Abstract

Oral pyogenic granuloma (OPG) is a reactive vascular lesion that may worsen during orthodontic treatment due to biofilm-induced inflammation. This clinical case describes the surgical and mucogingival management of an OPG associated with fixed orthodontic appliances in an adolescent patient. A 12-year-old male patient presented with an oval, pedunculated lesion with a smooth surface and soft consistency, measuring approximately 8.5 × 6.5 mm, located on the attached gingiva adjacent to tooth #21. Therapeutic management consisted of complete surgical removal of the lesion under local anesthesia; additionally, mucogingival management was performed via partial dissection, lateral displacement, and coronal advancement of the tissue to promote preservation of the gingival architecture. Histopathological examination confirmed the diagnosis of OPG. Adequate healing was observed during clinical follow-up. This case highlights the importance of identifying reactive gingival lesions in young patients with fixed orthodontic appliances, in whom inflammatory and hormonal factors may play a parallel role.

Introduction

Oral pyogenic granuloma (OPG) is a reactive vascular and granulation tissue hyperplasia that primarily affects gingiva, most commonly in the upper jaw [1–3]. This condition may occasionally be found in areas such as the oral mucosa, lips, or tongue [4, 5]. Although OPG affects people of all ages, recent studies show a higher recurrence rate in children and adolescents due to hormonal surges during development and external irritants [6–9].

The success of OPG treatment does not depend exclusively on the use of precise techniques for excision of the lesion and its histopathological analysis [4, 7, 9]; it is also necessary to restore the gingival architecture, allowing the patient to regain both the health and aesthetics of their smile in the long term [10, 11]. The aim of this case report is to describe the surgical and mucogingival management of an OPG associated with fixed orthodontic appliances in an adolescent patient.

Case report

A 12-year-old male patient with no history of medical conditions, currently undergoing orthodontic treatment and suffering from generalized gingivitis associated with dental plaque, visited the dental clinic with the following complaint: “I have a red spot on my gingiva.”

Intraoral examination revealed an increase in mucogingival tissue volume on the attached gingiva, appearing erythematous, oval, lax, smooth, and without signs of active ulceration, measuring approximately 8.5 × 6.5 mm. The lesion originated in the masticatory mucosa medial to the vestibular surface of tooth #21, presenting a pedunculated base that extended from mesial to distal to that tooth (Fig. 1A–C). No significant radiographic findings were observed (Fig. 2).

For image description, please refer to the figure legend and surrounding text.
Figure 1

(A) Frontal view of the intraoral lesion: Growth of mucogingival tissue on the attached gingiva, appearing firm, oval, fibrous, and smooth, with no signs of active ulceration. (B) Right lateral view of the lesion. (C) Left lateral view of the lesion.

For image description, please refer to the figure legend and surrounding text.
Figure 2

Periapical radiograph of tooth #21. No signs of bone pathology are observed.

The surgical procedure was aimed at the complete removal of the hyperplastic lesion, with the goal of obtaining a definitive diagnosis and, simultaneously, eliminating the pathological tissue. Under aseptic and antiseptic conditions, local anesthesia was administered using 4% articaine with epinephrine 1:100 000. Subsequently, using a No. 15c scalpel blade, the base of the hyperplastic tissue was resected up to the mesial and distal angles of tooth #21, ensuring adequate margins to guarantee complete removal of the lesion. Next, bone preparation was performed using a Gracey mini-five ½ curette (Fig. 3). The removed tissue was placed in 10% formalin and sent for histopathological examination. To achieve primary healing, an oblique incision was made from mesial to distal of tooth #11 along the mucogingival line, and partial dissection was performed to laterally displace the mucosal tissue. Simultaneously, the mucosa was advanced coronally over the defect toward the cementoenamel junction of tooth #21 via partial dissection. Once the tissue was released, it was positioned over the wound with 6-0 nylon sutures using simple stitches, and a Cornick suture was placed in the fundus of the pouch to ensure the stability of the repositioned tissue and primary healing of the wound (Fig. 4). Pain medication (ibuprofen 400 mg every 8 h as needed) was prescribed, along with rinses using 0.12% chlorhexidine for one minute, twice daily, for 15 days.

For image description, please refer to the figure legend and surrounding text.
Figure 3

Resection of the base of the hyperplastic tissue and bone shaping using Gracey mini-five ½ curettes.

For image description, please refer to the figure legend and surrounding text.
Figure 4

Lateral and coronal repositioning of the mucosal tissue on the buccal surface of tooth #21 using 6-0 nylon simple sutures and a 5-0 nylon Cornick suture.

The definitive diagnosis was an OPG (Figs 5 and 6). At the 15-day follow-up, adequate primary healing and favorable soft tissue recovery were observed. The sutures were removed without signs of inflammation, infection, or complications (Fig. 7).

For image description, please refer to the figure legend and surrounding text.
Figure 5

Histological section stained with hematoxylin and eosin (H&E, 10×). The lesion is lined by a non-keratinized stratified squamous epithelium, which shows marked spongiosis and leukocyte migration; beneath it, there is a severe diffuse inflammatory infiltrate.

For image description, please refer to the figure legend and surrounding text.
Figure 6

Histological sections stained with H&E (40×). Granulation tissue consisting of blood capillaries, some of which are congested, active fibroblasts, loose and irregularly compacted collagen fibers, and a severe, chronic, diffuse inflammatory infiltrate with a predominance of lymphoplasmacytic cells.

For image description, please refer to the figure legend and surrounding text.
Figure 7

Healing at 15 days.

Discussion

OPG is a reactive proliferative condition that can occur at any stage of life. Adolescence is a stage in which this condition is not merely an accidental lesion but can become the response of “hormone-sensitive” gingival tissue to mechanical irritation [4, 11]. Consequently, the endocrine changes characteristic of puberty has an impact by exacerbating the inflammatory and angiogenic mechanisms associated with the development and progression of OPG.

During male puberty, increased testosterone may play a role in modulating the behavior of gingival tissue in the presence of dental biofilm, leading to an exacerbated inflammatory process. This mechanism may promote increased blood vessel permeability, inflammatory infiltration, and elevated levels of cytokines such as IL-1β, IL-6, IL-8, TNF-α, and prostaglandin E2, thereby facilitating leukocyte recruitment, vasodilation, and destruction of extracellular connective tissue [1, 12]. This inflammatory microecosystem is linked to increased levels of growth factors such as VEGF, FGF/bFGF, and angiopoietins, which trigger uncontrolled angiogenesis, endothelial cell proliferation, and excessive granulation tissue formation in response to even the slightest stimulus [4, 6]. In adolescent males, this biological vulnerability is present in fixed orthodontic appliances; consequently, the situation becomes critical, as brackets act as traps for biofilm and dental calculus, as well as causing recurrent mechanical microtrauma.

When comparing this clinical case with previous ones, we undoubtedly find quite clear clinical similarities: the preferred location, especially in the maxilla, as well as the therapeutic approach involving surgical excision [4, 13, 14]. However, there are some significant variations: first, the size can increase progressively over a matter of weeks, and bleeding is usually profuse at the slightest touch due to the high density of capillaries. These variations depend directly on the intensity of the hormonal stimulus and the duration of the irritant [7].

The therapeutic management of oral gingivitis must be thorough and precise; therefore, both the removal of the lesion and the elimination of local irritants such as plaque and dental calculus are essential [4, 10]. Additionally, in this clinical case, advanced mucogingival surgery was indispensable, as it is the superior option because it allows for the removal of the implant base, the curettage of the hidden periosteum, the assurance of aesthetic health through primary healing, the restoration of gingival architecture, and the prevention of deformities in a patient who is still developing—a critical consideration in a young patient. Otherwise, the remaining cells in the gingiva may regenerate a lesion through hormonal stimulation [1, 4, 10].

The prognosis depends on an interdisciplinary approach; it is vital to educate the patient on how hormonal changes during puberty can exacerbate any lapses in oral hygiene and to help them understand that their own endocrine development makes them vulnerable. Prevention involves not only maintaining oral hygiene but also neutralizing irritants so that the gums can coexist with orthodontic treatment and hormones without developing permanent pathologies [4, 15].

Conclusion

In adolescent patients, the manifestation of OPG associated with orthodontic treatment is highly complex, as it involves hormonal, inflammatory, and mechanical factors simultaneously. In the present case, comprehensive therapeutic treatment allowed for the complete removal of the lesion, its confirmation through histopathological analysis, and the preservation of periodontal architecture through favorable primary healing.

Recognizing reactive lesions in adolescent orthodontic patients is a clinical challenge. Brackets are devices that facilitate the accumulation of dental biofilm, leading to an irritative stimulus. Early diagnosis is vital because an uncontrolled lesion could interfere with tooth movement, hinder oral hygiene, and cause permanent aesthetic deformities.

Author contributions

Francisco Javier Alcaraz-Baturoni: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Methodology, Formal analysis, Conceptualization. Jessica Paola Ibarra-González: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Methodology, Formal analysis, Conceptualization. Luis Fernando López-Hernández: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Formal analysis, Conceptualization. Mario Alberto Alarcón-Sánchez: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Formal analysis, Conceptualization. Daniel Ortuño-Sahagún: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Formal analysis, Conceptualization. Artak Heboyan: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Formal analysis, Conceptualization. Juan Pablo González-Cárdenas: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Formal analysis, Conceptualization. Sarah Monserrat Lomelí-Martínez: Writing—review and editing, Writing—original draft preparation, Visualization, Validation, Supervision, Methodology, Formal analysis, Conceptualization.

Conflicts of interest

All authors report no relevant conflicts of interest for this article.

Funding

None declared.

Data availability

The data supporting the findings of this study are available from the corresponding author upon reasonable request.

Patient informed consent

The study participant provided informed written consent prior to study enrollment.

CARE Checklist (2016) statement

The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).

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