Case Report Peripheral Giant Cell Granuloma A Review and Case Report Dr. Somya Maheshwari *, Dr. Girish Bhutada, Dr Vaishakhi Baisane, Dr Devendra Palve Name & Address of Institution: Swargiya Dadasaheb Kalmegh Smruti Dental College and Hospital, Waddhamna Road, Wanadongri, Nagpur, Maharashtra. Corresponding author* ABSTRACT Peripheral giant cell granuloma is among the reactive lesions of oral cavity present either on the gingiva or alveolar ridge. It can occur due to local irritational factors, trauma, etc. This case report presents a peripheral giant cell granuloma on the lingual aspect of mandibular premolars with hard bony consistency and a firm, consistent growth seen in interdental region between left mandibular premolars in a 48 year-old female patient. Traditional surgical excision was performed under local anesthesia. Keywords: Peripheral Giant Cell Granuloma (PGCG), Excisional Biopsy, Gingival Overgrowth, Mandible INTRODUCTION Oral cavity manifests a spectrum of lesions which could be either reactive, developmental and inflammatory to neoplastic. Constant external or internal stimuli causes the lesion to occur. 1 Reactive hyperplastic lesions represent the most frequently encountered oral mucosal lesions in humans. Peripheral giant cell lesions (PGCL) are reactive, extraosseous and exophytic, located in the alveolar ridge in edentulous area or in the gingiva. It usually occurs as a result of local irritants such as bacterial plaque, calculus, food retention, chronic infections, chronic irritation, trauma related to poorly fit dental prostheses, supernumerary teeth, poorly finished fillings, occlusal forces and exodontia. If the lesion is excised along with the elimination of local factors, the recurrence rate is low. Central giant cell lesions (CGCL) are intraosseous nonproliferative lesions whose etiology is unknown. It is less common than PGCL and occurs exclusively in maxillary bones. It has variable clinical manifestations with either rapid painful growth with recurrence or slow asymptomatic growth with no recurrence. PGCL are derived from periosteum and periodontal ligament and occurs frequently in young adults. It occurs in variable sizes, sessile or pedunculated. 2 PGCL appear as a reddish purple or purplish blue lump with smooth shiny or papillomatous surface. It is a well-defined lesion with exophytic growth and rarely exceeds 3 cm in their greater dimension. Although they are encountered at any age, the fourth to sixth decades are more frequent with a slight female predilection. 3 A few cases have been reported occurring in children, and in these cases the lesion appeared to be more aggressive with resorbtion of the interproximal crest area, displacement of the adjacent teeth and multiple recurrences. Previously, the lesion was called peripheral giant cell reparative granuloma. However, its reparative effect has not been proved yet, hence osteoclast activity seems doubtful. 4,5,6 Although PGCL arise in soft tissues, the cup-shaped resorption of the subjacent alveolar bone may be occasionally observed. 7,8 53
Peripheral giant cell lesion can be differentiated from other inflammatory hyperplastic lesions by presence of multinucleated giant cells whose origin is undetermined. The differential diagnosis of peripheral giant cell granuloma involves lesion with very similar clinical and histopathological features such as CGCL, fibrous hyperplasia, peripheral ossifying fibroma, pyogenic granuloma, inflamed irritation fibroma, hemangioma, lymphangioma, amelanotic melanoma and metastatic tumors. 12 Rarely a giant cell epulis may be due to hyperparathyroidism, representing the so-called osteoclastic brown tumours associated with this endocrine disorder (Smith et al, 1988; Burkes & White, 1989) and is also associated with other lesions in bones and changes in the blood chemistry. The gingiva in extra-osseous lesions of cherubism appears very similar to giant cell epulide. However, the other distinctive clinical and radiological features of cherubism indicate the correct diagnosis (Odell & Morgan, 1998). 2 Early diagnosis based on clinical and radiological findings and confirmed by pathological analysis allows for conservative management with less risk of destruction for the adjacent teeth and tissues. 13 CASE-REPORT A female patient of 48 years presented with chief complaint of soft to firm swelling in lower front region of the jaw (inner aspect) since few months. On examination generalized deposits of calculus and marginal recession of gingiva was also present. Intra oral periapical radiograph revealed bone resorption and widening of Lamina dura with lower second premolar (Fig 1 and Fig 2). Generalized bleeding on probing of the periodontal pockets was present. The lesion present was painless, as well as elastic on palpation, sessile, extending from distal aspect of left first premolar to mesial aspect of left first molar covered by red-white mucosa and measuring about 10 7 mm 2 (Fig 3 and Fig 4). The provisional diagnosis for the case was moderate chronic periodontitis with pyogenic granuloma. The differential diagnosis could be Fibrous hyperplasia, inflamed irritational fibroma and Hemangioma. The patient underwent complete blood investigations. Phase1 periodontal therapy was performed, and patient was recalled after 15 days for excisional biopsy. The lesion was excised under local anaesthesia, and flap of that quadrant was raised for complete debridement and root planing in order to prevent recurrence. Obtained tissue specimens were sent for histopathological examination. On microscopic examination the excised specimen shows single bits of tissues consisting of epithelium and connective tissue. The epithelium was parakeratinized stratified squamous type (Fig 5). At one part of the epithelium there were long pushing rete ridges and at the other part it was flat. The lamina propria adjacent to epithelium showed loosely arranged collagen fibres, few chronic inflammatory cells, many diffusely arranged fibroblast and blood vessels which appeared engorged as well as dilated with blood elements in it. Deeper connective tissue showed many multinucleated giant cells distributed evenly with variable number of nuclei ranging from 4-10 in number with mild to moderate chronic inflammatory cells like plasma cells and lymphocytes (Fig 6). The lesion was diagnosed as Peripheral Giant Cell Granuloma. 54
Fig 1 - Intra-oral peri-apical radiograph revealing reduction of the level of crestal bone in premolar area. Fig 2 OPG revealing generalized bone loss Fig 3 - Specimen removed by excisional biopsy (about 7 10 mm 2 ) 53 55
Fig 4- Showing overgrowth on lingual aspect below mandibular premolar. Fig 5 Low Power Microscope showing Surface Epithelium Fig 6 High Power Microscope showing many Multinucleated Giant Cells 56 54
DISCUSSION Two members of the tumor necrosis factor The present case was histopathologically (TNF) group: receptor activator of nuclear diagnosed as peripheral giant cell granuloma. factor- β ligand (RANKL) and osteoprotegerin The peripheral giant cell granuloma, also known (OPG) helps Stromal mononuclear cells as giant cell epulis, PGCL or giant cell (monocytes and macrophages) to participate in hyperplasia though is the most common giant the formation of multinucleated giant cells. The cell lesion, it is not a true neoplasm, but rather a transmembrane molecule RANKL is produced by reactive lesion caused by local irritation or osteoblasts/stromal cells and binds to its RANK trauma. Moreover, its etiology is still receptor, which is situated on osteoclast contentious. These lesions have been described progenitor cells surface. Differentiation of as reddish or purple with a smooth surface and osteoclast progenitor cells into mature consistency that varies from soft to firm. In the osteoclasts is promoted by RANK RANKL present case, the lesion was reddish in color in binding. OPG, also produced by stromal cells/ accordance to the literature. osteoblasts, competitively binds to RANKL The preferential location of the lesion is thereby blocking and neutralizing its binding to premolar and molar zone, though Shafer, 9 the RANK receptor, resulting in the reduction of Giansanti and Waldron 10 suggest that it osteoclastogenesis. 12 commonly occurred anterior to molars. The Treatment consists of local surgical excision occurrence of PGCG is 2 times more common in down to the underlying bone, for extensive females than males. When compared maxilla to clearing of the base (Neville et al, 2009).Removal mandible, it is more frequent in latter. 11 All the of local factors or irritants is also required characteristic features present in our study were (Regezi et al, 2008). If resection is only in accordance to the literature. superficial, the growth may recur. Exposure of The characteristic histopathological features all bony walls following thorough surgical include a non-encapsulated highly cellular mass resection responds satisfactorily most of the with abundant giant cells, hemosiderin deposits, times. Recurrence rate of 5.0-70.6% (average inflammation, mature bone or osteoid, 9.9%) has been reported in various interstitial hemorrhage. Incipient lesions may epidemiologic studies (Mighell et al, 1996). 2 bleed and induce minor changes in gingival CONCLUSION contour but large ones adversely affect normal Early and precise diagnosis of the lesion can oral function. Interference with occlusion may allow conservative management without cause ulceration of the lesion due to which it destruction of tooth and adjacent bone. becomes infected and painful. 3 Treatment consists of local surgical excision As the exact origin of the giant cells remains down to the underlying bone, with removal of unclear, several hypotheses were generated to local factors or irritants. The growth may recur if explain their proliferation: osteoclasts, spindleshaped mesenchymal cells, osteoblasts, foreign the lesion along with regular recall visits is the superficially resected. So complete excision of body cells, phagocytes reacting to hemorrhage treatment of choice for Peripheral Giant Cell and endothelial cells. 5 Granuloma. 57 53
ACKNOWLEDGEMENT We would like to acknowledge all the staff of Department of Periodontology, Swargiya Dadasaheb Kalmegh Smruti Dental College and Hospital and Dr. Devendra Palve Professor, Department of Oral and Maxillofacial Pathology, Swargiya Dadasaheb Kalmegh Smruti Dental College and Hospital for performing histological examination. The authors report no conflicts of interest related to this study. REFERENCES 1. Nareddy G, Shettar L, Bajaj M, Datta A, Thakur S. Multiple Peripheral Giant Cell Granuloma: 18 Months Recall. Int J Oral Health Med Res 2016; 2(6):88-90. 2. S. Moghe, M.K. Gupta, A. Pillai, A. Maheswari. Peripheral Giant Cell Granuloma: A Case Report and Review of Literature. People s Journal of Scientific Research. 2013; 6(2): 55-59. 3. Bacem AE Ottoman. Peripheral Giant Cell Granuloma Reaching an Impressive Overgrowth: A Case Report. Open Journal of Dentistry and Oral Medicine. 2015; 3(4): 91-93. 4. Etoz, O. A. Et Al. The Peripheral Giant Cell Granuloma in Edentulous Patients: Report Of Three Unique Cases. Eur J Dent. 2010; 4(3): 329-33. 5. Mannem, S, Chava, V. K. Management Of An Unusual Peripheral Giant Cell Granuloma: A Diagnostic Dilemma. Contemp Clin Dent. 2012; 3(1): 93-96. 6. Tandon, P. N. Et Al. Peripheral Giant Cell Granuloma. Contemp Clin Dent, V. 3, N. 1, (Suppl 1), P. 118-21, 2012. 7. Papanicolaou, P. Et Al. Increased Tnf-, IL-6 And Decreased IL-1β immunohistochemical Expression By The Stromal Spindle-Shaped Cells In The Central Giant Cell Granuloma Of The Jaws. Med Oral Patol Oral Cir Bucal.2012; 7(1): 56-62. 8. Saygun, I. Et Al. Human Cytomegalovirus In Peripheral Giant Cell Granuloma. Oral Microbiol Immunol. 2009; 24(5): 408-10. 9. Rajendran R., Sivapathasundharam B. Benign and malignant tumors of the oral cavity. Shafer s Textbookof Oral Pathology. 5th ed. New Delhi: Elsevier Publishers; 2006; 113-308. 10. Giansanti JS, Waldron CA. Peripheral giant cell granuloma: Review of 720 cases. J Oral Surg. 1969; 27:787-91. 11. Rodrigues SV, Mitra DK, Pawar SD, Vijayakar HN. Peripheral giant cell granuloma: This enormity is a rarity. J Indian Soc Periodontol. 2015;19(4): 466-9. 12. Rodrigo Gadelha Vasconcelos; Marcelo Gadelha Vasconcelos; Lélia Maria Guedes Queiroz.Peripheral and central giant cell lesions: etiology, origin of giant cells, diagnosis and treatment. J Bras Patol Med Lab. 2013; 49(6): 446-452. 13. Alaa Z. Abu Gharbyaha, Mohammad Assa. Management of a Peripheral Giant Cell Granuloma in the esthetic area of upper jaw: A case report. International Journal of Surgery Case Reports. 2014; 5: 779 782. 58 54