Fibroepithelial Hyperplasia: A Case Report

Fibroepithelial hyperplasia is a reactive lesion of the oral cavity, commonly found in the interdental papilla. It is believed to result from chronic, low-grade irritation caused by microbial plaque, trauma, and other irritants. Classified as a non-neoplastic lesion, its enlargement can lead to aesthetic and functional concerns, including difficulty in chewing and challenges in maintaining oral hygiene, further exacerbating the hyperplastic tissue. This case report represents fibroepithelial hyperplasia in a 35-year-old female patient who reported with a painless growth persisting for 1.5 years in the maxillary anterior region.

Introduction

The oral mucosa is continuously exposed to various external and internal stimuli, leading to a broad spectrum of developmental, inflammatory, reactive, and neoplastic conditions. Reactive proliferations manifest clinically and histologically as non-neoplastic nodular swellings, often resulting from chronic and repeated tissue injury [1]. These proliferative responses may regress upon elimination of the underlying irritant. However, due to their overlapping clinical presentations, diagnosing reactive lesions may become challenging. Such lesions are frequently triggered by local irritants, including dental plaque, calculus, masticatory forces, defective restorations, and iatrogenic factors [2]. Bhaskar and Jacoway classified reactive gingival lesions as: pyogenic granuloma, peripheral giant cell granuloma, fibrous hyperplasia, and peripheral fibroma with calcification [3].

Method and Results

Case Report

A 35 years old female patient presented to the Department of Periodontology with a chief complaint of swelling in the left anterior maxillary region persisting for 1.5 years (Fig. 1). Additionally, she reported an increasing interdental space in the same region, affecting her esthetics. Initially, the lesion appeared as a small, painless growth; progressively enlarging to its current size.

Fig. 1. Preoperative intraoral picture showing fibrous growth between teeth # 22 and 23.

Her medical history was non-contributory, and extraoral examination revealed no abnormalities. Intraorally, she exhibited fair oral hygiene with moderate gingival inflammation near the affected teeth. A probing pocket depth (PPD) of 5 mm was recorded at the distoproximal surface of tooth #22 and the mesioproximal surface of tooth #23, whereas other sites showed a PPD of 3–4 mm. The clinical attachment level (CAL) was 5 mm in the same region. The lesion was sessile, ovoid, pinkish with a finely pebbled surface. It measured approximately 3 mm buccolingually and 3 mm mesiodistally. It was firm, non-reducible, and non-compressible with slight bleeding on probing.

Intraoral periapical radiographs revealed a radiolucent area in the interproximal region of teeth #22 and #23, with an interdental space measuring 4 mm (Fig. 2). Full-mouth scaling and root planing were performed, with particular emphasis on the affected site. The patient underwent routine blood investigations, all of which were within the normal range.

Fig. 2. Preoperative intraoral periapical radiograph showing radiolucency between teeth #22 and 23.

Under local anesthesia, an excisional biopsy was performed. A No. 12 blade was used to make an incision around the lesion, followed by a crevicular incision around teeth #22 and #23 on both the labial and palatal aspects. The flap was reflected, and the interdental fibrous tissue along with granulation tissue was excised (Figs. 3a and 3b). Subgingival calculus was meticulously removed through root planing. The excised tissue was preserved in 10% formalin, and the surgical site was irrigated with betadine before repositioning the flap. Silk sutures were placed interdentally.

Fig. 3. Immediate postoperative pictures after removal of growth.

Postoperatively, the patient was prescribed Brufen (400 mg) and Amoxicillin (500 mg) three times daily for three days. Standard postoperative instructions were provided. The excised tissue was sent for histopathological examination.

At the one-week follow-up visit, suture removal revealed uneventful healing (Figs. 4a and 4b). The patient was advised to resume brushing. Follow-up assessments over a six-month period showed no signs of recurrence, with no reported pain or regrowth. PPD was reduced to 3 mm interproximally between teeth #22 and #23, and the interdental space remained unchanged (4 mm) (Fig. 5a). Intraoral periapical radiograph revealed no further bone loss in the same region (Fig. 6).

Fig. 4. Intraoral pictures showing healing following suture removal on 8^th day.

Fig. 5. Intraoral pictures after 6 months follow-up.

Fig. 6. Intraoral periapical radiograph after six months follow-up.

Histopathological Findings

Microscopic analysis of the excised tissue revealed multiple soft tissue fragments composed of hyperplastic parakeratinized stratified squamous epithelium overlying a fibrocellular stroma. The stroma exhibited irregularly arranged thick collagen bundles, numerous small to medium-sized compressed blood vessels, and extravasated red blood cells (RBCs). These findings were consistent with a diagnosis of fibroepithelial hyperplasia.

Discussion

Gingival tissues frequently respond to chronic irritation by forming localized overgrowths, historically referred to as “epulis”. This reactive hyperplastic inflammatory condition is considered non-neoplastic. The histologic classification of hyperplastic gingival lesions remains complex, with the exception of the peripheral giant cell granuloma, which exhibits distinct features. Shafer, Hine, and Levy argued that the term epulis is inadequate as it fails to describe the histopathological characteristics of the lesion [4]. Cooke introduced the term fibroepithelial polyp, defining it as the mature stage of a fibrous or giant cell epulis [5]. Daley et al. further categorized fibromas into peripheral fibroma and peripheral fibroma with calcification [6].

The lesion in this case represents a reactive, non-neoplastic growth unrelated to drug-induced factors. It typically arises in the interdental papilla due to irritation of periodontal ligament fibers. Due to its slow growth and mild symptoms, these lesions often go unnoticed until they interfere with oral hygiene or esthetics. Although generally asymptomatic, these lesions may become ulcerated due to repetitive trauma.

Some researchers suggest that hyperplastic gingival lesions represent different stages of a single pathological process. Chronic irritation in a localized area may lead to mesenchymal cell proliferation, initially manifesting as a pyogenic granuloma, which may progress into a calcifying fibroblastic granuloma or a fibroepithelial polyp. While the precise etiology remains uncertain, contributing factors include individual susceptibility, local irritants, and certain medications [7].

The enlargement of such lesions may lead to esthetic concerns, speech difficulties, impaired mastication, and compromised oral hygiene, all of which may have psychological repercussions. Clinically, these lesions present as raised masses, either pedunculated or sessile, with a smooth or slightly roughened surface. Their color generally matches the surrounding gingiva, although variations exist. These lesions constitute approximately 2% of all oral tumors and 9% of gingival overgrowths [8].

Daley et al. hypothesized that pyogenic granuloma may undergo gradual transformation into fibrous hyperplasia [9]. Al-Rawi reported that fibrous hyperplasia shares a strong predilection for females and occurs in similar age groups and anatomical locations as gingival pyogenic granuloma [10]. This supports the theory that fibrous hyperplasia represents the fibrous maturation of pyogenic granuloma in chronic cases. Some reports also highlight the role of certain medications in inducing hyperplastic gingival overgrowth, although drug-induced cases are considered an exaggerated response rather than a distinct pathological entity [11].

Differential diagnosis is crucial for the appropriate diagnosis and management of reactive hyperplastic gingival lesions. These must be clinically and histologically distinguished from other entities, including pyogenic granuloma, which predominantly affects females and occurs most frequently between the second and fourth decades of life [12]. Peripheral fibroma with calcification shares clinical similarities with pyogenic granuloma however, the former primarily affects younger individuals and has a predilection for the anterior maxillary gingiva [13]. Fibrous hyperplasia is more common in older individuals [12].

Management involves thorough oral prophylaxis, root planing and elimination of the underlying irritant. Surgical excision with a deep incision is often required. Regular follow-up and strict oral hygiene maintenance are essential to prevent recurrence [14].

Conclusion

Reactive gingival hyperplasia arises as a response to chronic gingival irritation of varying intensities. Accurate clinical and histopathological evaluation is imperative for precise diagnosis and treatment planning. Systemic conditions should also be considered, as oral lesions may reflect underlying systemic diseases. Initial management includes phase I therapy, while persistent lesions necessitate surgical intervention. Long-term follow-up is strongly recommended due to the potential for recurrence.