Download Citation on ResearchGate | Displasia cemento-óssea florida: relato de caso | Lesões fibro-ósseas benignas são caracterizadas pela substituição do. Florid cemento-osseous dysplasia has been described as a condition that characteristically . A displasia cemento-óssea florida tem sido descrita como uma. 18 nov. Focal. Thalyta Brito Santos LIMA. Renan de Souza BONFIM. Gefter CORREA. Rafael MOURA. TRATAMENTO. DISPLASIA CEMENTO-ÓSSEA.

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Florid cemento-osseous dysplasia is a sclerosing disease that affects the mandible, especially the alveolar process, and that is, in most cases, bilateral; however, in ossfa cases it affects up to three or even four quadrants. During the disease, normal bone is replaced with a thinly formed, irregularly distributed tissue peppered with radiolucent areas of soft tissue.

Newly formed bone does not seem to invade periodontal space, but, in several images, it is confused with displaaia roots, without, however, compromising pulp vitality or tooth position in the dental arch. There is no replacement resorption, not even when the images suggest dentoalveolar ankylosis.

Orthodontists should make an accurate diagnosis when planning treatments, as this csmento, when fully established, is one of the extremely rare situations in which orthodontic treatment is contraindicated.

This contraindication is due to: Densely mineralized and disorganized bone is unable to remodel or develop in an organized way in the periodontal ligaments and the alveolar process. Organized bone remodeling is a fundamental phenomenon for tooth movement. Without a normal adequate bone remodeling process, there is no orthodontic movement, or, when there is some movement, it is not enough to restore the normal esthetics and functions. In this new century, Brazil has adopted a new National Oral Health Plan, and at the same time, social and economic conditions allowed lower-income populations to have access to health services.

At the same time, there displaisa been an increase in the knowledge about florid cemento-osseous dysplasia ossda the number of diagnosed cases, particularly by using panoramic radiographs.

Florid cemento-osseous dysplasia is not rare, and a large number of cases are diagnosed in the imaging documentation centers Figs 1 to 4. It is more frequent in black women about 40 years old at the time of diagnosis, with a prevalence of 5. Black woman aged dispkasia years and 3 months. No symptoms associated with lesion and no systemic diseases reported.

Frontal and lateral views. No clinical signs of disease. Mandibular lesions are mixed, some radiopaque, some radiolucent, and are confused with roots of molar teeth, as they are randomly distributed in posterior region. Maxilla was not affected; implant is normal and functioning. Mandibular lesions are mixed and overlap roots of molar teeth, as they are randomly distributed in posterior region; cotton-wool appearance.

Florid cemento-osseous dysplasia, a sclerosing disease that affects the mandible, is associated with the alveolar process and, in most cases, is bilateral; however, it may affect up to three or even four quadrants in some cases. In this process of intense and abnormal bone sclerosis, normal bone is replaced with a densely formed tissue, irregularly distributed and peppered with radiolucent areas of soft tissue found primarily in the alveolar process Figs 1 to 4including the interdental and interradicular septa.


After some time, newly formed bone invades the periodontal space and is confused with the dental roots, without, however, compromising pulp osxea and displlasia position in the dental arch. The characteristics described above indicate that orthodontists must make an accurate diagnosis of florid cemento-osseous dysplasia in the analyses conducted for their treatment planning, as this disease, when fully established, is one of the rare conditions that contraindicate orthodontic treatment.

The human skeleton undergoes full renewal every 1 to 4 years in children and 4 to 10 years in adults. Bones have both soft and mineralized tissues. Osteoblasts, osteocytes and osteoclasts are mature bone cells that, in association with other components, such as macrophages, promote bone remodeling, which exists, primarily, to control the levels of mineral ions in the blood and tissues. Constant bone remodeling gives bone greater adaptability. According to the stimuli applied to its structure, the form and volume that define bone design may be remodeled.

This adaptive and reactional capacity of bone is clinically very important in everyday practice in Dentistry.

The reactional capacity of bone and its resistance to stimuli or aggressors depend on three fundamental factors, which may determine the type of lesion a certain cause may inflict on the affected bone:. A more compact or dense cancellous bone has small medullary spaces, and, consequently, not much space for more abundant inflammatory exudates.

Any inflammation may increase, at an early stage, the pressure inside these reduced medullary spaces, thus compressing the vases and creating barriers to venous return, which leads to medullary tissue necrosis in a shorter time. An area of necrotized medullary tissue may be the ideal site for bacteria to lodge and build microbial biofilm. On the other hand, bone with more space or loosely distributed trabeculae offers more space for inflammatory exudates and infiltrate when there is an insult.


Logical deduction leads to the conclusion that bone that is more compact is much stronger physically, but fragile biologically, as it requires that the inflammatory process function more rapidly. The opposite is seen when the bone is less compact but spongier: In the same way as other insults, mild and constant irritation, or irritation described as chronic, leads to initial acute inflammation, but rapidly goes into a mild or moderate chronic phase, in which there is restricted accumulation of mediators at the site of inflammation.

Several inflammatory exudate mediators induce bone resorption, but some have bipolar effects: Inducing mediators of new bone formation on the trabecular and subperiosteal surfaces gradually change local bone morphology, which remains organized. As irritation increases its insulting power, the reaction to form new bone may still occur, but in a not so organized way. Rapid and intense irritation, or that referred to as acute, in the same way as all other insults, promotes acute initial inflammation, but much more exudative and rich in terms of mediators inducing bone resorption, and may, therefore, induce the formation of areas of medullary and endosteal tissue and osteocyte necrosis.

Mild or chronic insults induce new bone formation or production, predominantly as synthesis, whereas severe or acute insults lead to bone resorptive, osteolytic or destructive reactions. The systemic state of the host is determinant in bone reactions to insults.

Osteomyelitis occur only in:. In radiotherapy, osteoradionecrosis and osteoradiomyelites occur when common cemeento invade the areas of irradiated bone, as a result of: When the patient is systemically healthy, the same causes that induced osteomyelitis promote osteitis, also an inflammation, but local and focal and with less serious consequences, because the osteolytic areas are restricted and small, the areas of bone sclerosis are predominant, and symptoms are very few.

The prognosis of osteitis is very good. Sincethe WHO, in studies such as the one conducted by Pindborg and Kramer, 6 among others, has attempted to unify the nomenclature and classification of odontogenic neoplasia, among which are the fibro-osseous lesions. In that first study, six lesions were defined, four of which were classified in cemenot group called cementomas: The other two diseases included as odontogenic fibro-osseous lesions were ossifying fibroma and fibrous dysplasia, although much more closely associated with bone.

Defining a uniform nomenclature and classification of these lesions is difficult because it is impossible to distinguish whether the mineralized material in these lesions is cement or bone, even when analyzed under transmission or scanning electron microscopy or immunocytochemistry.

InBurkhardt 7 analyzed two fibro-osseous lesions using optical and electron microscopy and cejento and found that some mineralized tissues may also have a dentinal nature. In the present study, the priority and focus is on one of these formerly called cementomas, which was also called a gigantiform cementoma for a long time. Currently, the classification most commonly used universally is florid cemento-osseous dysplasia.

Initially, gigantiform cementoblastomas were characterized as a typically multiple and symmetrically distributed benign odontogenic lesion that affected middle-aged black women. Radiographically, they are dense lesions and lobulated masses that are microscopically composed of tissue that resembles cement. Later, inthe term florid cemento-osseous dysplasia was coined by Melrose et al 8 to describe an exuberant multi-quadrant fibro-osseous lesion in which the bone was gradually replaced with diisplasia tissue, as described for gigantiform cementomas.

The name florid cemento-osseous dysplasia was widely accepted to describe also the condition previously described as multiple cemento-ossifying fibroma, multiple sclerosing osteomyelitis and sclerotic cemental masses.

Cemento-osseous dysplasia | Radiology Reference Article |

The term florid cemento-osseous dysplasia was also adopted for gigantiform cementomas. However, the need to use the term gigantiform cementoma or familial gigantiform cementoma was demonstrated by Young et al 9 inwho described five generations of a family with familial gigantiform cementoma of dominant autosomal character. Although the two lesions are indistinguishable under imaging and microscopic examination, familial gigantiform cementomas have a familial or hereditary history, whereas florid cemento-osseous dysplasia does not.

Florid cemento-osseous dysplasia, but not gigantiform cementomas, has a greater prevalence among black women. Familial gigantiform cementoma is characterized by great expansive and asymmetrical growth, not found in florid cemento-osseous dysplasia. Several authors recommend that the two lesions, although they have some points in common, should be classified separately as two distinct entities.

The term florid cemento-osseous dysplasia was used for the first time inwhen Melrose et al 8 described an exuberant multi-quadrant fibro-osseous lesion characterized by bone replacement with fibro-cement in the jawbones. That classification was largely accepted to describe conditions that had been previously reported as multiple cemento-ossifying fibroma, sclerosing osteomyelitis and sclerotic cemental masses.


Summerlin and Tomich 10 reanalyzed cases of more localized lesions, such as cementifying fibroma and central ossifying fibrous dysplasia of the jawbones, chronic sclerosing osteomyelitis, sclerotic cemental masses and fibro-osseous lesions, under several focuses, in They concluded that the clinical entity called focal cemento-osseous dysplasia was an initial phase of florid cemento-osseous dysplasia that gradually compromises the other areas to result in the complete or generalized symptoms of the disease.

This initial lesion of florid cemento-osseous dysplasia, called focal cemento-osseous dysplasia, may simulate several other fibro-osseous lesions of the jawbones, especially cementifying or central ossifying fibromas, and special attention should be paid at the time of differential diagnosis, as its nature is benign, with variable degrees of local aggressiveness.

Focal cemento-osseous dysplasia seems to compose only a localized and still initial form of florid cemento-osseous dysplasia, but it is not a new clinical entity or disease. In contrast, periapical cemental or cemento-osseous dysplasia in the region of the mandibular incisors may only be a uniform manifestation of the same focal cemento-osseous dysplasia, but this is still controversial.

May periapical cemental or cemento-osseous dysplasia evolve into florid cemento-osseous dysplasia? Clinical experience and literature reveal that it may not.

Their occurrence together in the same patient seems to be a fortuitous and rare occurrence. In a certain point of the region of the mandibular molars and premolars, probably simultaneously in both sides, bone tissue is resorbed and replaced with fusiform and polyhedral cells that form discretely fibrosed connective tissue. These areas, if examined using imaging techniques, are radiolucent or hypodense, as they are osteolytic and irregular. After some time, these polyhedral cells initiate the deposition of an irregularly and randomly distributed, disorganized collagen matrix, over which basophilic mineralized bone begins to form.

Its structure and organization resemble that of immature or still disorganized mature bone, or, at other times, that of a cementum-like tissue.

The radiolucent areas reveal irregular and focal irregular radiopaque areas that gradually unite to form radiopaque masses, usually surrounded by irregular radiolucent areas that interface with normal neighboring bone and are filled with soft tissue that has not yet been mineralized.

In these initial stages, there are no clinical signs, not even any signs on CT scans or radiographs Figs 1 to 4. This process tends to affect the mandible bilaterally and asymptomatically and gradually increases until it is eventually diagnosed on imaging studies indicated due to other clinical conditions.

Which factor triggers this pathologic process?

Florid cemento-osseous dysplasia mimicking multiple periapical pathology–an endodontic dilemma.

Florid cemento-osseous dysplasia probably originates in the periodontal ligament as a result of irregular cementum formation and a disorder in the displasis of periodontal ligament stem cells. Under normal conditions, these cells differentiate into cementoblasts, fibroblasts and osteoblasts of the alveolar bone every day. This disorder of the periodontal ligament stem cells may explain why this mineralized material has already been described as similar to cementum and bone, between fibrous tissue similar to the periodontal ligament.

It may also explain why these mineralized masses are not encapsulated. Florid cemento-osseous dysplasia has no symptoms or clinical signs.

Teeth in the areas affected by this condition show pulp vitality and normal color. There is no expansion of the cortical bone, and, therefore, no jawbone volume increase or asymmetry. The areas affected have a normal texture to palpation, and the overlying mucosa is completely normal Figs 1 to 4. Imaging studies reveal mixed radiopaque and radiolucent areas Figs 1 to 4.

In the space limited by the jawbone cortical bones, florid cemento-osseous dysplasia gradually involves all alveolar process in the interdental and interradicular spaces. In the region of the affected teeth, displaia is not possible to detect the radiolucent periodontal space or the radiopaque lamina dura, but there is no root replacement reabsorption, no matter how advanced the disease is, which is a sign of presence of the periodontal ligament.

This overlapping reveals that these radiopaque and radiolucent masses are random in a variety of radiographic images. The aspects described above are particularly detailed on CT scans and three-dimensional reconstructions.

Between these masses and teeth, no periodontal spaces are seen at osssea points, not even in thinner CT sections, but there is no replacement resorption. CT sections reveal that these masses extend from one cortical to the other. With time, the involvement of the jawbone, particularly the mandible, may extend from the area of third molars to that of canines, and lesions may be found in both quadrants.