Peripheral giant cell granuloma associated with dental prostheses: A case report

Abstract

BACKGROUND

Peripheral giant cell granuloma (PGCG) is a reactive lesion of the gingiva or alveolar ridge that usually develops in response to chronic local irritation. Plaque, calculus, trauma, and periodontal inflammation are established contributors, and defective dental prostheses may intensify these effects by creating plaque-retentive areas and repeated soft-tissue injury. This article combines a focused narrative review with an illustrative case to discuss diagnosis, treatment, recurrence, and prosthodontic implications.

CASE SUMMARY

A 60-year-old man presented with a 1.0 cm × 0.5 cm palatal gingival mass beneath a three-unit ceramometal fixed dental prosthesis in the maxillary anterior region. Clinical examination, radiographic assessment, excisional biopsy, and histopathologic evaluation confirmed PGCG. Management included prosthesis removal, complete excision with curettage, and extraction of a non-restorable abutment tooth. Healing was uneventful, and no recurrence was observed at 6 months. PGCG is a reactive gingival lesion associated with chronic local irritation. This case report illustrates PGCG arising beneath a defective fixed dental prosthesis in a multifactorial inflammatory setting that also included plaque retention and periodontal breakdown. Its value lies in the practical lessons for diagnosis, differential diagnosis, complete excision, elimination of local irritants, prosthodontic redesign, and follow-up to reduce recurrence.

CONCLUSION

This case supports interpreting a defective prosthesis as a contributing local factor rather than an isolated proven cause. The report highlights the need for clinicopathologic correlation, cautious causal wording, elimination of local irritants, appropriate prosthodontic redesign when indicated, and follow-up to reduce recurrence.

Key Words: Peripheral giant cell granuloma; Dental prostheses; Fixed dental prosthesis; Reactive gingival lesion; Oral pathology; Case report

Core Tip: Peripheral giant cell granuloma is a relatively common reactive lesion of the oral cavity that arises exclusively on the gingiva or edentulous alveolar ridge. It is generally regarded as a non-neoplastic proliferation associated with chronic local irritation or trauma, likely originating from the periodontal ligament or periosteum. The report highlights the need for clinicopathologic correlation, cautious causal wording, elimination of local irritants, appropriate prosthodontic redesign when indicated, and follow-up to reduce recurrence.

INTRODUCTION

Peripheral giant cell granuloma (PGCG) is a reactive lesion that arises exclusively on the gingiva or edentulous alveolar ridge and is generally associated with chronic local irritation or minor trauma[1,2]. Clinically, it usually presents as a red to reddish-purple nodular enlargement that may be sessile or pedunculated and can resemble several other reactive or neoplastic gingival lesions. Because of this overlap in appearance, diagnosis requires correlation of the clinical presentation with radiographic and histopathologic findings[3].

Dental prostheses may contribute to a chronic inflammatory environment by promoting plaque retention, repeated soft-tissue irritation, poor cleansability, and unfavorable emergence profiles. However, prosthetic factors should be interpreted cautiously as contributory rather than isolated causes. The present case is clinically relevant because it illustrates PGCG developing beneath a defective fixed dental prosthesis in a multifactorial setting that also included periodontal inflammation and compromised abutment teeth[4].

CASE PRESENTATION

Chief complaints

A 60-year-old man presented with a painless swelling on the palatal aspect of the maxillary anterior region.

History of present illness

The patient reported that the lesion had been present for approximately 3 months. He described difficulty cleaning the area and occasional bleeding during toothbrushing. The swelling was located beneath a fixed dental prosthesis and had gradually become more noticeable, although it remained painless.

History of past illness

The medical history was significant for controlled hypertension and controlled type 2 diabetes mellitus treated with losartan and metformin. There was no reported history of systemic giant cell disease or previous similar oral lesions.

Personal and family history

The patient was a non-smoker. No relevant family history of oral tumors, metabolic bone disease, or other related conditions was reported.

Physical examination

Intraoral examination revealed a sessile, exophytic, erythematous nodular lesion on the palatal gingiva of the maxillary anterior region. The lesion measured approximately 1.0 cm × 0.5 cm, was firm on palpation, and had a lobulated surface. It was located directly beneath the pontic-connector region of a three-unit ceramometal fixed dental prosthesis extending from tooth #11 to tooth #22. The prosthesis showed marginal discrepancy, an overcontoured plaque-retentive emergence profile, and defective cervical adaptation at the abutment margins. The adjacent gingiva was inflamed and edematous (Figure 1).

Figure 1 Dental/periodontal clinical examination. A: Frontal intraoral view demonstrating the three-unit ceramometal fixed dental prosthesis (FDP) in situ and the associated marginal inflammation; B: Palatal close-up view showing the defective prosthetic margins and the exophytic lesion emerging from the gingival crevice; C: Occlusal view following removal of the FDP, revealing the exophytic palatal lesion originating beneath the ill-fitting prosthesis.

Laboratory examinations

No routine hematologic or biochemical abnormalities were documented. Because the lesion was solitary and the histopathologic findings were typical for PGCG, biochemical evaluation for hyperparathyroidism, including serum calcium, phosphate, and parathyroid hormone levels, was not pursued[5]. Histopathologic examination of the excised specimen showed a non-encapsulated lesion beneath stratified squamous epithelium with a highly cellular and vascular connective tissue stroma containing numerous multinucleated giant cells, hemorrhage, hemosiderin deposition, and inflammatory infiltrate, consistent with PGCG.

Imaging examinations

Periapical radiographs demonstrated generalized horizontal bone loss consistent with chronic periodontitis, together with severe vertical bone loss around the involved abutment teeth. Widening of the periodontal ligament space was also noted. No convincing central osteolytic lesion or distinct cup-shaped resorption was identified.

MULTIDISCIPLINARY EXPERT CONSULTATION

The case was assessed through clinicopathologic correlation involving prosthodontic/periodontal clinical evaluation, radiographic interpretation, and histopathologic examination of the excised tissue (Figure 2). This integrated assessment supported a reactive peripheral lesion rather than a primary central bony process.

Figure 2 Imaging examination. A: Periapical radiograph of the right maxillary anterior region demonstrating severe alveolar bone loss; B: Periapical radiograph of the left maxillary anterior region showing the pattern of bone loss and widening of the periodontal ligament space.

FINAL DIAGNOSIS

PGCG of the palatal gingiva associated with a defective fixed dental prosthesis in a multifactorial inflammatory setting.

TREATMENT

Treatment focused on elimination of local irritants and definitive surgical management. The fixed dental prosthesis was removed to allow full visualization of the lesion and proper assessment of the abutment teeth (Figure 3A). Under local anesthesia with 2% lidocaine containing 1:100000 epinephrine, the lesion was completely excised down to the periosteum, and the base was curetted to reduce the possibility of residual lesion tissue (Figure 3B). Tooth #22 was extracted during the same procedure because it was non-restorable and periodontally compromised. The specimen was fixed in 10% formalin and submitted for histopathologic examination (Figure 4). Postoperatively, the patient received ibuprofen 400 mg as needed, chlorhexidine gluconate 0.12% mouthwash, and oral hygiene instructions.

Figure 3 Intraoperative view and gross specimen photograph. A: Intraoperative view of the surgical site immediately following complete excision of the lesion and extraction of tooth #22; B: Gross specimen photograph of the excised lesion placed adjacent to a ruler, measuring approximately 1.0 cm.

Figure 4 Hematoxylin and eosin stained photomicrograph showing numerous multinucleated giant cells within a cellular vascular stroma (original magnification ×200). Scale bar = 100 µm.

OUTCOME AND FOLLOW-UP

At 20 days postoperatively, the surgical site showed satisfactory healing with healthy pink mucosa and no evidence of infection or residual lesion (Figure 5). A transitional acrylic removable partial denture was delivered to restore function and esthetics during healing and subsequent prosthetic planning. At 6-month follow-up, the surgical site remained clinically stable with no evidence of recurrence. The patient reported satisfactory function with the transitional prosthesis and remained under periodic review for definitive rehabilitation and maintenance.

Figure 5 Occlusal view of the maxillary arch at the 20-day postoperative follow-up appointment demonstrating complete mucosal healing.

DISCUSSION

The narrative review was structured and reported with reference to the Scale for the Assessment of Narrative Review Articles[6], and the case was documented in line with the CARE reporting guidelines[7]. PGCG should be interpreted as a reactive lesion arising within a multifactorial local inflammatory environment rather than being attributed to a single isolated cause (Table 1). In the present case, the lesion developed beneath a defective fixed dental prosthesis; however, plaque retention, gingival inflammation, periodontal destruction, and compromised abutment teeth were also present and likely contributed to lesion development (Table 2). Therefore, the prosthesis is best considered a contributory local irritative factor rather than definitive proof of causation.

Table 1 Local factors relevant to peripheral giant cell granuloma.

Category	Examples	Clinical relevance
Biofilm-related factors	Plaque, calculus, food impaction	Sustain chronic gingival inflammation
Prosthetic/restorative factors	Overhanging margins, poor marginal adaptation, rough surfaces, defective pontic design, poor emergence profile	Increase plaque retention and/or soft tissue trauma
Periodontal factors	Chronic periodontitis, deep inflammation around abutment teeth	May contribute to a reactive gingival environment
Traumatic factors	Repetitive mechanical irritation, impinging prosthetic components	Promote persistent local injury
Systemic/contextual contributors	Hormonal changes, xerostomia, impaired hygiene access	May increase susceptibility, though usually not sufficient alone

Table 2 Diagnostic considerations in gingival nodular lesions.

Lesion	Typical clinical clues	Role of histopathology
Peripheral giant cell granuloma	Red-purple gingival/alveolar ridge nodule; may ulcerate; reactive setting	Confirms multinucleated giant cells in vascular stroma with hemorrhage/hemosiderin
Pyogenic granuloma	Soft, highly vascular, bleeds easily	Distinguishes capillary granulation tissue pattern from PGCG
Peripheral ossifying fibroma	Firmer, often paler, gingival mass	Demonstrates fibrous proliferation with mineralized material
Fibroma	Firm, mucosal-colored nodule	Shows dense fibrous connective tissue
Brown tumor of hyperparathyroidism	Giant cell lesion pattern with systemic metabolic context	Requires clinicopathologic and biochemical correlation
Plasma cell gingivitis	Diffuse erythematous/plasma cell-rich gingival changes	Histology and, if needed, adjunctive workup aid exclusion of mimics
Hematologic/neoplastic lesions (e.g., plasmacytoma, leukemia-related enlargement)	Atypical appearance, systemic signs, rapid progression, or unusual site/course	Biopsy is essential; immunohistochemistry may be required

PGCG: Peripheral giant cell granuloma.

This case also highlights the importance of clinicopathologic correlation. Clinically, PGCG may resemble pyogenic granuloma, peripheral ossifying fibroma, and fibroma[8,9]; in selected situations, less common systemic or neoplastic lesions must also be considered[10,11]. Histopathologic confirmation was therefore essential. Central giant cell granuloma was also considered in the broader differential diagnosis[12], but the lesion was centered in soft tissue and radiographs did not show a convincing central osteolytic process. The observed bone loss and widening of the periodontal ligament space were more consistent with chronic periodontitis and pressure-related local effects than with a primary intraosseous giant cell lesion (Table 2).

From a therapeutic standpoint, successful management requires not only complete excision but also elimination of local irritants and appropriate prosthodontic correction. Curettage of the base and removal of compromised local factors are important because recurrence has been reported when irritants persist[13,14]. The absence of recurrence during the 6-month follow-up in this patient supports the value of combined surgical management, local debridement, and prosthetic reassessment[15] (Table 3).

Table 3 Timeline of clinical events and follow-up.

Time point	Event
Day 0	Initial clinical assessment; lesion identified beneath the defective FDP; periapical radiographs obtained; FDP removed; complete excision with curettage performed; non-restorable tooth #22 extracted during the same procedure
Day 20	Suture removal; favorable healing observed; transitional acrylic removable partial denture delivered
6 months	No clinical recurrence; continued maintenance and definitive prosthetic planning

FDP: Fixed dental prosthesis.

CONCLUSION

PGCG is a reactive gingival lesion that should be interpreted within a multifactorial setting of chronic local irritation. Defective dental prostheses may contribute to plaque retention and repeated mucosal trauma, but they should be regarded as contributory rather than sole causative factors. Accurate diagnosis depends on correlation of clinical, radiographic, and histopathologic findings. Effective management requires complete excision, elimination of local irritants, appropriate prosthodontic redesign when necessary, and follow-up to detect recurrence.

ACKNOWLEDGEMENTS

This case was managed in accordance with the ethical principles of the Declaration of Helsinki[16]. The authors thank the patient for consenting to publication of the clinical details and images. They also acknowledge the contribution of the clinical and pathology teams involved in the diagnosis and management of this case.