a purplish-red nodule consisting of multinucleated giant cells in the background of mononuclear stromal cells and extravasated red blood cells. This case report describes the unusual appearance of a PGCG extending from left maxillary interdental gingiva to palatal area in 32-year-old female patient.

INTRODUCTION

Peripheral giant cell granuloma (PGCG) is a benign, generally asymptomatic hyperplastic lesion of the attached gingiva or alveolar mucosa. This lesion is usually around 1–1.5 cm in diameter. Very rarely we come across a lesion that is >1.5 cm. It is thought to arise from the gingival connective tissue or the periosteum of the alveolar ridge in response to injury.[1] The etiology of PGCG is unclear. It is probably a reactive lesion caused by local irritation or trauma.[2]

Clinically, PGCG is seen exclusively on gingiva, especially in the area between the first permanent molars and incisors and presents itself as sessile or pedunculated lesion. Ulceration may occur secondary to trauma. Females are more frequently affected than males, with lesions occurring more frequently in the mandible than in the maxilla. The lesion can be found in all age groups, with a relative predilection for those 40–60 years old.[3]

The microscopic appearance of giant cell lesion is unique. The lesion is characterized by a nonencapsulated, highly cellular mass with abundant multinucleated giant cells and inflammatory cells. Interstitial hemorrhage, hemosiderin deposits, and mature bone or osteoid are also seen. Furthermore, a variable number of chronic inflammatory cells and neutrophils usually are present, underlying ulcerated areas. Surgical excision is the treatment of choice for PGCG, with removal of local factors or irritants.

This case report describes the clinical and histopathological findings and management of a uniquely large PGCG (around 2.5 cm in diameter) found in the maxilla of a young female.

CASE REPORT

A 32-year-old woman reported to Department of Periodontology, TPCT's Terna Dental College, Nerul, Navi Mumbai with the chief complaint of swelling in upper left back region of the mouth since 3 months. Patient's history revealed that a small swelling appeared 3 months back on left buccal aspect of the jaw, which gradually extended palatally and increased to attain present size. The patient reported the lesion to be asymptomatic, but bleeding tendency was observed if accidentally bitten on during mastication. Patient also gave the history of mishri use twice daily since 10 years. Extraoral examination did not reveal any pathological findings and facial asymmetry. Medical history of the patient revealed no systemic diseases; examination of lymphonodes in the head and neck region revealed no lymphadenopathy. Patient was systemically healthy and was not taking any medications.

Intra-oral examination revealed a nodular growth on the maxillary buccal interdental gingiva in relation to the second premolar and first molar which was extending to palatal mucosa. Swelling was exophytic, sessile, bluish-red in color, firm in consistency which measured 1 cm × 1 cm on the buccal aspect [Figure 1]. Palatal swelling was pedunculated, irregular and multilobulated which measured 2.5 cm × 2.5 cm [Figure 2]. Other oral findings included an over-retained root piece of deciduous second molar distal to the growth and overall simplified oral hygiene index for the patient was 3.66 indicating poor oral hygiene.

Figure 1.

Intra-oral clinical presentation of swelling (buccal view)

Figure 2.

Intra-oral clinical presentation of swelling (palatal view)

Her complete blood count revealed normal results. Superficial erosion of the alveolar crest in relation to the growth was seen in periapical radiograph [Figure 3], such superficial erosions of alveolar bone are usually observed in cases of PGCG.[4] In occlusal radiographs, no significant bone loss was found [Figure 4]. Orthopantomogram of patient showed interdental bone loss with second premolar and first molar [Figure 5]. Cone beam computed tomography revealed soft tissue growth originating from left maxilla measuring 23.28 mm × 16.57 mm in greatest dimensions [Figure 6a and b].

Figure 3.

Intra-oral periapical radiograph showing superficial erosion of alveolar crest between second premolar and first molar

Figure 4.

Occlusal radiograph reveals no significant bone loss

Figure 5.

Orthopantomogram showing interdental bone loss between second premolar and first molar

Figure 6.

(a) Cone beam computed tomography (CBCT) showing soft tissue shadow of swelling and antero-posterior dimension; (b) CBCT showing soft tissue shadow of swelling and medio-lateral dimension

After phase I periodontal treatment, incisional biopsies were performed for both the buccal and palatal lesions. Biopsy specimens were embedded in 10% formalin and sent to Department of Oral Pathology. Routine histological examination with hematoxylin and eosin (H and E) stains were performed. After confirmation of the diagnosis of the lesion complete surgical excision was performed [Figure 7]. The H and E section showed hyperplastic parakeratinized stratified squamous epithelium exhibiting acanthosis and ulceration. The underlying connective tissue stroma showed high cellularity. Nodular proliferation of multinucleated giant cells along with mesenchymal cells was observed, with few areas of hemorrhage interspersed with zones of bone formation and chronic inflammatory cells [Figure 8a and b]. The microscopic features of the lesion were consistent with PGCG.

Figure 7.

Excised lesion measuring around 2.5 cm in diameter

Figure 8.

(a) Hematoxylin and eosin staining section of lesion (×4) showing nodular proliferation of multinucleated giant cells covered by parakeratinized stratified squamous epithelium; (b) hematoxylin and eosin staining section of lesion (×40) showing multinucleated giant cells and spindle shaped mesenchymal cells

Due to likelihood of recurrence, a wide excision of the lesion was performed to minimize the chance of further recurrence. Subgingival band of calculus was observed with second premolar region after excision of the lesion [Figure 9]. High power diode laser of wavelength 810 nm with a treated tip in continuous mode at 0.6–1 W was used to cauterize the bleeding tissue. To extend the periphery of excision treated tip in continuous mode at 1.2–1.5 W was used [Figure 10a and b]. The excised specimen was embedded in 10% formalin and sent to the Department of Oral Pathology. The histology of the excised lesion re-confirmed the diagnosis of PGCG.

Figure 9.

Subgingival band of calculus with respect to palatal aspect of second premolar

Figure 10.

(a) Postexcision after laser cauterization (buccal view); (b) postexcision after laser cauterization (palatal view)

Healing was uneventful till 4 months postoperative [Figure 11a and b]. Patient is still under follow-up.

Figure 11.

(a) Four months postoperative photo showing uneventful healing (buccal view); (b) 4 months postoperative photo showing uneventful healing (palatal view)

DISCUSSION

The PGCG is not a neoplasm, but rather a reactive lesion caused by trauma or irritation. PGCGs account for <10% of all hyperplastic gingival lesions. It is seen in the young as well as in the elderly population with the highest incidence in the fourth to sixth decades of life. The maximum capacity of PGCGs to enlarge is 0.1–3 cm and 94% of these lesions are <1.5 cm.[5] In present case size of the lesion was >1.5 cm. This lesion was uniquely large and required special care during surgical excision. PGCG can be sessile or pedunculated, spreading through penetration of the periodontal membrane and may or may not be ulcerated.[4]

The preferential location of the lesion is premolar and molar zone, though Shafer,[4] Giansanti and Waldron[6] suggest that it generally occurs in the incisor and canine region. The lesions have been reported to be 2 times more common in females than males and more frequent in the mandible than the maxilla.

In present case sex predilection and age of the patient were compatible with the literature but not compatible in case of size and location of the lesion. The size of the lesion was unusually large and grew aggressively over a period of 3 months, which initially gave an impression of being a malignancy.

It has been reported that lesions may cause mobility or displacement of neighboring teeth.[7] In present case postexcision mobility of the associated tooth was encountered. The lesion was painless as it did not interfere with the occlusion, therefore, might not have been affected by traumatic forces. The consistency of the lesion is dependent on the age of lesions because with time, there is an increase in the collagen fibers, characterizing the mature lesion as being of a firm consistency instead of soft. In our case, the consistency was firm.

The etiology of this lesion is still not precisely defined, local irritating factors such as tooth expulsion, ill-fitting prosthesis, poor restorations, plaque, calculus, chronic infections or the effects of nutrients may play a vital role in the etiology.[8] Previously, the lesion was called peripheral giant cell reparative granuloma. However, its reparative effect has not been proved yet, hence osteoclast activity seems doubtful.[9,10] The probable etiological factors in present case could be plaque, calculus or an over-retained root piece.

The distinctive feature of PGCG is mainly due to excess number of giant cells that are disseminated in the connective tissue stroma. The exact basis of giant cells is uncertain. Many opinions have been identified in the literature as osteoblasts, phagocytes, endothelial cells, and spindle cells are thought to be responsible for giant cell proliferation.[4,10] The proliferation of giant cells associated with resorption of deciduous teeth has been implicated in the development of giant cell lesions,[1] but this theory has not received any attention because such lesions also may develop in edentulous areas. The origin of the multinucleated giant cells is unknown; some believe them to show immunohistochemical features of osteoclasts while others suggest them to arise from mononuclear phagocyte system.[2,10]

Microscopic examination is required for definitive diagnosis. The PGCG has numerous foci of multinuclear giant cells and hemosiderine particles in a connective tissue stroma. Areas of chronic inflammation are scattered throughout the lesion, with acute involvement occurring at the surface. The overlying epithelium is usually hyperplastic, with ulceration at the baseline.[4] In present case, all of these features were present, except the presence of hemosiderine particles.

There are no pathognomic clinical features whereby these lesions can be differentiated from other forms of gingival enlargement. The differential diagnosis of PGCG includes pyogenic granuloma, peripheral ossifying fibroma, and peripheral cemento-ossifying fibroma, all of which present with similar clinical and radiographic findings. Another lesion, with very similar clinical and histological characteristics, is central giant cell granuloma. This is located within the jaw itself and exhibits more aggressive behavior. Only radiological evaluation can establish a distinction. Definitive diagnosis can be established through histopathologic examination.

Traditional treatment consists of local surgical excision down to the underlying bone,[2] for extensive clearing of the base.[5] Removal of local factors or irritants is also required. If the resection is only superficial, the growth may recur. Recurrence rate of PGCG varies between 5% and 70.6%, but it is generally accepted that the recurrence incidence for PGCG is approximately 10%.[3] These wide variations probably are related to the surgical technique utilized. Therefore to minimize the chances of recurrence wider excisions extending to the periosteum and including the entire base of the lesion are warranted. The high power diode laser is an excellent soft tissue surgical tool indicated for cutting and coagulating gingiva and mucosa.[11] In our case for postsurgical excision we used soft tissue laser to cauterize the bleeding tissue and to extend the excision till the periosteum. This will probably reduce the chances of recurrence.

CONCLUSION

Although the PGCG is a relatively common entity, dental practitioners may be confronted with cases of PGCG with such a large size during their practice. Consequently, timely histopathological examination, diagnosis, and treatment are essential to prevent greater loss of periodontal attachment.