Neha Solunke* 1
Shivani Tawade 2
The oral mucosa is constantly subjected to multiple endogenous and exogenous influences, rendering it vulnerable to a broad range of pathological alterations that may be developmental, reactive, inflammatory, or neoplastic in nature. ¹ Gingival enlargement is a common clinical presentation associated with gingival disorders and has historically been described using terminology such as gingival hyperplasia and hypertrophic gingivitis. The term hyperplasia denotes an increase in the number of cells resulting in tissue overgrowth, whereas hypertrophy refers to enlargement caused by an increase in the size of individual cells. ² Reactive hyperplastic lesions represent some of the most frequently observed conditions within the oral cavity, aside from dental caries and periodontal or periapical inflammatory pathologies. ³ These lesions generally arise as a consequence of sustained low-grade trauma or chronic local irritation. Contributing factors include masticatory forces, food lodgment, dental calculus, fractured teeth, and iatrogenic sources such as improperly extended denture borders and overhanging restorations. ³ Among these conditions, fibrous hyperplasia—whether associated with removable prostheses or occurring independently—accounts for the largest proportion of cases. In addition, reactive lesions affecting the gingiva and alveolar mucosa, including inflammatory gingival hyperplasia, pyogenic granuloma, peripheral giant cell lesion, and peripheral cemento-ossifying fibroma, constitute the second most prevalent category. ⁴ Despite similarities in causative factors, variations in tissue response lead to distinct histopathological characteristics. Although clinical assessment and radiographic evaluation contribute to the diagnostic process, microscopic examination remains the gold standard for definitive diagnosis. Gingival enlargement may also develop secondary to chronic inflammatory changes marked by edema, discoloration, and cellular infiltration due to persistent plaque accumulation; such conditions typically respond to conventional periodontal therapy.⁵ Conversely, lesions demonstrating a pronounced fibrotic component and lacking spontaneous regression often necessitate surgical management.⁵ Inadequate oral hygiene practices and continuous mechanical irritation from defective restorative or orthodontic appliances are significant predisposing factors in the development of inflammatory fibrous hyperplasia.⁶
Case Report
A middle-aged male patient presented with the chief complaint of a painless enlargement of the gingiva in the maxillary posterior region, which had progressively increased in size over a period of several months. The patient’s medical history did not reveal any relevant systemic conditions. Intraoral examination demonstrated inadequate oral hygiene, the presence of multiple dental caries, and a clearly demarcated sessile gingival mass located in the posterior maxillary region (Figure 1). The lesion appeared erythematous and exhibited a firm consistency on palpation. Local irritative factors were noted in proximity to the growth. Considering the clinical presentation, a provisional diagnosis of inflammatory fibrous hyperplasia was established. Initial therapy consisted of professional oral prophylaxis along with removal of contributing local factors. The lesion was then completely excised under local anesthesia. The surgical specimen was forwarded for histopathological analysis, which verified the diagnosis of inflammatory fibrous hyperplasia. Postoperative recovery was satisfactory without complications. The patient received detailed instructions regarding maintenance of optimal oral hygiene. Follow-up evaluation revealed no evidence of recurrence.
Treatment
Management was initiated with a non-surgical phase aimed at controlling local inflammation. The patient received comprehensive oral hygiene instructions along with professional scaling and root planing to eliminate plaque and calculus deposits. ³ This phase led to partial improvement in gingival inflammation; however, the enlargement persisted and did not regress completely. Consequently, surgical intervention was planned. Routine hematological investigations were performed preoperatively to assess the patient’s fitness for the procedure. The patient was reinforced with oral hygiene measures and scheduled for surgical excision three days later. ³
Surgical Procedure
Local anesthesia was achieved using an inferior alveolar nerve block with 2% lignocaine containing 1:200,000 adrenaline. ³ The base and extent of the lesion were carefully evaluated with a William’s periodontal probe to determine the appropriate excision margins. ³ Complete removal of the lesion was performed using a No. 15 surgical blade, proceeding from the coronal aspect toward the apical region.³ Following excision, the operative field was thoroughly inspected to confirm complete removal of the lesion and to reduce the likelihood of recurrence.³ Residual calculus deposits were eliminated, and meticulous root planing was carried out to remove any remaining irritants. ³ Gingivoplasty was subsequently performed to re-establish physiologic gingival architecture. ³ A periodontal dressing was placed over the surgical site and maintained for one week. ³ Postoperative care instructions included avoidance of spicy foods and application of external cold compresses in case of swelling. Warm saline rinses were advised to begin 24 hours after surgery, to be performed three to four times daily. In addition, a 0.2% chlorhexidine mouth rinse was prescribed twice daily for one week starting the day after the procedure. ³ the patient was prescribed antibiotics (NovaMox CV-625) and analgesics (Combiflame) three times daily for three days. At the one-week follow-up visit, healing was satisfactory, and periodic reviews were scheduled to monitor for recurrence. ³ the excised tissue specimen measured approximately 1.8 × 1.4 × 0.8 cm, exhibited a reddish-pink appearance, and had a firm consistency. It was submitted for histopathological examination. ³
Histopathology
Microscopic examination demonstrated stratified squamous epithelium exhibiting areas of epithelial thickening along with focal parakeratosis. The underlying connective tissue stroma showed dense, irregularly arranged collagen bundles. Numerous spindle-shaped fibroblasts were evident, suggestive of active fibrous tissue proliferation. A moderate chronic inflammatory infiltrate, predominantly composed of lymphocytes and plasma cells, was observed within the connective tissue, indicating ongoing inflammatory activity. No evidence of cellular atypia or malignant change was identified. These histopathological features were consistent with inflammatory fibrous hyperplasia, confirming the lesion as a reactive overgrowth secondary to chronic irritation.
DISCUSSION
Inflammatory fibrous hyperplasia represents a non-neoplastic, reactive enlargement of the oral mucosa that arises secondary to persistent mechanical irritation or chronic low-grade trauma. Contributing factors commonly include inadequate oral hygiene, accumulation of plaque and calculus, and irritation from defective restorations or prosthetic appliances. ³ In the present case, poor plaque control and the presence of multiple carious teeth were probable contributing factors in the development of the lesion. Clinically, such lesions are generally characterized by firm, non-tender gingival masses, which correlated with the findings observed in this patient. Establishing a definitive diagnosis requires histopathological evaluation to distinguish this entity from other lesions with comparable clinical appearances. The microscopic features noted in this case—dense collagenous connective tissue, active fibroblastic proliferation, and chronic inflammatory cell infiltration—are typical of inflammatory fibrous hyperplasia. The lack of dysplastic changes or cellular atypia further confirms the benign and reactive nature of the condition. Effective management requires a comprehensive strategy. Initially, local inflammatory factors must be controlled through professional debridement and reinforcement of oral hygiene practices. When fibrotic tissue persists despite conservative measures, complete surgical excision becomes necessary. ³ Thorough removal of the lesion along with elimination of etiological factors is essential to reduce the likelihood of recurrence. Furthermore, patient awareness and consistent follow-up appointments play a crucial role in maintaining periodontal health and evaluating postoperative healing.
CONCLUSION
This case highlights the clinical significance of identifying inflammatory fibrous hyperplasia as a reactive overgrowth resulting from sustained irritation within the oral environment. Accurate diagnosis depends on careful clinical evaluation supplemented by histopathological confirmation. Management involves elimination of local irritants through non-surgical therapy, followed by surgical excision of residual fibrotic tissue when required. Maintenance of optimal oral hygiene and regular monitoring are fundamental to preventing recurrence and ensuring favorable treatment outcomes.
Source of Funding
None.
Conflict of Interest
None.
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10.5281/zenodo.19597970