Dental radiologyPathology
Diseases occurring in other parts of the skeleton also appear in the jaws, but the most common lesions are associated with the teeth or derived from dental tissues. Different pathological entities may have similar radiographic features. On the other hand, the very same pathological entity can have a varied radiographic appearance. Many lesions cannot be diagnosed solely through imaging.
Malformations
Malformations of the jaws and teeth may be confined to the jaws or may occur as part of a syndrome causing morphological and functional impairment of the facial region, the entire skull, and other body organs. Tooth anomalies can involve single teeth or the entire dentition. In the latter case, the permanent dentition is more frequently involved than the primary.
Dens invaginatus (Fig. 13) is the descriptive name of a common tooth anomaly caused by an invagination of the enamel organ. In its advanced forms, it affects the size, shape, as well as the structure, of the permanent teeth. It may occur in any tooth, but is most commonly found in the
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Figure 14.
Supernumerary tooth in inverted position.
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Figure 15.
Mandibular incisors in a patient with dentinogenesis imperfecta. The pulps are obliterated, the roots are short, and the incisal enamel is worn by attrition.
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maxillary lateral incisors. Frequently, it is impossible to discover the invagination at a clinical examination. The only sign may be a palatal pit.
Mineralization defects in the invaginated hard tissues provide routes of infection of the pulp and the periapical bone.
Increased numbers of teeth, hyperodontia, or supernumerary teeth (Figs. 14, 16) are predominant in the anterior maxillary part of the permanent dentition. Supernumerary teeth are prevalent in certain syndromes, such as cleidocranial dysplasia (cleidocranial dysostosis), Gardner's syndrome, and orofaciodigital syndrome (mandibulofacial dysostosis, Treacher Collins' syndrome). A decreased number of teeth, hypodontia, is unusual in the primary dentition, but is rather common in the permanent dentition. Total absence of teeth, anodontia, is rare; it is one of the expressions of ectodermal dysplasia.
Among structural changes are amelogenesis imperfecta (hereditary hypoplasia of enamel) and dentinogenesis imperfecta (hereditary opalescent dentin). Dentinogenesis imperfecta occurs either as a solitary phenomenon (Fig. 15), or in conjunction with osteogenesis imperfecta.
Hyperplasia of the maxillary tuberosities, hyperplasia of the coronoid processes, and congenital hypoplasia of the mandible (micrognathia) are among malformations that are confined to the jaws. The most common
malformations that extend beyond the jaws include congenital unilateral hypo- and hyperplasia of the face, progressive facial hemiatrophy, cleidocranial dysplasia, craniofacial dysostosis (for example: Apert, Crouzon and Pfeiffer syndromes), and orofaciodigital syndrome.
Facial clefts predominantly affect the maxilla. Cleft lip and palate are by far the most common. They may be solitary or combined with malformations in multiple organs. The clefts can be either uni- or bilateral. Palatal clefts may be incomplete or complete, in which case they run through the soft and hard palates and the alveolar ridge anteriorly, usually in the region of the lateral incisor (Fig. 16). The lateral incisor is frequently malformed or missing. Although there are racial differences in the prevalence of cleft lip and palate, approximately one in 800 infants is born with either cleft lip or cleft palate.
The so called latent or static cyst, also referred to as idiopathic bone cavity or Stafne cyst, is a malformation, which consists of an excavation on the lingual aspect of the mandible. It is typically located in the angular region below the mandibular canal. Radiographically it resembles a cystic lesion with varying size and border characteristics (Fig. 17). It usually develops after the first to second decade but appearance after the age of 30 has also been observed. When the lesions have been explored surgically, either an empty cavity or a cavity containing salivary gland tissue has been found.
Inflammatory changes in and around the teeth
The most prevalent oral diseases, caries and periodontal diseases, are caused by infection, which gives rise to inflammatory changes in and around the teeth.
Caries
Caries is the predominant cause of pain in the jaws. In the premolar and molar regions, carious lesions may be difficult to detect clinically. This holds true in particular for proximal, some occlusal, and deeply situated root caries. Radiographic examination is therefore of importance. Proximal and occlusal caries (Fig. 18) commonly show a narrow demineralised entrance in the enamel. When the lesion reaches the dentinoenamel junction, it spreads along the junction, undermining the enamel. Root caries (Fig. 18) has a much wider entrance that is frequently concealed by the gingiva. In an adult population, the most common type o
caries is recurrent (secondary) caries at the cervical margins of proximal restorations.
Pulpitis
Inflammation of the dental pulp is a common sequelae of caries. Pulpitis seldom causes radiographic signs. It may, however, be associated with periapical widening of the periodontal ligament.
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Figure 19.
a) Periapically, at the first premolar, an ill-defined osteolytic lesion (arrows) caused by an acute or a chronic abscess. b) Left maxillary lateral incisor with a well-defined osteolytic lesion periapically, typical of a granuloma. The borders of the lesion are sclerotic. |
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Periapical osteitis
lf untreated, pulpitis results in necrosis of the pulp tissue and an acute periapical abscess. The abscess can either become chronic, or more commonly, develop into a periapical granuloma, which is formed in response to the infection. The only sign of an acute abscess may be a widening of the periodontal ligament space. Usually, however, both an acute and a chronic abscess are represented by a discontinuity of the lamina dura and an ill-defined rounded osteolytic lesion (Fig. 19). Periapical granulomas have well-defined borders, frequently surrounded by bone sclerosis (Fig. 19). If a periapical granuloma becomes reinfected, the borders break down and it will take the shape of an abscess. The periodontal ligament contains epithelial cell rests, which may proliferate and form a lining around the granuloma, leading to radicular cyst formation.
Odontogenic infection via a root canal, a periodontal pocket or an extraction wound is the most common local cause of osteomyelitis of the jaws. Rarely, a fracture serves as in infection route. Haematogenous spread of an infective agent from another part of the body also occurs. A distinct type of osteomyelitis, osteoradionecrosis, occurs after therapeutic irradiation of oral and neck malignancies.
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Figure 20.
An ill-defined periapical and interdental osteolytic lesion in the mandibular anterior region three weeks after onset of clinical symptoms of osteomyelitis.
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Figure 21.
Chronic suppurative osteomyelitis with three sequestra (arrows). Osteolytic as well as sclerotic areas are present.
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Osteomyelitis is more common in the mandible than in the maxilla. In the mandible, it occurs predominantly in the posterior parts, the ramus included, whereas in the maxilla, it is more frequent in the anterior than in the posterior parts. In the acute phase, osteolysis is not visible radiographically until one or two weeks after the onset of clinical symptoms which are: pain, fever, local lymphadenopathy, increased white blood cell count, and teeth sensitive to percussion. Numbness of the lower lip is another common sign of mandibular osteomyelitis.
The initial radiographic changes are blurring and thinning of the trabeculae and subsequent enlargement of the bone marrow spaces. Without treatment, large volumes of the bone tissue can rapidly become involved, causing loosening of the teeth (Fig. 20).
If acute osteomyelitis becomes chronic, it is frequently possible to distinguish between chronic suppurative osteomyelitis (Fig. 21) and chronic sclerosing osteomyelitis (Fig. 22), both of which have ill-defined borders. In the suppurative form, radiolucent areas alternate with sclerotic, giving the bone a "moth-eaten" appearance. This is further enhanced when sequestra develop. In chronic sclerosing osteomyelitis, radiolucent areas occur, but there is a predominance of radiopaque changes due to the formation of sclerotic bone. The bone is often enlarged through periosteal bone formation (Figs. 22, 23). Over time, the distribution of
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Figure 22.
Chronic sclerosing osteomyelitis of right mandible with some osteolytic areas. Ramus is enlarged.
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Figure 23.
a) Right mandibular molars in a young patient. The alveolar bone is unevenly sclerotic; chronic sclerosing osteomyelitis. b) Occlusal view of the same patient. Periosteal bone formation (arrow) on the buccal side of the mandible.
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sclerotic and radiolucent areas varies, indicating disease activity.
Periodontal diseases
In periodontal disease, gingival pockets develop through a complex interaction between bacterial plaque formed on the tooth surfaces and the host. Untreated, it may result in a considerable loss of the bone that supports the teeth. The course of disease is episodic, i.e. bursts of disease activity alternate with periods of stability. Consequently, in the same dentition, at any given time, here may be disease active as well as disease inactive sites. Radiographs (Figs. 4, 24) do not yield information on disease activity, but on the total bone loss over time. Idiopathic juvenile periodontal disease affects children and young adults. It is characterized by aggressive bone destruction around the permanent first molars and incisors, leaving the rest of the periodontal bone intact (Fig. 25).
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Figure 24.
Generalized periodontal disease. The marginal bone loss is substantial and includes destruction of bone in the furcation areas of multirooted teeth (arrows).
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Figure 25.
a) Extensive alveolar bone loss at the mandibular first molars associated with juvenile periodontal disease (arrows). b) Maxillary incisors of the same patient with alveolar bone loss around the left central incisor, not visible in the panoramic radiograph.
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Cysts
The majority of cysts of the jaws are odontogenic. The most common are radicular and dentigerous cysts, less common are keratocysts, lateral periodontal, botryoid, and non-odontogenic developmental cysts.
Cysts present well-defined radiolucent lesions, usually with a thin cortical lining (Figs. 26, 28). If the cyst is infected, the lining may be diffuse or more sclerotic. Also, if the hydraulic pressure within the cyst decreases bone formation may give rise to sclerotic walls. Large cysts expand and thin the cortical borders of the jaws. Occasionally the cortex may lose its integrity in discrete areas (Fig. 27). Large cysts may also cause an image suggestive of multilocularity, although the lesion is merely lobulated. In the lower jaw the mandibular canal may be displaced by an expanding cyst (Fig. 26). In the upper jaw expansion may occur into the maxillary sinus and the nasal cavity where the thin layer of bone covering the cyst forms an upward convex bony border (Fig. 27). An expanding cyst may cause divergence of the roots of adjacent teeth. Root resorption is sometimes seen, particularly in conjunction with infected cysts. Radicular or periapical cysts are associated with non-vital teeth.
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Figure 26.
Large radicular cyst in the mandible displacing the mandibular canal inferiorly (arrows) and thinning the inferior cortex.
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Figure 27.
Transversal (a) and frontal (b) CT i ages of a large dentigerous cyst expanding into the maxillary sinus. Note loss of cortical lining (arrow).
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Figure 28.
Dentigerous cyst of a mandibular third molar.
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A residual cyst is a radicular cyst, which remains or recurs after removal of the tooth associated with the cyst (Fig. 29). It shows the same characteristics as the radicular cyst. Dentigerous cysts emanate from the cervical parts of impacted teeth and the crowns, but not the roots, are included in the cysts (Fig. 28). This is an important differential diagnostic sign. The affected tooth may be displaced by the cyst. The most common sites for dentigerous cysts are the lower third molar region and the upper cuspid region.
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Figure 29.
Residual cyst in the mandibular premolar region.
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Keratocysts differ from other odontogenic cysts in regard to their origin and way of growth but radiographically they are in many instances indistinguishable. They can appear unilocular or multilocular and their borders are not consistently evenly and thinly corticated (Fig. 30), areas of sclerosis can be seen. Root resorption is more frequently caused by keratocysts than by other odontogenic cysts. Keratocysts may be associated with impacted teeth and also with congenitally missing teeth when they are called primordial cysts. They show a high recurrence rate. In patients with multiple keratocysts the nevoid-basal cell carcinoma (Gorlin's) syndrome should be suspected. The lateral periodontal cyst (Fig. 31) is named after its location on the lateral aspect of a root. It has some histologic features that distinguishes it from other odontogenic cysts. Clinically and radiographically it cannot be differentiated from a keratocyst with the same location.
Non-odontogenic cysts occur at sites where parts of the facial skeleton fuse during development. Most common among the developmental cysts are the midline and incisive canal cysts (Fig. 32). They are similar in appearance and may very well be the same pathological entity. A
rounded, well-defined unilocularradiolucenty in the midline that exceeds approximately 6 mm in width suggests the presence of such a cyst. In intraoral radiographs the superimposition of the anterior inferior borders of the nasal cavity and the anterior nasal spine may give this cyst a heart shaped image.
The so-called traumatic or simple bone cyst is an obscure lesion, which mostly occurs in the lower jaw (Fig. 33). Anteriorly, it usually presents as a rounded well-defined radiolucency; whereas posteriorly it expands between the teeth causing a scalloped appearance. Toward the base of the mandible it tends to have less distinct borders. In about 30% the
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Figure 32.
Developmental cyst of the incisive canal. Note the superimposition of the anterior nasal spine region (arrows).
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Figure 33.
Traumatic bone cyst in the mandibular premolar region. Note the intact lamina dura and the poor definition inferiorly.
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cortex is expanded. Surgical reports have frequently described the traumatic bone cyst as an empty cavity lined with a thin "endosteum". These cysts may heal spontaneously. On the other hand, recurrences have been reported after surgery. A tentative diagnosis can usually be made when the lamina dura of adjacent roots is intact.
Tumours and tumorous conditions
The majority of benign tumours of the jaws are odontogenic. Odontogenic tumours can be divided into ectodermal, mesodermal, and mixed ectoand mesodermal. Ameloblastoma, adenomatoid odontogenic tumor, calcifying epithelial odontogenic tumour, compound and complex odontoma, ameloblastic odontoma, ameloblastic fibroma, odontogenic myxoma, and benign cementoblastoma are considered odontogenic tumours.
Ameloblastoma is a locally aggressive tumour often associated with a clinically missing tooth. Approximately 80% of ameloblastomas occur in the posterior part of the mandible. They are radiolucent and vary in
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Figure 34.
Ameloblastoma in the right mandible. Note the multilocular ("soap bubble ") appearance.
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Figure 35.
a) Large expansile unicystic ameloblastoma in the right mandible. Histologically, a very small ameloblastoma was found in the epithelial lining of what could be a dentigerous cyst. b) Occlusal cross-sectional radiograph demonstrates the expansion of the lesion and displacement of the mandibular canal (arrows).
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shape and size, although the multilocular appearance with a marked variation in size between the loculi is typical (Fig. 34). The ameloblastoma has a high recurrence rate if not removed with sufficient margins. The so called unicystic ameloblastoma radiographically appears like a dentigerous cyst since it apparently develops in the wall of a dentigerous cyst (Fig. 35). The adenomatoid odontogenic tumour is seen in the anterior regions mimicking a dentigerous cyst, except that parts of the root are encompassed in the lesion. When hard tissue appearing like" driven snow" occurs within the radiolucency this tumour should be easily diagnosed. The calcifying epithelial odontogenic tumour resembles the ameloblastoma radiographically but occasionally scattered areas of sclerotic foci indicate the possibility of this rare tumour.
The odontogenic tumours forming hard tissues are more easily diagnosed. The compound odontoma consists of a varying number of tooth-like formations, whereas the complex odontoma contains the tissues of
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Figure 36.
Compound odontoma in the mandibular incisor region with multiple tooth-like structures.
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Figure 37.
Complex odontoma in the left maxilla. The first permanent molar is missing.
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Figure 38.
Odontogenic myxoma in the right maxilla with straight bony trabeculation and poorly defined borders.
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a tooth in a much less organized arrangement producing a more homogeneous radiopacity than the compound odontoma (Figs. 36, 37). Compound odontomas are usually seen in the anterior regions. They are occasionally associated with a clinically missing tooth, whereas complex odontomas are mostly found in the posterior regions, typically in combination with unerupted or missing teeth. The odontogenic myxoma has a varying radiographic appearance. It occurs most commonly in the posterior regions. Typically, it is a less well delineated multilocular lesion with more straight bony septa than, for instance, the ameloblastoma (Fig. 38). Odontogenic myxomas are frequently associated with a missing tooth.
Fibroosseous lesions and tumours include ossifying and cementifying fibromas (Fig. 39), as well as periapical cemental dysplasia, florid osseous dysplasia, and fibrous dysplasia. Differential diagnosis would
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Figure 39.
Ossifying fibroma in the left mandible with divergence of teeth and erosion of the inferior cortex (arrows).
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Figure 40.
Periapical cemental dysplasia at mandibular incisors (arrows). Some lesions contain hard tissue (open arrows).
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include Paget's disease, osteopetrosis, sclerosing osteomyelitis, and sclerosing osteogenic sarcoma. These lesions can be anything from radiolucent to completely radiopaque depending on the stage of development at which the examination is undertaken. Intraoral radiographs are valuable because they depict the finer structures of diagnostic importance, such as a radiolucent capsule in cases of ossifying or cementifying fibromas. The distinction between periapical cemental dysplasia and florid osseous dysplasia is not clear-cut (Fig. 40).
Periapical cemental dysplasia occurs most commonly anteriorly in the mandible, often at multiple teeth. It is more prevalent in women than in men, with a typical age range at the time of diagnosis of between 30-40 years. The lesions are initially radiolucent, when they can be mistaken for inflammatory lesions. The periodontal ligament is widened and there is a loss of lamina dura. The borders are well defined and in places slightly sclerotic. At a later stage a cementum like tissue is formed centrally in the lesions. In the final, mature stage, the lesions are radiopaque and surrounded by thin radiolucent
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Figure 41.
Monostotic fibrous dysplasia of the right maxilla with ground glass appearance.
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Figure 42.
Osteosclerosis posterior to mandibular second molar following extraction of a third molar. Histologically, the diagnosis was "dense bone formation ".
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capsules. Periapical cemental dysplasia should not be confused with hypercementosis, which is a deposition of cementum on the root surface.
All three types of fibrous dysplasia can be found within the jaws. A typical site for the most common variety, monostotic fibrous dysplasia, is the posterior maxilla where it can encroach upon the maxillary sinus and expand the alveolar process (Fig. 41). The typical ground glass or stippled appearance of the bone is pathognomonic for fibrous dysplasia. Histologically, the bone in fibrous dysplasia resembles the primary bone laid down initially when fractures heal and after bone surgery. A number of lesions, originally diagnosed as fibrous dysplasia, have be en shown to be chronic sclerosing osteomyelitis with reactive bone formation. In fibroosseous lesions bone scintigrams will demonstrate increased activity, which should be taken into account if screening for metastatic disease is performed.
Osteomas and exostoses are masses on the outer surfaces of bones. Dense bony structures within the jaws without apparent relation to an inflammatory process are usually referred to as bone islands, idiopathic osteosclerosis, enostosis, focal sclerosis, fibrous dysplasia, or reactive bone formation. These lesions have a varying size and radiographic appearance and sometimes they suggest a tumorous condition (Fig. 42). Once established, they seem to change very little over time and are clinically
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Figure 43.
Giant cell granuloma in the mandible with faint bony septa within the lesion (arrows).
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Figure 44.
Soft tissue calcifications (phleboliths) in a cavernous haemangioma of the neck (arrows).
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symptom less. Occasionally, osteosclerosis is associated with root resorption.
The giant cell granuloma is commonly found in the mandibular posterior regions. It is an expansile tumour, which can displace and resorb adjacent teeth. It often presents with some delicate wispy bony septa within a radiolucency (Fig. 43). The aneurysmal bone cyst is also expansile and shows faint bony septa within the lesion. Periapical and occlusal cross-sectional radiographs are helpful in the differential diagnosis of these lesions. Typically, these lesions are found in young individuals. Giant cell tumours ("brown tumours") in conjunction with hyperparathyroidism have the same radiographic appearance but they are found in adults. Haemangiomas occur both in the jaw bones and in the adjacent soft tissues. Soft tissue calcifications (phleboliths), typical of cavernous haemangiomas, are serendipitous findings in radiographs of the jaws (Fig. 44). The radiographic presentation of intraosseous haemangiomas varies but the occurrence of straight trabeculae separated by larger spaces than in normal bone is fairly typical for these lesions (Fig. 45).
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Figure 45.
Intraosseous haemangioma in the right maxillary incisor region (arrows) with straight septa and lack of normal trabeculation.
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Figure 46.
Invading carcinoma of the floor of the mouth eroding the mandible on the right side creating a broad-based rounded defect.
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Figure 47.
Mucoepidermoid carcinoma in posterior mandible with partly distinct borders and resorption of the roots of the first and second molars (arrows). The lesion resembles a cyst.
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Malignant tumours comprise those that invade the jaws from the periphery, those arising primarily within the jaws, and those which are metastases from distant primary tumours. The most prevalent malignant tumour is the invading squamous cell carcinoma which presents as a broad-based erosive change with variable definition of the borders (Fig. 46).
Squamous and mucoepidermoid carcinomas, osteogenic sarcomas, lymphomas, and myelomas are among the primary malignancies of the jaws. Squamous and mucoepidermoid carcinomas may appear radiographically similar to a cyst since these tumours may arise within a dental cyst (Fig. 47). Osteogenic sarcomas, sclerosing osteogenic sarcoma
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Figure 48.
Sclerosing osteogenic sarcoma of the anterior maxilla.
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Figure 49.
Osteogenic sarcoma of the left maxilla. Root resorption of first molar (arrow).
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and chondrosarcomas are seen at older ages in the jaws than in the long bones (Figs. 48, 49). Adjacent teeth may show a widening of the periodontal ligament, which is then suggestive of a sarcoma. Primary myeloma (Fig. 50), multiple myeloma, and malignant lymphomas of the jaws are rare. In multiple myeloma the jaws are involved in less than 50%. Metastatic tumours produce a variable radiographic image (Figs. 51, 52). Typical is an irregular radiolucency with mostly ill-defined borders and a moth-eaten appearance, occasionally with sclerotic areas. The most common tumours that metastasize to the jaws are breast, lung, kidney, prostate, and colon adenocarciomas and the most frequent site is the posterior mandible.
Lars Hollender and Karl-Åke Omnell