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CASE REPORT |
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Year : 2017 | Volume
: 8
| Issue : 1 | Page : 41-45 |
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Peripheral ossifying fibroma: A case report and brief review
Meyyappan Arunachalam1, Thalaimalai Saravanan2, KR Shakila2, Noorulla Anisa2
1 Department of Oral Pathology and Microbiology, Karpaga Vinayaga Institute of Dental Sciences, Kanchipuram, Tamil Nadu, India 2 Department of Oral Medicine and Radiology, Karpaga Vinayaga Institute of Dental Sciences, Kanchipuram, Tamil Nadu, India
Date of Web Publication | 30-Mar-2017 |
Correspondence Address: Meyyappan Arunachalam No. 19, Siva Shanmugam Street, West Tambaram, Chennai - 600 045, Tamil Nadu India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0976-433X.203485
Gingival growths are one of the most frequently encountered lesions in the oral cavity. Most of these lesions are innocuous, but some do have malignant potential. Different lesions with similar clinical presentations make it difficult to arrive at a correct diagnosis. One of the infrequently occurring gingival lesions is peripheral ossifying fibroma (POF) which is a reactive gingival overgrowth occurring frequently in the anterior maxilla. Lesions with histological features similar to POF have been given various names, adding to the confusion. Exuberant connective tissue response to chronic irritation due to plaque, calculus, restorative, or orthodontic appliances are thought to be responsible for the initiation of the lesion. Moreover, persistent irritation can cause metaplasia of the mesenchymal cells resulting in calcifications. The diagnosis is often challenging as the lesion masquerade as other reactive lesions of gingiva. This article describes a case of POF in a 29-year-old male in an unusual location with rare involvement of bone. Clinical, radiographic, and histologic characteristics are discussed and recommendations regarding differential diagnosis, treatments are provided. Keywords: Gingiva, ossifying fibroma, peripheral ossifying fibroma
How to cite this article: Arunachalam M, Saravanan T, Shakila K R, Anisa N. Peripheral ossifying fibroma: A case report and brief review. SRM J Res Dent Sci 2017;8:41-5 |
How to cite this URL: Arunachalam M, Saravanan T, Shakila K R, Anisa N. Peripheral ossifying fibroma: A case report and brief review. SRM J Res Dent Sci [serial online] 2017 [cited 2023 Mar 28];8:41-5. Available from: https://www.srmjrds.in/text.asp?2017/8/1/41/203485 |
Introduction | |  |
Many types of localized reactive lesions may occur on the gingiva, including focal fibrous hyperplasia, pyogenic granuloma, peripheral giant cell granuloma (PGCG), and peripheral ossifying fibroma (POF). These lesions may arise as a result of such irritants as trauma, microorganisms, plaque, calculus, restorations, and dental appliances.[1],[2],[3]
POF is a nonneoplastic enlargement of gingiva that is classified as a reactive hyperplastic inflammatory lesion, a common gingival growth, which is typically seen on the interdental papilla and is believed to comprise about 9% of all gingival growths.[4]
POF appears as a slow growing solitary mass which is usually sessile with a smooth or ulcerated surface. Adjacent teeth are usually unaffected, but in some cases, migration, mobility, and delay in the eruption of permanent teeth may occur.[5]
As POF occurs usually in the gingiva which is close to the periodontal ligament (PDL), origin is thought to be from the PDL. However POF is not a counterpart of the central ossifying fibroma (COF) but a reactive lesion of the gingiva.
Ossifying fibroma occurs mostly in craniofacial bones and is generally categorized into two types: Central and peripheral. The central type of ossifying fibroma arises from the endosteum or the PDL adjacent to the root apex and expands from the medullary cavity of the bone. On the other hand, the peripheral type shows a contiguous relationship with the PDL, occurring solely on the soft tissues overlying the alveolar process.[6],[7]
In 1982, Gardner coined the term “POF” for a lesion that is reactive in nature and is not the extraosseous counterpart of a COF of the maxilla and mandible.[3]
The purpose of this article is to present a case of POF, briefly review the current literature on this condition and emphasize the importance of discussion of a reasonable differential diagnosis with the patient.
Case Report | |  |
A 29-year-old male patient reported to the Department of Oral Medicine and Radiology, Karpaga Vinayaga Institute of Dental Sciences, Maduranthakam, Tamil Nadu, with the complaint of swelling of the gums near upper left back tooth region for the past 3 years. The swelling started as small nodule that progressed gradually to the present size. There was no relevant family and medical history and patient did not give any history of trauma, injury, or food impaction. On intraoral examination, a well-defined growth was present in relation to 24, 25, 26 measuring about 2 cm × 2 cm in diameter extending from distal aspect of 23 to 26 along the occlusal and palatal surface [Figure 1] and [Figure 2]. On palpation, swelling was nontender, sessile, and soft in consistency. Radiographic examination in the region of 24, 25, 26 reveals the presence of irregular radiopacity evident in the mesial aspect of 24 and distal aspect of 25 with areas of cuffing evident in crestal region between 25 and 26 [Figure 3]. Based on the history, clinical examination and investigations, the case was provisionally diagnosed as POF. The differential diagnosis considered were PGCG and pyogenic granuloma. Under local anesthesia, excisional biopsy was performed using scalpel [Figure 4] and the tissue was submitted to the Department of Oral Pathology for histopathological investigations. Histologically, the tissue section revealed hyperkeratinized stratified squamous epithelium with fibro vascular connective tissue. The epithelium showed slender rete ridges with atrophy in some areas. The connective tissue exhibited reticular arrangement of collagen bundles interrupted with vital bone. The section also showed numerous dilated capillaries [Figure 5]. On the basis of clinical, histopathological, and radiographic examination, the diagnosis of POF was given. The patient presented for a follow-up examination 15 days postoperatively. The surgical site appeared to be healing well. | Figure 1: A well-defined growth in relation to 24, 25, 26 extending from distal aspect of 23 to distal aspect of 26 along the occlusal and palatal surface
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 | Figure 2: A well-defined growth in relation to 24, 25, 26 extending from distal aspect of 23 to distal aspect of 26 along the occlusal and palatal surface
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 | Figure 3: Radiographic examination reveals presence of irregular radiopacity evident in the mesial aspect of 24 and distal aspect of 25 with areas of cuffing evident in crestal region between 25 and 26
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 | Figure 5: Histological section revealing hyperkeratinized stratified squamous epithelium with fibro vascular connective tissue. The epithelium showing slender rete ridges and connective tissue exhibiting reticular arrangement of collagen bundles interrupted with vital bone
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Discussion | |  |
In 1982, Gardner coined the term POF for a lesion that is reactive in nature and is not the extraosseous counterpart of a COF of the maxilla and mandible.[3]
Intraoral ossifying fibromas have been described in the literature since the late 1940s. Many names have been given to similar lesions, such as epulis, peripheral fibroma with calcification, POF, calcifying fibroblastic granuloma, peripheral cementifying fibroma, peripheral fibroma with cementogenesis and peripheral cemento-ossifying fibroma. The sheer number of names used for fibroblastic gingival lesions indicates that there is much controversy surrounding the classification of these lesions.[8],[9]
It has been suggested that the POF represents a separate clinical entity rather than a transitional form of pyogenic granuloma, PGCG, or irritation fibroma.[1]
Eversole and Rovin [2] stated that, with the similar sex and site predilection of pyogenic granuloma, PGCG and POF, as well as similar clinical and histologic features, these lesions may simply be varied histologic responses to irritation.
Gardner [3] stated that POF cellular connective tissue is so characteristic that a histologic diagnosis can be made with confidence, regardless of the presence or absence of calcification.
Buchner and Hansen [10] hypothesized that early POF presents as ulcerated nodules with little calcification, allowing easy misdiagnosis as a pyogenic granuloma.
Ossifying fibroma elaborates bone, cementum, and spheroidal calcifications, which has given rise to various terms for these benign fibro-osseous neoplasms. When bone predominates, ossifying is the appellation, while the term “cementifying” has been assigned when curvilinear trabeculae or spheroidal calcifications are encountered. When bone and cementum like tissue are observed the lesions have been referred to as cemento-ossifying fibroma. Cementifying fibromas may be clinically and radiographically impossible to separate from ossifying fibromas.[2],[11]
The term cementossifying is outdated and scientifically inaccurate, because clinical presentation and histopathology of cemento-ossifying fibroma are the same in areas where there is no cementum, such as skull, femur, and tibia they are all ossifying fibromas. Those that happen to occur in the jaws should not be termed cemento-ossifying fibromas merely because of teeth. Moreover, there is no histologic or biochemical differences between cementum and bone.[12],[13]
Although the etiopathogenesis of POF is uncertain, an origin from cells of PDL has been suggested. The reasons for considering PDL origin for POF include exclusive occurrence of POF in the gingival (PDL), the proximity of gingiva to the PDL and the presence of oxytalin fibers within the mineralized matrix of some lesions. Excessive proliferation of mature fibrous connective tissue is a response to gingival injury, gingival irritation, sub gingival sulcus, or a foreign body in the gingival sulcus. Chronic irritation of the periosteal and periodontal membrane causes metaplasia of the connective tissue with resultant initiation of bone formation and dystrophic calcification. Rare manifestation of multicentric lesion in recent times point toward a possible role of genetics in the etiopathogenesis of this disease. Multicentric lesion present in the oral cavity are not typical, but have been observed in the conditions such as nevoid basal cell carcinoma syndrome (multiple odontogenic keratocysts), multiple endocrine neoplasia type 11 (multiple neuromas), neuro fibromatosis (multiple neuro fibromas), and Gardners syndrome (multiple neoplasms), all of these conditions have been associated with inherited genetic mutations so the potential exists that POF can also be due to genetic mutations that predisposes to gingival soft tissue overgrowths that contain mineralized product or ossification.[14]
Clinically, POF appears as a solitary nodular mass that is either pedunculated or sessile. The surface mucosal color ranges from red to pink, and the surface is frequently ulcerated. The mass usually arises from the interdental papilla. Lesions occur slightly more frequently in the maxillary arch (60%) and the incisor cuspid region (50%).[15] Whereas, in our present case, the lesion was associated with upper posteriors.
Although they are generally <2 cm in diameter, size can vary; reports range from 0.2 to 3.0 cm to 4–8 cm and some lesions may be as large as 9 cm in diameter.[10] The cases of tooth migration and bone destruction have been reported, but these are not common.[16]
POF tends to occur in the first and second decades of life, with peak prevalence between the ages of 10 and 19. The female to male ratio reported in the literature varies from 1.22:1 and 1.7:1 to 4.3:1.[17]
Hormonal influences may play a role, given the higher incidence of POF among females, increasing occurrence in the second decade, and declining incidence after the third decade.[18]
Radiographically, POF may not show significant changes in certain cases. However, some cases show varying radiodensity within the lesion, depending on the degree of mineralization. Superficial bone loss, cupping defect, and focal areas calcification have been rarely reported like in the present case which showed involvement of bone with cuffing defect. Additional investigations such as computed tomography and magnetic resonance imaging are also helpful in larger lesions.[19],[20]
Clinical differential diagnosis for gingival growths includes fibroma, peripheral giant cell granuloma, pyogenic granuloma, peripheral odontogenic fibroma, and POF. The definitive diagnosis of POF is made by the histologic evaluation of biopsy specimen. Histologically, the key feature of this lesion is exceedingly cellular mass of connective tissue comprising large number of plump, proliferating fibroblasts intermingled throughout with delicate fibrillar stroma. Buchner and Hansen [10] observed that the mineralized tissues observed in POF can be of three basic types: (1) Bone that may be woven, lamellar or trabecular, sometimes surrounded by osteoid, (2) cementum– like material that appears as spherical bodies resembling cementum or large acellular round– to– oval eosinophilic bodies, which seemed to have coalesced to form islands in various sizes and shapes, (3) dystrophic calcification, which can range from small clusters of minute basophilic granules or tiny globules to large, solid irregular masses.
Treatment of these lesions is complete surgical excision as was performed in the present case. Proper excision and aggressive curettage of the adjacent tissues is required for prevention of recurrence. The recurrence rate (8%–20%) of POF has been considered high for reactive lesions and it probably occurs due to incomplete initial removal, repeated injury, or persistence of the local irritants.[18],[21]
Conclusion | |  |
POF is a slow growing lesion with a limited growth potential. Many cases will progress for a long period before patients seeks treatment due to its asymptomatic nature as in our case. Etiopathogenesis of POF still remains unclear although origin from PDL is considered, recent reports of multicentric lesions also goes in favor of genetic involvement. Unfortunately, little is known in respect to molecular or genetic profile of these lesions; therefore, further analysis like karyotyping may give insight into chromosomal or genetic abnormalities that could be present and whether or not they are constitutional and can be passed to offspring. Close postoperative follow up is required because of its high recurrence rate in incompletely removed lesions.
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Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
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