7: Diseases of bone and the maxillary sinus

Diseases of bone and the maxillary sinus

7.1 Diseases of bone

Normal jaw skeleton

The mandible and maxillary bones form in membrane and are unusual in that they contain odontogenic epithelium and neurovascular bundles within their substance. Most diseases arising in the jaws are of odontogenic origin, but both non-odontogenic local and systemic disorders may affect the jaws.

The mandible is formed of a cortex and rather coarse trabecular medulla. A depression into the cortex may form around the submandibular salivary gland during development. It can give rise to a radiolucent area at the angle of the mandible, referred to as Stafne’s cavity (Fig. 7.1). It is important to be aware of this normal structure, which appears below the inferior alveolar nerve canal on radiographs, to avoid confusion with bone cysts. Another important normal structure is the torus mandibularis. Tori are smooth bone prominences found on the lingual aspect of the mandible, below the canine/premolar teeth (Fig. 7.2). They are often bilateral and may consist of single, double or triple prominences. The maxilla is often extensively pneumatised to form the maxillary sinus, described later in this chapter. The hard palate forms by elevation and fusion of embryonic shelves. A bony prominence may form in the midline, which is referred to as torus palatinus. Both the torus palatinus and pterygoid hamulus can be discovered by anxious patients and reassurance may be required.

At a histological level, bone is composed of mineralised collagenous matrix containing osteocytes. It is organised into an outer cortex and an inner cancellous (trabecular) structure, which is adaptive to stresses (Fig. 7.3). Endosteal surfaces are lined by bone lining cells; remodelling is achieved by the coordinated activity of osteoclasts (bone-resorbing cells) and osteoblasts (bone-forming cells) in bone metabolic units. Bone is surrounded by periosteum, which is continuous with oral mucosa in certain places in the jaws. The vascular supply to bone is via periosteal vessels and marrow spaces. Fatty and haemopoetic marrow may be present in the jaws.

Bone fractures and tooth extraction sockets heal by similar processes, which involve demolition of blood clot, formation of initial woven bone in a fibrous scaffold and subsequent remodelling to restore normal architecture. In tooth sockets, there is simultaneous epithelial healing. Alveolar remodelling occurs over a prolonged period, resulting eventually in a rounded ridge form. The lamina dura can be detected radiographically for up to 2 years after extraction.

Fibrous dysplasia

Fibrous dysplasia is caused by mutation of the GNAS1 gene. Normal bone is replaced with fibrous tissue, which, in turn, undergoes gradual calcification. Monostotic (single bone) and polyostotic (more than one bone) types are seen. Around 30% of those affected have the polyostotic form of the disease.

Clinical features

An affected bone or area within a bone undergoes painless expansion. Other symptoms are few, but when the skull base is involved, neurological signs may occur, presumably owing to pressure on foramina. In the jaws, teeth are often affected, with effects upon eruption and developing malocclusion. The maxilla is affected twice as commonly as the mandible. The disease is most commonly unilateral but may involve multiple craniofacial bones and typically produces a visible facial asymmetry (Fig. 7.4). Fibrous dysplasia develops during childhood, usually before 10 years of age, with no sex predilection (except Albright’s syndrome). The disease becomes quiescent in early adult life, but the deformity persists.

The polyostotic form of fibrous dysplasia shares these general characteristics but has additional signs. There are two types: Jaffe’s type and Albright’s syndrome. In the first, multiple bones are affected and there are patches of skin pigmentation (café-au-lait spots). In Albright’s syndrome, which is almost always a disease found in females, there are usually various endocrine abnormalities, such as precocious puberty, hyperthyroidism and hyperparathyroidism.


Radiology shows:

Initially an affected area appears radiolucent, reflecting the fibrous tissue content. As bone forms, the lesion becomes more radio-opaque. The alteration in trabecular pattern is particularly notable: the trabeculae are very small and fine, resulting in a picture that has been described as like ‘ground glass’, although coarser forms are often described as resembling a ‘fingerprint’ or ‘orange peel’ (Fig. 7.5). Where teeth are present, another commonly noted sign is loss of lamina dura. With age, there is a tendency for lesions to increase their radio-opacity. While lesions classically merge into surrounding normal bone, mandibular lesions sometimes have better defined margins.

Cemento-ossifying fibroma

The cemento-ossifying fibroma shares much with fibrous dysplasia in its histopathology, but clinically and radiologically it is different. Its general behaviour is typical of a benign neoplasm in bone.

Paget’s disease of bone

In Paget’s disease, there is abnormal formation and resorption of bone. It is usually polyostotic, but invariably some bones in the skeleton will remain normal while others will be at different stages of the disease. Its aetiology may be viral.

Clinical features

Paget’s disease affects individuals in middle and old age. Males are more commonly afflicted than females. The clinical symptoms reflect the enlargement and weakening of bone that results from Paget’s disease. Slowly growing swelling of bones may lead to shape changes and enlargement of the skull and jaws (Fig. 7.6). Deformity of bones, typically of those bearing weight, may lead to bowing of legs and spinal curvature. Bone pain may occur and, if the skull base is affected, various neurological effects may develop.

In the jaws, the maxilla is affected more commonly than the mandible. In contrast to fibrous dysplasia, the disease is bilateral in the jaws. Spacing of teeth may develop and dentures may cease to fit. Extraction of teeth may be difficult, as a result of hypercementosis and ankylosis, and can be complicated by excessive bleeding, infection and slow healing. Other complications of Paget’s disease include high-output cardiac failure and an increased risk of sarcoma, in particular osteosarcoma.


Paget’s disease can be roughly divided into three overlapping phases. During the first of these, osteoclastic activity predominates, normal bone is resorbed and is replaced by well-vascularised cellular fibrous tissue. The surface of the bone is rimmed by giant osteoclasts resting in Howship’s lacunae. As the disease progresses, this osteolysis is accompanied by osteogenesis as new bone forms within the cellular fibrous tissue in the second phase of the disease. This combination of bone resorption and deposition gives rise to the classic mosaic appearance of bone in Paget’s disease (Fig. 7.7). The basophilic reversal lines that outline ‘the pieces of the mosaic’ mark switches in activity from bone resorption to bone deposition. Ultimately, in the third phase, osteoblastic activity predominates and the trabeculae of bone fuse together to give rise to masses of dense, sclerotic bone that is relatively avascular. Cementum is affected by Paget’s disease in a similar manner to bone, resulting in hypercementosis and, when bone and cementum fuse, ankylosis.


There are three stages:

1. Radiolucent (osteolytic): bone resorption results in radiolucency and cortical thinning; the lamina dura of teeth may disappear.

2. Mixed: the bony trabecular pattern is altered and often appears like ‘ground glass’ or may show a striking appearance of lines with few connections (Fig. 7.8); a few radio-opaque patches may appear in the bone.

3. Radio-opaque (osteoblastic): with time, the radio-opaque patches increase in number, grow and coalesce; tooth roots often have hypercementosis.

The affected bone will always enlarge. In maxillary lesions, the enlargement encroaches on the maxillary sinuses, often obliterating them entirely (Fig. 7.9).

Giant-cell granuloma (central giant-cell granuloma)

Giant-cell granuloma (GCG) is a non-neoplastic lesion of bone.


Osteoporosis is a disease characterised by a microarchitectural deterioration of bone structure and a low bone mineral content, leading to increased bone fragility and an increase in fracture risk. It is a generalised disease, the effects of which are of greatest clinical importance in the hip, spine and forearm, but which will also occur in the jaws.


Hyperparathyroidism is an endocrine abnormality in which there is an excessive amount of parathyroid hormone (PTH). This causes bone resorption and hypercalcaemia. The disease may be primary, caused by excessive PTH formation by a parathyroid tumour (usually a functioning adenoma), or secondary to hypocalcaemia resulting from poor diet, vitamin D malabsorption, liver or kidney disease.


There is increased radiolucency of bone, either generalised or localised. The earliest sign is subperiosteal resorption of the terminal phalanges. In the jaws, lamina dura of teeth is classically lost, along with the cortex of the inferior dental canal. There may be demineralisation of the cortex of the lower border of the mandible. Localised fairly well-defined radiolucencies (brown tumours) may be seen throughout the skeleton but are more common in facial bones than elsewhere (Fig. 7.13).

Genetic disorders

Numerous genetic disorders affect the jaws, and a good reference source for evaluation of individual cases is the Online Mendelian Disorders in Man (OMIM) database (www.ncbi.nlm.nih.gov/sites/entrez?db=omim). A number of disorders have effects in the jaw bones:

• Familial adenomatous polyposis (Gardner’s syndrome): multiple osteomas and odontomes, hazy sclerosis and hypodontia may be found in the jaws; numerous polyps develop in the large bowel and there is a very high risk of malignant change (adenocarcinoma of the bowel).

• Osteogenesis imperfecta: multiple bone fractures occur after minor trauma and soft tissues are typically lax, with hernia formation; the sclera may look blue and some patients develop dentinogenesis imperfecta; short stature is typical.

• Osteopetrosis: also known as marble bone disease, the medullary cavity infills with dense bone; the maxillary sinus may fail to pneumatise and bone appears dense and structureless on radiographs; there may be partial failure of tooth eruption.

• Vitamin-D-resistant rickets (hypophosphataemia): description of condition to follow from author

• Cleidocranial dysplasia: description of condition to follow from author

• Cemento-osseous dysplasia: description of condition to follow from author

• McCune–Albright syndrome: description of condition to follow from author

Bone tumours

A simple classification of bone swellings is given in Box 7.1. Osteomas occur most frequently in the paranasal sinuses and are dealt with in the section on maxillary sinus. Primary malignant bone tumours are rare and include osteosarcoma, chondrosarcoma and multiple myeloma. Direct invasion of bone by squamous-cell carcinoma arising in the oral mucosa is common in advanced oral cancers. Metastatic deposition of carcinoma from colon, lung, breast, kidney and other primary sites is more likely to be the cause of a destructive malignant lesion in bone than primary sarcoma.

Box 7.1   Simple classification of bone swellings in the jaws


Torus mandibularis and torus palatinus

Reactive exostosis






Central giant-cell granuloma

Fibrous dysplasia

Cemento-ossifying fibroma

Cemento-osseous dysplasias





Metastatic deposits in bone

7.2 Diseases of the maxillary sinus

The maxillary sinus (antrum) has a close anatomical and pathological relationship with the oral cavity. It is relevant in dentistry because:

Jan 9, 2015 | Posted by in Oral and Maxillofacial Pathology | Comments Off on 7: Diseases of bone and the maxillary sinus
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