|Year : 2015 | Volume
| Issue : 1 | Page : 152-155
Medical management of a case of central giant cell granuloma masquerading as a periapical pathosis
Balaji Babu Bangi, Lakshmi Kavitha Nadendla, Revath Vyas Devulapalli, Archana Pokala
Department of Oral Medicine and Radiology, Kamineni Institute of Dental Sciences, Narketpally, Telangana, India
|Date of Submission||19-Dec-2014|
|Date of Acceptance||13-Sep-2015|
|Date of Web Publication||12-Oct-2015|
Revath Vyas Devulapalli
Department of Oral Medicine and Radiology, Kamineni Institute of Dental Sciences, Narketpally - 508 254, Telangana
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Lesions of non-endodontic origin may mimic periapical pathosis. Errors in one or more of the clinical reasoning steps of diagnosis of such lesions may ultimately lead to misdiagnosis and ensuing complications. Central giant cell granuloma (CGCG) is one such lesion of non-endodontic origin which can present as periapical pathosis. Here, we present a case of CGCG in a 33-year-old female patient who visited our department with a complaint of growth from the extraction sockets of upper front teeth, which were extracted 1 month back after a misdiagnosis as periapical pathosis. Suspecting a non-endodontic lesion, radiographic examination and incisional biopsy were performed and a final diagnosis of CGCG was made. Biweekly intra-lesional steroids were given for 6 weeks and patient was followed up for 6 months.
Keywords: Central giant cell granuloma, jaw, non-surgical treatment, steroid, surgery
|How to cite this article:|
Bangi BB, Nadendla LK, Devulapalli RV, Pokala A. Medical management of a case of central giant cell granuloma masquerading as a periapical pathosis. J Indian Acad Oral Med Radiol 2015;27:152-5
|How to cite this URL:|
Bangi BB, Nadendla LK, Devulapalli RV, Pokala A. Medical management of a case of central giant cell granuloma masquerading as a periapical pathosis. J Indian Acad Oral Med Radiol [serial online] 2015 [cited 2020 Mar 29];27:152-5. Available from: http://www.jiaomr.in/text.asp?2015/27/1/152/167150
| Introduction|| |
Periapical lesions generally have an etiology that is associated with necrosis and infection of the root canal system;  they are usually identified as radiolucency located in the apex of the teeth on radiographic examinations. However, there are lesions of neoplastic sources, cystic lesions of non-endodontic origin, and anatomic variations such as a stafne bone cavity (SBC) that when located in the periapical area of the teeth might radiographically and clinically mimic lesions of endodontic origin, leading to misdiagnosis.  A detailed review of the patient's past medical and dental histories, clinical aspects and specific radiographic findings represent important steps in the diagnostic process and may prevent a diagnostic dilemma.  Central giant cell lesions (CGCL) are infrequent intraosseous lesions that affect the jaws.  They may occur rarely in periapical region and may be misdiagnosed as periapical pathosis. This report describes a clinical case of central giant cell granuloma (CGCG) in the periapical region of 21 and 22 with emphasis on radiological features and management.
| Case Report|| |
A 33-year-old female patient presented to our department with a complaint of growth from the extraction socket of upper front teeth since 1 month. She got her 21 and 22 teeth extracted 1 month ago due to swelling and mobility which developed 3 months after trauma. Shortly after the extraction of the teeth she noticed a mass growing from the extraction site. It was associated with very mild pain and tingling sensation. Physical examination revealed a smooth, non-tender and fluctuant swelling below the left ala of the nose causing elevation of left nostril and mild facial asymmetry [Figure 1]. Intraorally, a solitary well-defined cystic swelling was seen in the edentulous region of 21 and 22 causing vestibular obliteration and was associated with bluish purple growth which was of size 2 × 2 × 1 cm (buccolingually, mesiodistally and superoinferiorly) extending from the extraction sockets of 21 and 22 on to the incisal edges of lower incisors [Figure 2]. Provisionally a diagnosis of epulis granulomatosa was made as it appeared to be a growth from the extraction socket. Aspiration yielded thin blood-tinged fluid [Figure 3]. Under differential diagnosis central or peripheral giant cell granuloma or infected radicular cyst were considered. Intra-oral periapical radiograph (IOPA) showed a well-defined radiolucency of size 1.5 × 1.5 cm with irregular, undulating, non-sclerotic scalloping borders. Internal structure was completely radiolucent with granularity at the periphery [Figure 4]. The remnant bone at periphery resulted in V-shaped wispy trabeculae. Maxillary anterior occlusal and orthopantomograph (OPG) [Figure 4] showed similar findings. Computed tomographic sections and 3D reconstruction image showed an aggressive osteolytic lesion causing breach of buccal and lingual cortical plate, filled with a mass which was isodense with the adjacent soft tissue. Central portion of the lesion was hypodense and the lesion appeared to be well encapsulated [Figure 5]. These radiological findings excluded peripheral origin of the lesion and the lesion appeared to be either CGCG or infected radicular cyst. But non-corticated outline and wispy septa were more in favor of CGCG. Incisional biopsy was performed. Microscopic examination showed large number of multinucleated giant cells in a background of cellular stoma with large number of extravasated RBC [Figure 6]. These features were suggestive of CGCG. Histologically Brown's tumor may also show similar features. But, laboratory investigations showed normal levels of parathormone, calcium, phosphorus and alkaline phosphatase. Considering the size of the lesion, its close proximity to the maxillary sinus and possible facial deformity that could arise as a result of surgery, medical management with 2 ml of intralesional corticosteroid, triamcinolone acetonide at a dose of 10 mg/ml was given twice weekly for 6 weeks. During the course of the treatment, there was a gradual decrease in size of the lesion clinically and radiographically [Figure 7] and significant amount of resistance while giving intra lesional injections developed. Lesion was followed up for next 6 months. There was a significant clinical improvement with a residual radiological defect. After 6 months follow-up, extraction of adjacent mobile teeth was carried out and prosthetic rehabilitation was performed [Figure 8].
|Figure 1: Showing extra-oral presentation with obliteration of nasolabial fold|
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|Figure 2: Showing intra-oral presentation with bluish purple mass from the extraction socket|
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|Figure 4: Showing a unilocular lesion with wispy trabeculae at periphery|
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|Figure 5: Showing osteolytic lesion in the anterior maxilla causing labial and lingual cortical perforation|
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|Figure 6: Showing numerous giant cells interspersed in the connective tissue|
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|Figure 7: Showing resolution of the lesion clinically and radiographically|
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| Discussion|| |
Central giant cell granulomas appearing as small periapical lesions constituted 9% of all examined CGCG cases in one study.  Furthermore, the largest retrospective study on CGCG (n = 79) found in a periapical location revealed that 20% of the lesions were associated with teeth with necrotic pulps and that the majority of these necrotic teeth had been endodontically treated.  In addition, as in our case, periapical CGCG was encountered in patients older than 30 years of age, while the non-periapical-CGCG is usually diagnosed in younger patients; single cases of periapical-CGCG or small case series were also reported.  Normal predilection of CGCG is anterior to 1 st molar in the deciduous tooth-bearing regions. Mandible is more commonly involved than maxilla.  Non-speciﬁc pain and swelling are the most common clinical manifestations. The overlying mucosa may have a purple color. Our case also presented as a non-specific pain and swelling with a purplish overlying mucosa. Multiple lesions are rare but have been reported. But, when multiple lesions occur investigations should be done to rule out hyperparathyroidism.  Though our case presented as a solitary lesion, hyperparathyroidism was ruled out.
Radiologically, CGCG enlarge in a sequence of three phases. Early, smaller lesions begin as a cyst-like radiolucency. As the lesion enlarges, adjacent areas of bone are replaced and septa may separate adjacent lacunae of resorbed bone, thus forming a multilocular appearance. At the same time there is expansion and thinning of peripheral cortex. Ultimately septa are resorbed from the most central part of the lesion towards the periphery, leaving only crenations at the margins.  Current case presented in its 3 rd stage with no septa in the center but with crenations at the periphery. Histopathologically, CGCG is composed of proliferating endothelial cells, numerous small capillaries, multinucleated giant cells, and active fibroblasts and myofibroblasts embedded in a fibrous stroma.  Present case also showed similar histological features which confirmed the diagnosis of CGCG. Biochemical analysis of the alkaline phosphatase, parathormone and evaluation of renal function are mandatory to distinguish between the brown tumour of hyperparathyroidism and CGCL; these conditions may present identical radiographic and histopathologic features.  Our case showed normal levels of calcium, parathormone and alkaline phosphatase ruling out Brown's tumor of hyperparathyroidism. Depending on clinical, radiographic and histopathologic features, CGCG has been classified into two types- non-aggressive and aggressive. The clinical features of a more aggressive pattern include pain, rapid growth, swelling and recurrence. The radiographic features of the aggressive type include resorption of adjacent root apices, perforation of the expanded cortex and diameter exceeding 2 cm. Histological features like relative size of giant cells, stromal characteristics, mitotic index, presence of inflammation and amount of hemosiderin indicate the behavior pattern.  The traditional treatment of CGCG of the jaws has been surgical excision either by curettage or enbloc resection, depending on aggressive versus nonaggressive behaviour, location, size, and radiographic appearance.  Treatment of CGCG with intralesional steroid injections can be used as an alternative to surgery, especially in large lesions, which could compromise vital structures as in the present case. On the basis of experimental evidence it was hypothesized that intralesional steroids have inhibitory action on the extracellular production of lysosomal proteases which mediate osteoclastic bone resorption by creating an acidic extracellular medium or by steroidal apoptotic action on osteoclast-like cells or by inhibition of transcription factors for intracellular proliferation. These three mechanisms cause cessation of bone resorption.  A large CGCG can be treated with intralesional steroid injections either as a single modality, as in our case for deﬁnitive treatment or as a neoadjuvant treatment to shrink the lesion and decrease the morbidity of subsequent surgery.  Other treatment options include radiation,  systemic injections and intra-nasal spray of calcitonin  and α-interferon.  Reported recurrence rate of CGCG was 11-35%. Recurrences are more common in aggressive lesions with size greater than 3 cms and in patients younger than 20 years of age. 
| Conclusion|| |
Central giant cell granuloma may rarely mimic a periapical pathosis and present as a diagnostic dialemma. Early diagnosis of such lesions can help in providing prompt treatment to the patient. Intralesional injections may be considered as primary modality of treatment for CGCG as they are easy to perform, involve minimal morbidity, their cost is negligible and there will be a chance to treat the lesion surgically in the future, if necessary.
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Conflicts of interest
There are no conflicts of interest.
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