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| CASE REPORT |
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| Year : 2020 | Volume
: 14
| Issue : 1 | Page : 26-29 |
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Florid osseous dysplasia complicated by secondary periapical infection
N Girish Kumar1, Sumeet Sehgal2
1 Department of Oral and Maxillofacial Surgery, Army Dental Corps, New Delhi, India
2 Department of Oral Pathology and Microbiology, Army Dental Corps, New Delhi, India
| Date of Submission | 30-Dec-2019 |
| Date of Acceptance | 02-Jan-2020 |
| Date of Web Publication | 31-Jan-2020 |
Correspondence Address:
Sumeet Sehgal
200 MDC C/o 56 APO
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/JODD.JODD_11_19
Florid osseous dysplasia (FOD) is a benign fibro-osseous lesion that involves multiple quadrants of the jaws and is histopathologically characterized by the replacement of normal bone tissue by fibrous connective tissue which may contain a variable amount of bone and/or cementum like tissue. The lesion is usually asymptomatic and is mostly diagnosed with a chance finding on radiographic examination, and no treatment is necessary. However, a secondary infection may occur and cause complications in an existing FOD. We present a case of florid osseous dysplasia which was complicated by secondary infection from the adjacent tooth.
Keywords: Fibro osseous lesion, florid cement osseous dysplasia, florid osseous dysplasia
How to cite this article:
Kumar N G, Sehgal S. Florid osseous dysplasia complicated by secondary periapical infection. J Dent Def Sect. 2020;14:26-9 |
| Introduction | |  |
Florid osseous dysplasia (FOD) is a reactive osseous dysplasia rarely presenting in the jaws and belongs to the spectrum of fibro-osseous lesions and the subset of cemento osseous dysplasia. It represents an idiopathic reactive process characterized by the replacement of normal bone by poorly cellularized cementum-like materials and fibrocellular connective tissue.[1]
In the past, cases of FOD have been reported as multiple enostosis, multiple cement ossifying fibroma, multiple periapical osteofibromatosis, florid cement osseous dysplasia, and gigantiform cementoma among other names.[2],[3]
FOD is mostly asymptomatic and generally diagnosed with a chance finding on radiographic examination. However, it may become secondarily infected and progress to osteomyelitis and due to its avascular nature treatment by antibiotic therapy alone does not resolve the infection and sequestration and surgical debridement are required to remove the infected and necrotic tissue.[1]
We present a case of FOD that was diagnosed because of secondary infection from an adjacent carious tooth and which did not respond to any conservative treatment modality.
| Case Report | | |
A 52-year-old female patient presented with dull pain in the right posterior region of the jaw. Extraoral examination showed no signs and swelling was not detectable. There was no history of trauma or previous episode of pain. Intraoral examination showed a swelling which had caused the obliteration of the vestibule. It was a diffuse hard swelling extending from the region of 46–48 [Figure 1]. 47 was carious. Both 46 and 47 were tender on percussion. Mucosa over the swelling was normal. The pulp vitality tests for both 46 and 47 were altered. | Figure 1: Clinical photograph showing intra-oral swelling causing obliteration of the vestibule
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Intra oral periapical radiograph showed pulpal involvement of carious 47 and radiolucency associated with the mesial root. The periapical area of 46 showed diffuse, lobular and irregular shaped radiopacities surrounded by a well-circumscribed radiolucency [Figure 2]. | Figure 2: Intra-oral periapical radiograph X-ray showing diffuse radio opacities surrounded by a well-circumscribed radiolucency
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Computed tomography scan showed multiple mixed density lesions involving the maxilla and mandible, which were diffuse, lobular, and irregularly in shape. These lesions were seen only in the tooth-bearing areas and appeared to be attached to the root apices. The slight lingual expansion was seen posterior to the lower right first molar region [Figure 3] and [Figure 4]. | Figure 3: Coronal computed tomography scan showing mixed radiopaque and radiolucent lesions involving the maxilla
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 | Figure 4: Axial computed tomography scan showing mixed radiopaque and radiolucent lesions involving the mandible
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The blood chemistry for serum alkaline phosphatase, calcium, and phosphorus was done and was shown to be within the normal limits.
Root canal treatment of 47 was attempted with antibiotic cover for 10 days, but the pain was not relieved and tenderness in 46 persisted. Sequestration and surgical debridement were carried out, but the pain did not subside. The decision to extract both 46 and 47 was taken and the patient informed accordingly.
Excisional biopsy was performed. The histopathological findings showed young fibrous connective tissue intersected by delicate collagen fibers and plum fibroblasts. Stroma had basophilic compact masses scattered resembling immature bone, which did not show any cellular structure. Irregular basophilic cementum-like material was seen scattered throughout the lesional tissue. The soft tissue also showed a dense inflammatory infiltrate surrounding the hard tissue from the region of 46 [Figure 5] and [Figure 6]. | Figure 5: H and E stained section (×10) shows irregularly basophilic compact masses with no cellular structure
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 | Figure 6: H and E stained section (×10) shows calcified masses resembling immature bone interspersed with young fibrous connective tissue stroma
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The clinical, radiographic, biochemical, and histopathologic findings were all consistent with the diagnosis of FOD. The patient was reviewed after 2 months and was clinically normal [Figure 7]. | Figure 7: Clinically normal appearing mucosa with no significant clinical findings was seen 2 months post op
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| Discussion | | |
The term FOD was first suggested by Melrose et al. in 1976 to describe a condition of exuberant multiquadrant masses of cementum and/or bone in both jaws. The term florid was introduced to describe the widespread, extensive manifestations of the disease.[1] This disorder is unusual, and there are only 21 cases reported in the English literature in the past 10 years.[4]
The pathogenesis of FOD is unknown, and Waldron had proposed that possibly, reactive or dysplastic changes in the periodontal ligament might be a cause for this pathology,[5] which has been contradicted by Kawai et al. and the origin from medullary bone has been proposed as an alternative.[6]
The radiographic appearance of FOD varies with the degree of maturation of the lesion. The initial immature lesion appears radiolucent, the intermediate lesion is a mixed, radio-opaque and radiolucent lesion, and the later mature lesion appears as radio-opaque masses attached to root apices.[7]
FOD is a reactive fibro-osseous lesion that should be differentiated from other fibro-osseous lesions such as fibrous dysplasia, ossifying fibroma, Paget's disease, and sclerosing osteomyelitis based on a combined clinical, radiographic, and histological assessment.
Fibrous dysplasia is hamartomatous in nature, and facial disfigurement is noted at an early age. Ossifying fibroma, on the other hand, is localized and neoplastic in nature.
Paget's disease of the bone may have a cotton wool appearance. However, this condition affects the entire mandible and shows the loss of lamina dura, whereas FOD is usually seen confined to the interradicular and periapical alveolar area above the inferior alveolar canal and the lamina dura in the cervical two-thirds is normal.[8] Paget's disease is often polyostotic, involving other bones such as the spine, femur, skull, pelvis, and sternum and produces biochemical serum changes, such as elevated alkaline phosphate levels.[9]
Another disease that may mimic FOD is chronic diffuse sclerosing osteomyelitis. It appears as a single, poorly delineated opaque mass in the mandible, whereas FOD is seen as multiple round or lobulated opaque masses seen in the tooth-bearing areas.[10] Chronic diffuse sclerosing osteomyelitis is often seen as a complication of FOD and may present concomitantly with it, although it can also present as a primary condition of the mandible characterized by cyclic episodes of unilateral pain and swelling and is not always confined to tooth-bearing areas.
FOD can also suggest multiple endosteomas in Gardner syndrome, but in FOD, the involvement of other bones or the presence of dental abnormalities and benign skin tumors is not seen.[11]
Asymptomatic patients of FOD generally do not require treatment and periodic recall and observation suffice unless complications occur. It may emerge as the result of progressive alveolar atrophy under a denture or after extraction of tooth in the affected area or after trauma. The use of antibiotics therapy is not helpful in the treatment as the lesion is avascular and sequestration and surgical debridement are required. Surgical intervention such as remodeling and resection is reserved for cases with gross disfigurement.
In this case however, the patient presented with pain which was secondary to the infection from the adjacent tooth. Treatment by antibiotics, endodontic therapy of the affected tooth did not resolve the pain or swelling. Sequestration and surgical debridement also did not help. The patient had to undergo extraction and remodeling due to the complex presentation of the condition. On recall and observation, the patient has not shown further complications or alterations of the condition which reiterates the effectiveness of the treatment and the need of recall and observation, especially in cases of associated lesions.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Melrose RJ, Abrams AM, Mills BG. Florid osseous dysplasia: A clinico-pathologic study of 34 cases. Oral Surg Oral Med Oral Path 1976;41:62-82.  |
| 2. | MacDonald-Jankowski DS. Florid cemento-osseous dysplasia: A systematic review. Dentomaxillofac Radiol 2003;32:141-9. |
| 3. | Pitak-Arnnop P, Dhanuthai K, Chaine A, Bertrand JC, Bertolus C. Florid osseous dysplasia: Report of a case presenting acute cellulitis. Med Oral Patol Oral Cir Bucal 2009;14:e461-4. |
| 4. | de Carvalho CH, de Araujo Lima EN, Santos Pereira JD, de Medeiros AM, da Silveira EJ. Florid cemento-osseous dysplasiaand osteomyelitis: A case report of a simultaneous presentation. Rev Odonto Cienc 2012;27:166-9. |
| 5. | Waldron CA. Fibro-osseous lesions of the jaws. J Oral Maxillofac Surg 1993;51:828-35. |
| 6. | Kawai T, Hiranuma H, Kishino M, Jikko A, Sakuda M. Cemento-osseous dysplasia of the jaws in 54 Japanese patients: A radiographic study. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87:107-14. |
| 7. | Resnick CM, Novelline RA. Cemento-osseous dysplasia, a radiological mimic of periapical dental abscess. Emerg Radiol 2008;15:367-74. |
| 8. | Langlais RP, Langland OE, Nortjé CJ, editors. Diagnostic Imaging of the Jaws. Malvern: Williams and Wilkins; 1995. |
| 9. | Loh FC, Yeo JF. Florid osseous dysplasia in Orientals. Oral Surg Oral Med Oral Pathol 1989;68:748-53. |
| 10. | Groot RH, van Merkesteyn JP, Bras J. Diffuse sclerosing osteomyelitis and florid osseous dysplasia. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1996;81:333-42. |
| 11. | Dghoughi S, ElWady W, Taleb B. Florid cemento-osseous dysplasia. Rev Odont Stomat 2010;39:211-21. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
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