Lumps and swellings
in the jaws
INTRODUCTION
Jaw swelling is most often caused by developmental enlarge-
ments (e.g. tori or exostoses), which are benign, painless,
broad-based and self-limiting, usually with normal overlying
mucosa and typically require no intervention.
Jaw swelling is less commonly due to odontogenic causes
(unerupted teeth, infections, cysts or neoplasms) (Box 16.1).
Jaw swelling may occasionally be caused by non-odonto-
genic inflammatory or neoplastic disorders, or metabolic or
fibro-osseous diseases (Box 16.2).
Metastasis to the mouth is rare but is typically to the jaws,
especially the posterior mandible.
Imaging and other investigations (often biopsy) are almost
invariably required to assist the diagnosis of a jaw swelling.
Many of these conditions are discussed elsewhere in
the text. Here we discuss alphabetically other relevant but
­uncommon or rare, conditions.
BOX 16.1  Main causes of jaw swelling
■ Congenital (torus palatinus, torus mandibularis, exostosis)
■ Odontogenic (teeth, infections, cysts or neoplasms)
BOX 16.2  More advanced list of causes of jaw
swellings
Congenital (e.g. torus, exostosis)
■
■ Odontogenic
■ Cysts
■ Infections
■ Neoplasms
■ Post-operative or post-traumatic oedema or haematoma
■ Unerupted teeth
■ Non-odontogenic
■ Infections
■ Cysts
■ Neoplasms (e.g. myeloma, histiocytoses)
■ Pseudotumours (e.g. haemophilic pseudotumour)
■ Foreign bodies
■ Bone disease
■ Fibrous dysplasia
■ Cherubism
■ Neoplasms (e.g. sarcomas)
■ Osteomas (and Gardner syndrome)
■ Paget disease
16
ANEURYSMAL BONE CYST
Aneurysmal bone cyst is a rare lesion, which is actually not a cyst.
The aetiology remains obscure: approximately one-third appear
to be associated with other bone disorders, such as a giant cell
lesion, fibrous dysplasia and ossifying fibromas. This rare lesion
presents as an asymptomatic hard swelling of the jaw, sometimes
following a history of trauma. It may occur in any part of the skele-
ton. Radiographs show a unilocular, or ­multilocular translucency
with a honeycomb or ­soap-bubble appearance. Preoperative aspi-
ration shows bloody fluid with a low haematocrit, differentiating
it from undiluted blood in a vascular ­anomaly, such as haemangi-
oma. Diagnosis is confirmed by histology, which shows numer-
ous capillaries and blood-filled spaces, areas of haemorrhage
associated with multinucleated giant cells and irregular areas of
osteoid. Treat by thorough curettage or excision.
CHERUBISM
Cherubism is a rare genetically determined jaw disease, which
closely resembles fibrous dysplasia except for the autosomal
dominant inheritance (but variable expression) and associa-
tion with chromosome 4p and mutated gene SH3BP2 which
codes for a c-abl-binding protein. Painless symmetrical enlarge-
ment at the angles of the mandible and in the maxilla leads to
the typical ‘cherubic’ facial appearance. Cherubism presents at
2–4 years of age, lesions growing progressively until puberty
when they arrest or regress. Expansion of the alveolar bone
results in irregular spacing and premature loss of teeth and
­possibly disturbances to a developing dentition. Imaging shows
well-defined multilocular radiolucencies in the mandible, but
maxillary lesions are less clearly defined. Blood ­chemistry is
normal, although there may a raised alkaline phosphatase dur-
ing active growth periods. Histologically, the lesions ­consist of
loose ­vascular connective tissue with numerous multinucleated
giant cells and, as in fibrous ­dysplasia, there is fibrous replace-
ment of bone (Fig. 16.1). Other fibro-osseous lesions and giant
cell lesions of bone (giant cell granuloma, hyperparathyroidism,
giant cell tumours) should be excluded. Treatment of cherubism
is as for fibrous dysplasia (see also Noonan syndrome, Ch. 56).
EXOSTOSES
Bone prominences are not uncommon in the jaws and are
given different names which are site-specific. Torus palatinus
is found only in the midline of the hard palate (see below). 121
16 SECTION 2 COMMON COMPLAINTS
Fig. 16.1 Cherubism showing multinucleated giant cells
(arrowed) in fibrous stroma
Torus mandibularis is found only on the lingual surface of the
mandible, near the premolar teeth. Buccal exostosis is found
only on the facial surface of the alveolar bone, usually in the
maxilla. Exostoses typically appear in early adulthood, are
painless and may slowly enlarge over time. Bone prominences
usually require no treatment, and have no malignant potential.
Bony proliferations in other sites are considered to be usu-
ally either trauma-induced inflammatory periosteal reactions
(exostoses), or true neoplasms (osteomas). Unless such a
bony prominence is specifically located, is pedunculated or
is associated with an osteoma-producing syndrome such as
Gardner syndrome (Ch. 56), there is no way to differentiate
exostosis from osteoma, even histopathologically.
FIBROUS DYSPLASIA
Fibrous dysplasia is an uncommon disorder character-
ized by the replacement of an area of bone with fibrous
tissue. Mutations in signalling protein gene GNAS 1 may
be involved. Fibrous dysplasia usually presents as a painless
bony hard swelling, most often in a child and in the maxilla or
adjacent bones. The maxillary sinus is often involved, when
there may be encroachment on the orbit (causing proptosis)
and nasal cavity (causing obstruction). Expansion of the alve-
olar bone leads to disruption of occlusion, displacement of
teeth and possibly failure of eruption of teeth. Lesions appear
to stabilize with skeletal maturation.
Three types of fibrous dysplasia (FD) are recognized:
■ Monostotic (MFD), in which there is a single lesion in only
one bone.
■ Polyostotic (PFD), in which several lesions are present in
one or more bones.
■ McCune–Albright syndrome, PFD plus cutaneous pig-
mentation (cafe-au-lait type) on the same side as the bony
lesion, and precocious puberty (see Section 6).
Radiographically, there is either a translucent cystic appear-
ance in the affected bone, or mottled opaque areas likened
to ground glass. The lesions are often ill-defined and may
extend to, but not cross, suture lines. Serum calcium and
phosphate levels are normal but, in many, the serum alkaline
122 phosphatase level is high and urinary hydroxyproline is
Fig. 16.2 Fibrous dysplasia: Chinese characters formed
by bone
increased (findings similar to those in Paget disease).
Microscopically, the lesion consists of fibrous tissue that
replaces the normal bone and gives rise to osseous trabeculae
by metaplasia (Fig. 16.2). The osseous tissue is composed
of irregular (‘Chinese characters’) trabeculae of woven bone
lined by osteoblasts. Focal degeneration of fibrous tissue
accounts for the cystic spaces seen macroscopically. The
treatment of choice to correct any cosmetic defect is con-
servative surgery, preferably after the cessation of normal
skeletal growth. The lesion is not radio-sensitive; irradiation
may cause sarcomatous change.
GIANT CELL GRANULOMA
The central giant cell granuloma is an uncommon lesion only
seen in the tooth-bearing regions of the jaws, most commonly
in the mandible and typically in the second and third decades.
The true nature of these lesions is unknown but, as they are
invariably destructive, the term ‘reparative’ giant cell gran-
uloma would appear to be inappropriate. Lesions may be
symptomless or simulate a malignant neoplasm clinically and
radiographically. Occasionally, the lesion erodes through the
cortical bone where it presents as a domed, purplish submuco-
sal swelling. Radiography shows an ill-defined area of radio-
lucency and there may be resorption of the roots of related
teeth. Microscopy shows multinucleated giant cells irregularly
distributed in a cellular stroma of plump, spindle-shaped cells
which is often highly vascular. There may be areas of new
and old haemorrhage with haemosiderin pigment deposi-
tion. These microscopic features are indistinguishable from
the focal lesions of hyperparathyroidism, which can only be
excluded by the appropriate serological tests (calcium and
phosphate levels and alkaline phosphatase). Although central
giant cell granulomas may recur following curettage, they
virtually never metastasize.
METASTATIC TUMOURS IN THE JAWS
The jaws are not a common site for clinically obvious metas-
tases (‘secondaries’) but it is probable that sub-clinical
secondary deposits are not rare. The mandible is involved four

times as frequently as the maxilla, especially in the premo-
lar and molar region. In up to one-third of patients, the jaw
lesions are the first manifestation of a tumour. Most metasta-
ses originate from primary cancers of the breast, lung, kidney,
thyroid, stomach, liver, colon, bone or prostate via lymphatic
or haematogenous spread, and present as a lumps, ulceration,
pain, swelling, tooth loosening, sensory change or pathologi-
cal fracture. Metastases from the bronchus, breast, kidney or
thyroid gland are usually destructive and osteolytic. Prostatic
metastases tend to be osteoblastic and may be confused
radiographically with chronic osteomyelitis, Paget disease or
cemental lesions.
OSTEOID OSTEOMA AND
OSTEOBLASTOMA
These are benign bone tumours that are uncommon in the
skeleton generally and rare in the jaws, and their microscopic
features are similar, with a vascular stroma in which there are
trabeculae of osteoid surrounded by numerous, and darkly
staining, osteoblasts, but they have distinctive clinical and
radiological features.
Osteoid osteoma is usually seen in adolescents and young
adults, most frequently in the femur and fibia, is often painful
(particularly at night) and has a characteristic central radio-
lucent area or nidus surrounded by a rim of densely sclerotic
bone of variable thickness.
Osteoblastoma, on the other hand, shows progressive
growth without the osteosclerotic rim and is rarely painful.
OSTEOMA
Osteoma is a benign bone neoplasm which grows by the
continuous formation of lamellar bone. Osteomas are usually
unilateral, painless, hard smooth swellings covered by normal
oral mucosa. Multiple osteomas, cutaneous cysts or fibromas
and polyposis coli are features of Gardner syndrome; an auto-
somal dominant syndrome in which the polyps in the large
bowel may become malignant. Should a patient have multiple
bony growths or lesions not in the classic torus or buccal
exostosis locations, Gardner syndrome should be excluded.
PAGET DISEASE OF BONE
Paget disease of bone affects mainly older males. The
aetiology is unclear and incidence appears to be decreasing.
Viruses, particularly paramyxoviruses such as canine distem-
per or measles virus, have been implicated – but with little
evidence. There is a strong genetic component; 15–20% have
a first-degree relative with Paget disease. Mutations in seques-
tosome 1/p62 gene (SQSTM1/p62) are seen in about one-third,
and in 5–15% of patients with no family history. SQSTM1/
p62 protein is a selective activator of the transcription factor
NFB, which plays an important role in osteoclast differentia-
tion and activation in response to the cytokines RANK-ligand
and interleukin-1.
Paget disease is characterized by the total disorganization
of the normally orderly remodelling of bone and an anarchic
alternation of bone resorption and apposition (‘reversal lines’)
LUMPS AND SWELLINGS IN THE JAWS 16
Fig. 16.3 Paget disease showing bone reversal lines from
resorption/deposition with a ‘mosaic pattern’ (arrowed)
(Fig. 16.3) often with severe bone pain. In early lesions,
bone destruction predominates (osteolytic stage) and there
is bowing of long bones, especially the tibia, pathological
fractures, broadening/flattening of chest and spinal deformity.
If Paget disease is widespread, the increased bone vascular-
ity can lead to high output cardiac failure. As disease activity
declines, bone apposition increases (osteosclerotic stage) and
bones enlarge. If the skull is affected, the patient may notice
hat becomes tight. Constriction of skull foraminae may cause
cranial neuropathies. The maxilla often enlarges, particularly
in the molar region, with widening of the alveolar ridge and
any dentures may appear to become too tight. The dense bone,
hypercementosis and loss of lamina dura make extractions
difficult, and there is a liability to haemorrhage and infection.
Diagnosis is supported by imaging, biochemistry and histopa-
thology. In early lesions, large irregular areas of relative radio-
lucency (osteoporosis circumscripta) are seen, but later there
is increased radio-opacity, with appearance of an irregular
‘cotton wool’ pattern. There is progressive thickening of the
diploe and base of the skull as well as the sphenoid, orbital and
frontal bones. Isotope bone scanning shows localized areas of
very high uptake. Increase in plasma alkaline phosphatase and
urine hydroxyproline levels, but little or no changes in serum
calcium or phosphate levels. Differential diagnosis includes
other fibro-osseous lesions, such as fibrous dysplasia, and
conditions with a raised alkaline phosphatase, such as osteo-
malacia, hyperparathyroidism and osteoblastic metastatic
deposits (e.g. prostate carcinoma). Bisphosphonates are the
treatment.
TORUS PALATINUS AND MANDIBULARIS
Torus palatinus and mandibularis are common developmental
benign exostoses more common in Asians, especially Koreans.
They appear in late teens or adulthood and may become more
apparent with increasing age. They have a smooth or nodular
surface, and are of no consequence apart from occasionally
interfering with denture construction. The two types are not
necessarily associated one with another:
■ Torus palatinus occurs in the centre of the hard palate, is of
variable size and configuration (Fig. 16.4).
■ Torus mandibularis is lingual to the lower premolars and
usually bilateral (Fig. 16.5). 123
16 SECTION 2 COMMON COMPLAINTS
Fig. 16.4 Torus palatinus: central palatal symptomless bony
mass
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