Beruflich Dokumente
Kultur Dokumente
David P. Goldstein, M.D., Henry T. Hoffman, M.D., F.A.C.S., John W. Hellstein, D.D.S., and
Gerry F. Funk, M.D., F.A.C.S.
that involve the oral mucosa: for instance, well over 100 medications are associated with lichenoid drug reaction, and even more
are associated with xerostomia. Use of alcohol or tobacco is a
notable risk factor for the development of oral cavity carcinoma,
as is a previous head and neck carcinoma. The quantity of alcohol or tobacco consumed should be determined because a doseresponse relationship exists between the level of use and the risk
of cancer. Other risk factors for oral cavity carcinoma include sun
exposure (lip cancer), human papillomavirus infection, and nutritional deficiencies. Radiation exposure is a risk factor for soft tissue sarcoma, lymphoma, and minor salivary gland tumors, and
HIV infection is a risk factor for Kaposi sarcoma.
PHYSICAL EXAMINATION
Diagnosis is probable
Estimate likelihood of malignancy.
Inflammatory lesion
Infectious
Viral: symptomatic treatment, antivirals if
patient is immunocompromised
Bacterial: antibiotics
Fungal: antifungals, usually topical (systemic
for persistent infection)
Oral hairy leukoplakia or unusual infection:
rule out HIV infection, refer patient to
infectious disease specialist
Noninfectious
Aphthous ulcer: symptomatic treatment,
topical anti-inflammatories
Traumatic ulcer: symptomatic treatment
Autoimmune: symptomatic treatment, topical
or systemic steroids
Necrotizing sialometaplasia: observation,
biopsy to rule out cancer
Tumorlike lesion
Benign neoplasm
Hyperkeratosis
Diagnosis is uncertain
Investigate further with culture and sensitivity, imaging,
or lab tests.
Consult dermatologist or hematologist as appropriate.
Perform biopsy if malignancy is possible.
Treat identified condition as appropriate (see below).
Dysplasia or CIS
Assess margins. If clear,
consider reexcision with wider
margins or observation; if close
or positive, perform reexcision
with frozen-section control.
Invasive cancer
Ensure adequate margins.
Consider reexcision with
frozen-section control.
Mucosal melanoma
Stage with CT, MRI, or PET.
Perform wide local excision.
Clinically positive neck:
neck dissection.
Clinically negative neck:
consider selective neck
dissection.
Consider postoperative
irradiation.
Kaposi sarcoma
the associated inflammation, but in the setting of cervical lymphadenopathy, the initial diagnostic assumptions should emphasize
the strong possibility of a primary oral cancer with metastases to
the neck. Asymmetrical enlargement of the parotid or submandibular glands may result either from obstruction of the ducts by
an oral cavity mass or from enlargement of nodes intimately associated with the glands. Symmetrical enlargement suggests a systemic process (e.g., Sjgren syndrome or HIV infection). The
Table 1
Inflammatory
lesions
Tumorlike
lesions
Neoplasms
Upper
Alveolus
Hard
Palate
Retromolar
Trigone
Buccal
Mucosa
Oral
Tongue
Floor of
Mouth
Lower
Alveolus
Lip
Figure 1
cavity.
Table 2
Serologic Tests
SLE
Sjgren syndrome
Antinuclear antibody, rheumatoid factor, antiRo (SS-A), and anti-La (SS-B) antibodies
Wegener granulomatosis
Sarcoidosis
bacterial, or viral infection is suspected, a small portion of a specimen may be sent separately for culture. If there is an associated
neck mass [see 2:3 Neck Mass], fine-needle aspiration (FNA) may
be performed to rule out metastatic disease. In general, FNA is
not useful for biopsy of oral lesions: incisional biopsy is often technically easier and provides more tissue.
EXAMINATION UNDER ANESTHESIA AND PANENDOSCOPY
Infectious
Viral stomatitis may be caused by a number of different viruses, including herpes simplex virus (type 1 or type 2), varicellazoster virus, and coxsackievirus [see Figures 2a and 2b].8 It is most
common in children and immunocompromised patients. The
lesions of viral stomatitis are generally vesicular, occur in the oral
cavity and the oropharynx, and erupt over the course of several
days to form painful ulcers. Eruption may be preceded by local
symptoms (e.g., burning, itching, or tingling) or systemic symptoms (e.g., fever, rash, malaise, or lymphadenopathy). The diagnosis is usually established by the history and the physical examination and may be confirmed by means of biopsy or viral culture.
Treatment of viral stomatitis primarily involves managing
symptoms with oral rinses, topical anesthetics, hydration, and
antipyretics. Systemic antiviral medications may shorten the
course of herpetic stomatitis and are indicated in immunocompromised patients.9
Candidiasis is a common fungal infection of the oral cavity [see
Figures 2c and 2d]. Candida albicans is the species most commonly responsible; however, other Candida species can cause this condition as well, with C. glabrata emerging as a growing problem in
immunocompromised hosts. Factors predisposing to oral candidal infection include immunosupression, use of broad-spectrum
antibiotics, diabetes, prolonged use of local or systemic steroids,
and xerostomia.10 Oral candidiasis presents in several different
forms [see Table 3], of which pseudomembranous candidiasis
(thrush) is the most common. This form is characterized by
white, curdlike plaques on the oral mucosa that may be wiped off
(with difficulty) to leave an erythematous, painful base (the
Auspitz sign). Widespread oral and pharyngeal involvement is
common.The diagnosis is based on the clinical appearance of the
lesion and on evaluation of scrapings with the potassium hydroxide (KOH) test. Culture is generally not useful, because Candida
is a common commensal oral organism.11
Ideally, initial management of oral candidiasis is aimed at
Figure 2 Shown are infectious lesions of the oral cavity: (a) primary herpes stomatitis of
the buccal mucosa and soft palate; (b) primary herpes stomatitis of the tongue (in the
same patient as in frame a); (c) oral candidiasis (pseudomembranous form); and (d) oral
candidiasis (erythematous form).
reversing the underlying condition, though this is not always possible. Treatment typically involves either topically administered
antifungal agents or, if infection is severe or topical therapy fails,
systemically administered antifungals. Patients who are immunocompromised or have xerostomia may benefit from long-term
prophylaxis.
Noninfectious
Recurrent aphthous stomatitis Aphthous stomatitis is a
common idiopathic ulcerative condition of the oral cavity [see
Figures 3a and 3b].The ulcers are typically painful and may occur
anywhere in the oral cavity and the oropharynx but are rarely
found on the hard palate, the dorsal tongue, and the attached gingiva.9 Affected patients often have a history of lesions, beginning
before adolescence. There are three different clinical presentations of recurrent aphthous stomatitis, of which minor aphthous
Table 3
ulcers are the most common [see Table 4].9 The diagnosis is made
on the basis of the history and the physical examination; biopsy is
reserved for lesions that do not heal or that grow in size.
Numerous therapies have been tried for recurrent aphthous
stomatitis, most with only minimal success. The majority of aphthous ulcers heal within 10 to 14 days and require no treatment;
however, patients with severe symptoms may require medical
intervention. Temporary pain relief can be obtained with topical
anesthetic agents (e.g., viscous lidocaine). Tetracycline oral suspension and antiseptic mouthwashes have also been used, with
varying success.9 Topical steroids are the mainstay of therapy and
may shorten the duration of the ulcers if applied during the early
phase.11 These agents may be applied either in a solution (e.g.,
dexamethasone oral suspension, 0.5 mg/5 ml) or in an ointment
(e.g., fluocinolone or clobetasol). Ointments work much better in
the oral cavity than creams or gels do. Systemic steroids are indicated when the number of ulcers is large or when the outbreak
has persisted for a long time.
Presentation
Pseudomembranous
Hyperplastic
Erythematous
Angular cheilitis
Figure 3 Shown are noninfectious inflammatory lesions of the oral cavity: (a) minor apthous ulcer of the lower lip; (b)
minor apthous ulcer of the upper lip; (c) necrotizing sialotmetaplasia of the hard palate; (d) resolution of necrotizing
sialometaplasia without treatment (in the same patient as in frame c); (e) pyogenic granuloma of the upper alveolus;
(f) reticular lichen planus involving the buccal mucosa; (g) lichen planus of the lateral tongue; (h) pemphigus vulgaris of
the oral cavity, with an erythematous base after rupture of bullae (involving the left lateral tongue, the buccal mucosa, and
the lip); and (i) traumatic ulcer of the tongue secondary to dental trauma.
ductal squamous metaplasia, preservation of the lobular architecture, and a nonmalignant appearance of squamous nests.12,13
Lesions resolve without treatment within 6 to 10 weeks [see
Figure 3d].
Pyogenic granuloma A pyogenic granuloma is an aggregation of proliferating endothelial tissue [see Figure 3e] that occurs
in response to chronic persistent irritation (e.g., from a calculus
or a foreign body) or trauma.10 The lesion appears as a raised,
soft, sessile or pedunculated mass with a smooth, red surface that
bleeds easily and can grow rapidly.14 Surface ulceration may
occur, but the ulcers are not invasive. The gingiva is the most
common location, but any of the oral tissues may be involved.
Conservative excision with management of the underlying irri-
ritic papules.The diagnosis is generally made on the basis of the history and the physical examination; biopsy is not always necessary.
For asymptomatic lesions, no treatment is required other than
observation.17 For painful lesions, which are more common with
the erosive form of the disease, either topical or systemic steroids
are appropriate.17 There is some controversy regarding the risk of
malignant transformation; however, long-term follow-up is still
recommended.16,18 The main risk posed by lichen planus may be
the masking effect that the white striae cause, which can prevent
the clinician from observing the early leukoplakic and erythroplakic changes associated with epithelial dysplasia.
Ulcer from autoimmune disease Oral ulcers may be the
first manifestation of a systemic illness.The most common oral manifestation of systemic lupus erythematosus (SLE) is the appearance
of painful oral ulcers in women of childbearing age. Patients with
Behet disease present with the characteristic triad of painful oral
ulcers, genital ulcers, and associated iritis or uveitis. Patients with
Crohn disease or Wegener granulomatosis frequently manifest oral
ulceration during the course of the illness. These disorders should
be managed in conjunction with a rheumatologist.
Mucous membrane pemphigoid and pemphigus vulgaris are
chronic vesiculobullous autoimmune diseases that frequently affect
the oral mucosa [see Figure 3h]. In mucous membrane pemphigoid,
the antibodies are directed at the mucosal basement membrane,
resulting in subepithelial bullae.16 These bullae rupture after 1 to 2
days to form painful ulcers, which may heal over a period of 1 to 2
weeks but often do not display a predictable periodicity. Oral pain
is often the chief complaint, but there may be undetected ocular
involvement that can lead to entropion and blindness.
Pemphigus vulgaris is a more severe disease than mucous membrane pemphigoid. In this condition, the antibodies are directed at
intraepithelial adhesion molecules, leading to the formation of
intraepithelial bullae.9 The blisters are painful and easily ruptured
and tend to occur throughout the oral cavity and the pharynx.19 The
Nikolsky sign (i.e., vesicle formation or sloughing when a lateral
shearing force is applied to uninvolved oral mucosa or skin) is present in both pemphigus and pemphigoid. In most cases, biopsy with
pathologic evaluation (including immunofluorescence studies) is
Table 4
Type of Aphthous
Ulcer
Presentation
Time to
Resolution
Minor
Major (Sutton
disease)
46 wk, with
scarring
Herpetiform
12 wk
Palatal and mandibular tori are benign focal overgrowths of cortical bone [see Figures 4a and 4b].10 They appear as slow-growing,
asymptomatic, firm, submucosal bony masses developing on the
lingual surface of the mandible or the midline of the hard palate.14
When these lesions occur on the labial or buccal aspect of the
mandible and the maxilla, they are termed exostosis.20 Torus
mandibularis tends to occur bilaterally, whereas torus palatinus
arises as a singular, often lobulated mass in the midline of the hard
palate. Surgical management is required only if the tori are interfering with denture fit.
MUCOCELE AND MUCOUS RETENTION CYST
A fibroma is a hyperplastic response to inflammation or trauma [see Figures 4f and 4g].22 It is a pedunculated soft or firm mass
Figure 4 Shown are tumorlike lesions of the oral cavity: (a) torus mandibularis, with
bilateral bony protuberances on the lingual surface of the mandible; (b) mandibular
exostosis, with a unilateral bony protuberance on the labial-buccal surface of the
mandible; (c) mucocele of the lip (note the bluish hue of the cystic lesion; cf. frame e);
(d) mucocele of the floor of the mouth associated with the sublingual gland (ranula);
(e) mucous retention cyst of the lower lip (presenting much like mucocele, but appearing more transparent); (f) fibroma of the hard palate resulting from denture trauma;
(g) fibroma of the lower lip; and (h) dentigerous cyst (a unilocular radiolucency surrounding the crown of an unerupted tooth, with no bone destruction).
pressure resorption and to inflammation caused by retained keratin. Management involves either excision or debridement and
creation of a well-ventilated and easily maintained cavity.24
ODONTOGENIC CYST
Neoplastic Lesions
A dentigerous cyst is an epithelium-lined cyst that, by definition, is associated with the crown of an unerupted tooth [see
Figure 4h]. Such cysts cause painless expansion of the mandible
or the maxilla. Treatment involves enucleation of the cyst and its
lining and extraction of the associated tooth.23
An odontogenic keratocyst is a squamous epitheliumlined
cyst that produces keratin. Bone resorption occurs secondary to
BENIGN
Squamous Papilloma
Squamous papilloma is one of the most common benign neoplasms of the oral cavity [see Figures 5a and 5b].13 It usually presents as a solitary, slow-growing, asymptomatic lesion, typically
f
Figure 5 Shown are benign neoplasms of the oral cavity: (a) squamous papilloma of the frenulum; (b) squamous papilloma of the ventral tongue; (c) pleomorphic adenoma of the hard palate; (d) pleomorphic adenoma of the hard
palate on coronal CT (note the soft tissue thickening along the left hard palate,
with no bone erosion or destruction); (e) ameloblastoma of the left angle and
ramus of the mandible (a multilocular radiolucency); and (f) ameloblastoma on
CT, with a soft tissue mass in the left mandible and erosion of the lingual plate
of the mandible.
hematoma that leads to bony expansion and giant cell proliferation.26 Eventually, erosion of the buccal cortex may occur with the
development of facial swelling.
Management involves enucleation and curettage.26 The surgeon
should be prepared for bleeding during treatment. The use of calcitonin or intralesional steroid injections is gaining popularity.
Minor Salivary Gland Neoplasms
less than 1 cm in diameter. It is well circumscribed and pedunculated and has a warty appearance.16 The palate and tongue are the
sites most frequently affected13; occasionally, multiple sites are
involved. The presumed cause is a viral infection, most likely
human papillomavirus.25
Papillomas are managed with complete excision, including the
base of the stalk.
Giant Cell Lesions
Central giant cell granulomas, brown tumors of hyperparathyroidism, aneurysmal bone cysts, and lesions associated with genetic diseases (e.g., cherubism) may all be seen in the jaws. Of particular note is the aneurysmal bone cyst that may occur at sites of
trauma, which, in theory, is the consequence of an organizing
Leukoplakia
Leukoplakia is defined by
the World Health Organization as a whitish patch or
plaque that cannot be characterized clinically or pathologically as any other disease and
that is not associated with any physical or chemical causative agent
g
Figure 6 Shown are malignant lesions of the oral cavity: (a) polymorphous low-grade adenocarcinoma of
the hard palate (raised, erythematous lesion);
(b) extensive squamous cell carcinoma of the tongue,
the alveolar ridge, and the floor of the mouth; (c) squamous cell carcinoma of the right floor of the mouth,
with mandibular invasion on CT scan; (d) squamous
cell carcinoma of the lip (ulcerative lesion); (e) squamous cell carcinoma of the floor of the mouth (exophytic lesion); (f) squamous cell carcinoma of the hard
palate; and (g) squamous cell carcinoma of the retromolar trigone.
Table 5
Table 6
TX
T0
Tis
T1
T2
Amelanotic melanoma
Advanced stage at presentation
Tumor thickness > 5 mm
Presence of vascular invasion
Distant metastases
Primary
tumor (T)
Table 7
Growth Pattern
Ulceroinfiltrative
Exophytic
Endophytic
Superficial
T3
T4a
T4b
NX
N0
N1
Regional
lymph
nodes (N)
N2a
N2b
N2c
N3
Distant
metastases
(M)
MX
M0
M1
Stage 0
Tis
N0
M0
Stage I
T1
N0
M0
Stage II
T2
N0
M0
Stage III
T3
T1, T2, T3
N0
N1
M0
M0
Stage IVA
T4a
T1, T2, T3, T4a
N0, N1
N2
M0
M0
Stage IVB
Any T
T4b
N3
Any N
M0
M0
Stage IVC
Any T
Any N
M1
(70%80%) of alveolar ridge carcinomas occur on the lower alveolus, often in areas of leukoplakia.51
Oral cavity carcinoma is generally classified according to the
staging system developed by the American Joint Committee on
Cancer [see Tables 8 and 9].52 Staging is based on clinical examination and diagnostic imaging.The diagnosis is made on the basis of
biopsy and immunohistochemical staining (e.g., for cytokeratin
and epithelial membrane antigen).
Squamous cell carcinoma of the oral cavity is usually managed
with surgery, radiation therapy, or a combination of the two;
chemotherapy is used primarily for palliation of incurable disease.
For localized disease without bone invasion, the cure rate for radiation therapy is comparable to that of surgery.48 Advanced tumors
of the oral cavity are best managed with both surgery and irradiation. Traditionally, in North America, oral cavity cancer is treated
primarily with surgery, and postoperative radiotherapy is added if
the disease is advanced or if there are pathologic features indicative of a high risk of recurrence (i.e., positive margins on microscopy; extensive perineural or intravascular invasion; two or more
positive nodes or positive nodes at multiple levels; or nodal capsular extension). North American practice is reflected in the guidelines developed by the American Head and Neck Society (www.
headandneckcancer.org/clinicalresources/docs/oralcavity.php).
Postoperative radiation, if indicated, should be started 4 to 6
weeks after surgery. The total radiation dose depends on the clinical and pathologic findings; the usual range is between 50 and 70
Gy, administered over 5 to 8 weeks. Brachytherapy can be used as
an adjunct when close or positive margins are noted. Advances in
Incidence of Metastases
Lip
10%
Tongue
30%40%
Floor of mouth
50%
Alveoli
28%32%
Buccal mucosa
40%52%
Table 11
Tongue
Floor of mouth
Alveoli
50%60%
Retromolar trigone
Buccal mucosa
49%68%
Palate
Infectious and neoplastic oral cavity lesions are often the first
manifestation of HIV infection or the first indication of the progression to AIDS.
INFECTIONS
The two most common intraoral neoplasms in the HIV population are Kaposi sarcoma and non-Hodgkin lymphoma. Kaposi
sarcoma occurs most commonly in patients with HIV, though it is
not exclusive to this population. It frequently involves the oral cavity, showing a predilection for the attached mucosa of the palate
or the gingiva.68 The characteristic lesions are blue, brown, purple,
or red exophytic masses that may be either confined to the oral
mucosa or systemic. They are usually asymptomatic but may become painful or obstructive with growth or ulceration. Treatment
is aimed at palliation of symptoms and may involve sclerotherapy,
intralesional chemotherapy, laser ablation, cryotherapy, surgical
excision, or radiation therapy.69 Systemic chemotherapy may be
provided if the disease is systemic.
The risk of non-Hodgkin lymphoma is much higher in the
HIV population than in the general population.69 It should be
suspected in any HIV patient who presents with an intraoral mass
or an ulcerated lesion. Non-Hodgkin lymphoma appears as
painful lesions that show a predilection for the palate, the retromolar trigone, and the tongue. Associated symptoms include
facial paresthesias, loose dentition, fever, night sweats, and weight
loss. Local disease is managed with radiation, systemic disease
with chemotherapy.
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Acknowledgment
Figure 1
Tom Moore.