Fibro-osseous lesion is one in which bone is replaced by cellular fibrous tissue, which grows and then gradually matures back to bone. The degree of maturation varies between diseases and takes many months or years. Some- times the maturation never proceeds beyond woven bone, or the woven bone may mature further to disorganised lamellar bone or very dense sclerotic amorphous mineralisation.

Fibro-osseous lesions as a group are defined histologically and can be neoplasms, dysplasias, odon- togenic or non-odontogenic lesions

  • Fibrous dysplasia
    • Monostotic
    • Polyostotic
  • Cemento-osseous dysplasias
    • Periapical cemental dysplasia
    • Focal cemento-osseous dysplasia
    • lorid cemento-osseous dysplasia
  • Fibro-osseous neoplasms
    • Ossifying fibroma
    • Cemento-ossifying fibroma

Review all types PMID: 25409854

The following description of odontogenic fibro-osseous lesions is excerpted from Cawson’s Essentials of Oral Pathology and Oral Medicine:


These lesions are presumed to originate from periodontal ligament or lamina dura bone of the socket, part of which is odontogenic in origin.

Like other fibro-osseous lesions, the cemento-ossifying fibroma starts as a small radiolucency and expands slowly.

Calcification develops centrally while the lesion enlarges. Most become densely calcified given time and then appear largely radiopaque.

At all stages, the lesion has a sharply defined margin, often with a thin radiolucent rim sur- rounded by a narrow zone of cortication. This circumscrip- tion is a key diagnostic feature and can be detected both radiographically and histologically. Roots of related teeth can be fused to the lesion or displaced.

Densely mineralised lesions are relatively avascular and can become a focus for chronic osteomyelitis following dental extraction.

Juvenile ossifying fibroma

  • juvenile trabecular ossifying fibroma
  • juvenile psammomatoid (沙瘤样) ossifying fibroma. Now is called psammomatoid ossifying fibroma, as it is now known to develop at all ages.

Multiple and syndromic cemento-osseous fibromas

Syndrom Syndromes with cemento-ossifying fibromas:

  1. Hyperparathyroidism jaw tumour syndrome: Mutation in the CDC73 gene (also known as HRPT2 gene) encoding parafibromin, a tumour suppressor gene in the WNT signalling pathway. Inherited as an autosomal dominant but with very variable phenotype and expressivity. Additional features: Hyperparathyroidism caused by parathyroid adenomas or carcinomas, renal cysts, renal tumours and uterine tumours. Cemento-ossifying fibromas in both mandible and maxilla, often multiple.
  2. Gnathodiaphyseal dysplasia: Mutation in the ANO5 gene, which encodes a transmembrane ion channel, inherited as an autosomal dominant. Additional features: Presents in infants or children. Frequent bone fractures with normal healing, bowing and cortical thickening of the long bones.
  3. Familial ossifying fibroma: The cause is unkown. Additional features: Jaw lesions only. It is possible some of these cases are mildly affected patients with the two other syndromes.


These poorly understood diseases are non-neoplastic distur- bances of growth and remodelling of bone and cementum. They are, by far, the most common fibro-osseous diseases of the jaws. It is unclear whether the various subtypes are all truly related. They have similar histological and radiological features and differ mainly in their extent and radiographic appearances.

Previously these diseases have been known as osseous dysplasias. However, because they affect only the alveolar bone and appear odontogenic, the name cemento-osseous dysplasia has been reinstated.

Periapical cemental dysplasia

These simulate periapical granulomas but the related teeth are vital. During a period of years the separate lesions enlarge, may fuse and develop internal calcification. Mineralisation starts centrally and gives each lesion a target-like appearance radiographically. Eventually the lesions cease to enlarge, rarely exceeding 8–10 mm, and become densely radiopaque

Florid cemento-osseous dysplasia

In the florid form, multiple teeth are affected in more than one quadrant. The affected areas are frequently symmetrically distributed and may involve all teeth in all four quad- rants.

Individual lesions develop around the root apices exactly as in the periapical form but become larger and occasionally expand the jaw. The target-like appearance with central sclerosis resembling cementum on the root apex, surrounded by a radiolucent trim with a further outer zone of sclerosis in the surrounding bone is characteristic. Eventually dense radiopaque, somewhat irregular masses of sclerotic bone without a radiolucent border develop, producing a radiographic appearance similar to chronic osteomyelitis. As in the periapical form, tooth vitality is not affected.

The florid form becomes the most sclerotic and is particularly liable to become infected after extraction.

For cemento-osseous dysplasias, it must be emphasised that biopsy should not be performed for diagnosis. The diagnosis should be made radiographically, and biopsy avoided because it risks introducing infection into the sclerotic bone.

All types are fibro-osseous in nature with cellular fibrous tissue containing woven bone trabeculae and islands of dense cementum-like bone. Progressive calcification leads to the formation of a solid, bony mass with prominent resting and reversal lines.

Familial gigantiform cementoma

It is unclear whether the condition is one of multiple cemento-ossifying fibromas or a type of cemento-osseous dysplasia.