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Year : 2012  |  Volume : 2  |  Issue : 2  |  Page : 95-99

Endodontic misdiagnosis of periapical central giant cell granuloma: Report of case with 2 years of follow-up

1 Department of Conservative Dentistry and Endodontics, MGM Dental college and Hospital, Navi Mumbai, India
2 Department of Oral Medicine, Diagnosis and Radiology, CSMSS Dental College and Hospital, Aurangabad, India

Date of Web Publication6-Mar-2013

Correspondence Address:
Rahul Kumar
Department of Conservative Dentistry and Endoodontics MGM Dental College and Hospital, Sector 18, Kamothe, Navi Mumbai - 410 209, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1658-5984.108160

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Central giant cell granuloma is considered as reactive lesion of jaws possibly to intramedullary hemorrhage or trauma. It may manifest as radiolucencies anywhere in the mandible or maxilla. In rare cases, it can appear as a localized periapical area and mimic an endodontic lesion. This report presents a case where central giant cell granuloma was misdiagnosed as a periapical cyst in 20-year-old male and was treated by conventional endodontic treatment. However the lesion was refractory to endodontic treatment and proved to be central giant cell granuloma after surgical intervention and histopathological examination. The purpose of this case report is to emphasize on periodic follow-up of periapical lesions after endodontic treatment and surgical intervention if required.

Keywords: Central giant cell granuloma, endodontic lesion, misdiagnosis

How to cite this article:
Kumar R, Khambete N. Endodontic misdiagnosis of periapical central giant cell granuloma: Report of case with 2 years of follow-up. Saudi Endod J 2012;2:95-9

How to cite this URL:
Kumar R, Khambete N. Endodontic misdiagnosis of periapical central giant cell granuloma: Report of case with 2 years of follow-up. Saudi Endod J [serial online] 2012 [cited 2022 Aug 12];2:95-9. Available from: https://www.saudiendodj.com/text.asp?2012/2/2/95/108160

  Introduction Top

The central giant cell granuloma (CGCG) was first described by Jaffe in 1953 as a giant-cell reparative granuloma of the jaw bones. It was hypothesized that the lesion is not a true neoplasm but merely the result of a local reparative reaction. [1] Currently, CGCG is regarded as a destructive lesion of variable size and rate of progression. [2] The lesion more commonly affects females and has predilection for mandible, commonly occurring anterior to permanent molars and often crosses midline. The age of most patients ranges from 10-25 years. [3] Based on radiographic and clinical features, CGCG exhibits spectrum of behavior ranging from non-aggressive to aggressive. The former type exhibits slow growth and has a low recurrence rate. The aggressive form is less common, shows rapid growth and high recurrence rate. [4] In most of the cases it presents as a painless, slow growing swelling of the jaw. Pain and sensory disturbances are rare. Displacement of teeth can occur, which causes malocclusion. [5] Radiologic features of this lesion are diverse ranging from small unilocular lesion to large destructive multilocular radiolucency involving a large part of the maxilla or mandible. [6]

Histopathologically, CGCG is composed of lobules of spindle fibroblasts, numerous multinucleated osteoclast-like giant cells and hemorrhage and reactive woven bone rimmed by osteoblasts. In addition, scattered inflammatory cells within the stroma can be seen. The multinucleated giant cells are thought to be related to osteoclasts. [7],[8]

Although not related to dental pathoses, CGCG may be sometimes localized near the roots of teeth or the tooth apex and hence it can be misdiagnosed radiographically as a periapical granuloma or a radicular cyst. [9] If the pulp is vital the treatment can be directed towards intrabony lesion. However, if the pulp is non-responsive to vitality tests and tooth exhibits clinical features of apical periodontitis, CGCG can be easily mistaken for periapical pathology. Certain reports in literature report cases of CGCG associated with endodontically involved teeth. [10],[11],[12]

Here we present a case where a patient reported to the Department of Conservative Dentistry and Endodontics, with chief complaint of pain in the anterior mandible. The mandibular anteriors were non responsive to pulp vitality tests with intraoral radiographs showing a periapical radiolucency. Hence, conventional endodontic treatment was carried out. However the patient returned without any relief. The surgical intervention and histopathologic examination revealed the lesion to be CGCG.

  Case Report Top

A 20-year-old male patient reported to the Department of Conservative Dentistry and Endodontics, with complaint of pain and recurrent swelling in his anterior lower jaw in the symphysis and parasymphysis area. The history of complaint patient had a history of trauma to mandibular anteriors 10 years back. The patient then developed swelling one month back which subsided after discharging pus from the area. The swelling recurred 15 days back. The medical history was non-contributory. Intraorally, the oral mucosa was intact. Mandibular right central incisor was fractured and mandibular right central incisor and left incisors had grade two mobility [Figure 1]a. Intraoral periapical radiographs revealed well defined, non-corticated unilocular periapical radiolucency in region of mandibular right and left central incisors and mandibular left lateral incisors and also showed pathological displacement of left central and lateral incisors [Figure 1]b. Sensitivity tests of involved teeth were negative for the mandibular right and left central incisors and mandibular right lateral incisor. Initially, non-surgical endodontic therapy was planned. After application of rubber dam (Hygienic Dental Dam, Colténe Whaledent, Germany) and access cavity preparation, working length was determined. The root canals were cleaned and shaped using a ProTaper Ni-Ti rotary instrument (Dentsply, Maillefer) with a crown-down technique under copious irrigation with saline, 5% sodium hypochlorite solution (Dentpro, Chandigarh, India) and 17% EDTA (Prime Dental Product Pvt, Mumbai). The canal was dried with paper points (Dentsply Maillefer, Ballaigues, Switzerland) and calcium hydroxide (Metapex; Meta Biomed Ltd, Cheongju city, Chungbuk, Korea) was placed and the access was closed with a sterile cotton pellet followed by a provisional restorative material IRM (Caulk, Dentsply, Milford, DE). The patient was then reappointed for continuation of treatment approximately 2 weeks from the initial appointment. At the next appointment, rubber dam was placed as described above. The tooth was reaccessed, and calcium hydroxide was removed with 5.25% NaOCl irrigation with 27 gauges blunted needle disposable plastic syringe and instrumentation. The canals were finally rinsed with saline, dried with absorbent points (Dentsply Maillefer) and obturation was performed using cold lateral compaction of gutta-percha (Dentsply Maillefer) using AH Plus epoxy-resin sealer (Maillefer, Dentsply, Konstanz, Germany) [Figure 2]a. Finally, the tooth was then restored with glass ionomer cement (GC Fugi filling LC, GC India, Hyderabad). However, after 6 months, expansion and pain of the anterior region of mandible had increased gradually. Then, the patient was referred to department of oral medicine and radiology. Needle aspiration biopsy was carried out, unfortunately it demonstrated negative results. Clinical examination discovered no neurosensory defects by the department of oral medicine and radiology. These findings suggested a differential diagnosis of central giant cell granuloma (CGCG), Aneurysmal Bone Cyst or Cystic Calcifying Odontogenic Tumor. Because of persistent and expansion of periapical radiolucency surgery was planned.
Figure 1: Pre-operative clinical photograph (a) Pre-operative intra-oral periapical radiograph showing pathological displacement of left central and lateral incisors (b)

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Figure 2: Post-obturation radiograph (a) Horizontal and vertical incision (b) Reflection of buccal full-thickness triangular mucoperiosteal flap showing existing pathological cortical bone window (c) Surgical removal of periapical mass (d)

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Revised consent was obtained from the patient prior to the surgical treatment. Assessment of the surgical site showed adequate mouth opening, little attached gingiva and adequate depth of the vestibule. With inferior alveolar nerve block, local anesthesia of 2% lignocaine with 1:80,000 adrenaline was infiltrated in the alveolar buccal mucosa superficial to the periosteum at the level of root apices from mandibular left lateral incisor to mandibular right lateral incisor to get an added advantage of less surgical bleeding. The buccal full-thickness triangular mucoperiosteal flap was elevated to expose the area of the periapical lesion [Figure 2]b. Already existing pathological cortical bone window was expanded until underlying pathology was adequately exposed and sufficient space was available for thorough curettage [Figure 2]c. Gross examination of the lesion revealed many small soft elastic specimens, white-brown in color with [Figure 2]d. Sterilized gauze was placed between the pathological soft tissue mass and the lateral wall of the crypt, and lateral pressure was applied on the gauze with the concave surface of the curette facing the bone. This helped in separation of the periapical lesion from the surrounding bone. The enucleated lesion was stored in 10% buffered formalin solution and sent for histopathological examination [Figure 3]a. The root resection was not done to maintain maximum cemental covering on the root surface and to maintain the original root length to help tooth stability. Gutta-percha at the exposed root apex was burnished. The bone cavity was irrigated with sterile normal saline and gently dried with moist gauze [Figure 3]b. Careful clinical and radiographic inspection of the area was done to ensure no residual lesion tissue was left behind. The flap was repositioned and the flap margins were ensured to rest on sound bone. The flap was sutured using 5-0 silk with interrupted sutures and dressing given with COE-PAK. (GC, America) [Figure 3]c and d.
Figure 3: Clinical photographs of periapical mass (a) The mandible after surgical curettage (b), Suturing (c) and dressing (d)

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The patient was given postoperative instructions both verbally and in writing. Antibiotics, analgesics and mouthwash were prescribed. On the 4 th postoperative day, healing of covering mucosa with primary intention was observed and the sutures were removed. Histologically, multinucleated giant cells were distributed in a stroma that was highly cellular compromising both spindle-shaped and round cells which were found mostly in hemorrhagic and reactive bone areas. Ingested RBCs and scant collagen fibers were also seen [Figure 4]a-c. These findings confirmed diagnosis of CGCG.
Figure 4: Histological photos of the central giant cell granuloma exhibiting multinucleated giant cells among fibroblasts and a loosely fibrous connective tissue stroma. (a) original magnification, ×10, (b) original magnification, ×40 and (c) original magnification, ×100

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The patient was free from all symptoms and signs with optimal tissue healing at the 6-month follow-up visit. Radiographic examination revealed a decrease in the size of periapical radiolucency, as well as pathological migration between the left central and lateral incisors. A radiographic review at the 6, 9, 12, 24 months follow-up showed good evidence of bone healing between left central and lateral incisors [Figure 5].
Figure 5: Post-operative follow-up radiographs 3 months (a), 6 months (b), 12 months (c) and 24 months (d)

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  Discussion Top

The purpose of this case report is to demonstrate the role of pulp vitality tests and periodic follow-up of periapical radiolucencies following endodontic treatment. Certain lesions can project as periapical radiolucencies, which may not originate from pulpal tissues and are hence refractory to endodontic therapy. Unnecessary endodontic treatments have been reported to be performed in such cases. Spatafore et al., researched 1,659 periapical radiolucencies over a 10 year period and found that 52% of periapical lesions were granulomas, 42% cysts, 2% periapical scars and 4% other disorders, [13] Ortega et al., showed that from 43,706 biopsy specimens, 26 cases had a histopathologic diagnosis of non-endodontic pathology. The most common periapical non-endodontic radiolucency was Odontogenic Keratocyst (OKC) (11 cases) followed by CGCG (3 cases). No malignancy was reported. [14]

In 2005, De lange et al., reported that from 89 cases of CGCG, 79 cases were unilocular radiolucencies and 8 cases were localized in periapical areas of the tooth. [6] If these lesions are present near the root of a tooth with a necrotic pulp, or with doubtful sensitivity testing, it is reasonable to perform root canal treatment. This occurred in 14 out of the 16 (87%) cases reported by Dahlkemper et al., [2] Similarly in our case, the teeth were non-responsive to pulp vitality tests initially so endodontic treatment was performed.

Several case reports also describe root canal treatment of teeth with periapical radiolucent lesions later diagnosed histopathologically as CGCG. Martin [10] described a maxillary lateral incisor treated endodontically without proper vitality testing. Persistent pain and enlargement of the lesion led first to nonsurgical retreatment and then to eventual surgical treatment and biopsy. Sykaras [11] described a case in which a caries-free lower incisor was painful to percussion and tested nonvital to electric pulp testing. The beginning of root canal treatment showed a vital, but abnormal pulp. Continued pain, tenderness, and a lack of periapical healing 6 months after treatment led to apical curettage and a histopathologic diagnosis of CGCG. Glickman [12] described a restored mandibular premolar with a history of trauma and persistently symptomatic chronic apical periodontitis that underwent nonsurgical endodontic treatment twice before surgical curettage. Histologic examination showed the presence of a CGCG.

Despite a proper clinical diagnosis of a necrotic pulp and subsequent root canal treatment, a non-endodontic lesion may still be present. Pretreatment diagnosis is not 100% accurate, and nonsurgical endodontics is not 100% effective. These diagnostic and treatment shortcomings result in persistent and sometimes enlarged inflammatory lesions that cannot be distinguished from potentially more serious non-inflammatory lesions. Post-treatment follow-up clearly becomes an important issue at this point because it is the principal means to detect periradicular non-inflammatory disease that is unresponsive to endodontic treatment. Lack of adequate follow-up leaves the patient to decide when a lesion should be reexamined. That situation can lead to the development of an unnecessarily large lesion. Complete surgical excision of the lesion increases the likelihood of devitalizing or even sacrificing adjacent teeth. [2]

To conclude, the radiographic appearance of a CGCG is not pathognomonic and may be confused with other jaw lesions. The high incidence of common inflammatory periradicular lesions frequently leads clinicians to disregard the diagnosis of other pathological conditions. Thus, it is mandatory to follow-up the periapical radiolucencies after non-surgical endodontic treatment. If the lesions show no evidence of healing further surgical treatment with histopathologic examination should be carried out to confirm the diagnosis.

  References Top

1.Jaffe HL. Giant-cell reparative granuloma, traumatic bone cyst, and fibrous (fibro-osseous) dysplasia of the jawbones. Oral Surg 1953;6:159-75.  Back to cited text no. 1
2.Dahlkemper P, Wolcott JF, Pringle GA, Hicks ML. Periapical central giant cell granuloma: A potential endodontic misdiagnosis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000;90:739-45.  Back to cited text no. 2
3.Andersen L, Fejerskov O, Philipsen HP. Oral giant cell granulomas: A clinical and histological study of 129 new cases. Acta Pathol Microbiol Scand 1973;81:606-16  Back to cited text no. 3
4.Auclair PL, Cuenin P, Kratochvil FJ, Slater LJ, Ellis GL. A clinical and histomorphologic comparison of the central giant cell granuloma and the giant cell tumor. Oral Surg Oral Med Oral Pathol 1988;66:197-208.  Back to cited text no. 4
5.De Lange J, Van den Akker HP. Central giant cell granuloma of the jaw: Review of literature with emphasis on treatment options Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2007;104:603-15.  Back to cited text no. 5
6.De Lange J, Van den Akker HP. Clinical and radiological features of central giant-cell lesions of the jaw. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;99:464-70.  Back to cited text no. 6
7.Flanagan AM, Tinkler SM, Horton MA, Williams DM, Chambers TJ. The multinucleate cells in giant cell granulomas of the jaws are osteoclasts. Cancer 1988;62:1139-45.  Back to cited text no. 7
8.Tiffee JC, Aufdemorte TB. Markers for macrophage and osteoclast lineages in giant cell lesions of the oral cavity. J Oral Maxillofac Surg 1997;55:1108-12.  Back to cited text no. 8
9.Lombardi T, Bischof M, Nedir R, Vergain D, Galgano C, Samson J, et al. Periapical central giant cell granuloma misdiagnosed as odontogenic cyst. Int Endod J 2006;39:510-5.  Back to cited text no. 9
10.Martin LR. Systematic approach to endodontic diagnosis-a must! A case report. Clin Prevent Dent 1982;4:25-7.  Back to cited text no. 10
11.Sykaras SN. Central giant cell granuloma: Report of a case. Int Endod J 1981;14:185-7.  Back to cited text no. 11
12.Glickman GN. Central giant cell granuloma associated with a non-vital tooth: A case report. Int Endod J 1988;21:224-30.  Back to cited text no. 12
13.Seifi S, Fouroghi R Central Giant Cell Granuloma: A potential endodontic misdiagnosis Int Endo J 2009;4:4.  Back to cited text no. 13
14.Ortega A, Fariña V, Gallardo A, Espinoza I, Acosta S. Nonendodontic periapical lesions: A retrospective study in Chile. Int Endod J 2007;40:386-90.  Back to cited text no. 14


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]


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