Head and Neck






Figure 6.1


Normal tongue, gross

Viewed superiorly, the abundant submucosal lymphoid tissue (lingual tonsil) gives the posterior tongue (♦) a lobulated surface. The small indentation at the posterior tongue represents a vestigial foramen cecum (▲). The tongue surface has papillae. The filiform papillae impart a velvety texture to the upper surface and allow for a scraping function. Circumvallate papillae (+) arranged in a “V” pattern toward the back of the tongue have associated taste buds. Foliate papillae at the posterolateral aspects have associated taste buds. Fungiform papillae have a rounded surface and are nonkeratinized to give the appearance of a red dot pattern on the dorsum of the tongue and have associated taste buds.



Figure 6.2


Normal tongue, microscopic

The tongue is covered with thick stratified squamous epithelium. The bulk of the tongue consists of the genioglossus muscle with the muscle bundles arranged in three planes to provide movement in any direction. The squamous mucosa extends across the floor of the oral cavity to become the gingiva at the base of the teeth. Scattered throughout the tongue, but more prominent toward the back of the tongue, are minor salivary glands (♦).



Figure 6.3


Normal head, CT image

This normal axial CT scan of the head and neck shows the relationships of the maxilla (+) with teeth and nasopharynx (♦), tongue (□), ramus of mandible (∗), masseter muscle (◼), C2 and dens (▲), spinal canal (†), internal jugular vein (◀), internal carotid artery (▶), and parotid gland (×).



Figure 6.4


Cold sore, gross

The small “cold sore” seen here on the buccal mucosa just inside the lower lip is usually the result of herpes simplex virus type 1 (HSV-1) infection. Most adults have had past HSV-1 infection, but it remains latent, only to produce small sores during periods of stress, from local trauma, or with environmental changes such as exposure to cold. This vesicle may rupture to produce an ulcer, which can become secondarily infected. A similar lesion is the aphthous ulcer, or “canker sore,” which can appear under conditions of stress, local trauma, or hormonal changes but does not have an infectious etiology. Up to 40% of the population have had aphthous ulcers, particularly during the second decade of life. They spontaneously resolve.



Figure 6.5


Oral candidiasis, gross

The tongue is covered with a tan, matted layer of Candida organisms enmeshed in a fibrinopurulent exudate, forming the pseudomembranous form of candidiasis. This can be scraped off to reveal an erythematous base. Candida albicans is a frequent oral commensal, present in half of the population; it is normally held in check by normal oral flora. The “thrush” as seen here is most likely to occur in immunocompromised individuals.



Figure 6.6


Mucormycosis (zygomycosis), microscopic

Note the broad, nonseptate hyphae (▲) (6 to 50 μm wide) with necrotizing inflammation. Infection with Mucor circinelloides and related genera Rhizopus and Absidia of the “true” sexual fungi (Zygomycetes) can produce extensive tissue invasion and necrosis. Inhalation of airborne spores by immunocompromised individuals, particularly patients with diabetes mellitus in ketoacidosis, corticosteroid therapy, and neutropenia, can lead to nasopharyngeal, pulmonary, and gastrointestinal infection. Spread of these organisms into the orbit and intracranial cavity (rhinocerebral mucormycosis) is a feared complication.



Figure 6.7


Leukoplakia, microscopic

In this excised lesion from the buccal mucosa, the overlying squamous epithelium is thickened (acanthotic), producing the gross appearance of a white plaque (leukoplakia) on the oral mucosa. In addition, the underlying submucosa has increased collagen deposition, leading to the diagnosis of irritation fibroma in this patient with ill-fitting dentures. Although no cellular atypia is seen here, persistent leukoplakia can be a precursor to squamous atypia and carcinoma. Besides mechanical irritation, use of tobacco, alcohol, and betel nut can predispose to leukoplakia. Areas of grossly red and eroded epithelium denote erythroplakia, which carries a higher risk for malignant transformation.



Figure 6.8


Squamous cell carcinoma, CT image

Shown is a prominent mass (▲) involving the right posterior base of the tongue in the region of the lingual tonsil. There is a large confluent mass of adjacent lymph nodes (♦) involved with metastatic squamous carcinoma. The oral cavity, floor of the mouth, tongue, and soft palate are the most common locations for squamous carcinoma to arise, but multiple lesions may occur. Distant metastases may involve lungs, liver, and bone marrow. The major risk factors are tobacco use (particularly the “smokeless” tobacco products) and alcohol abuse. In regions where chewing betel nut is popular, the incidence of oral cavity cancers is higher. Half of oropharyngeal cancers are associated with human papillomavirus infection. Chronic mucosal irritation from trauma or infection may promote the neoplastic process. Approximately 95% of head and neck primary carcinomas are squamous cell carcinomas, and these currently constitute the sixth most common malignant neoplasm in the world. Mutations of p16 , p63 , and TP53 tumor suppressor genes are common.



Figure 6.9


Occult metastasis, positron emission tomography/CT image

Positron emission tomography (PET) is a nuclear medicine procedure that uses a radiolabeled substance, fluorodeoxyglucose (FDG), preferentially taken up by cells which use glucose more readily, such as cancer cells with the aerobic glycolytic metabolic pathway. The CT scanner uses x-rays for detailed imaging of a body site, and when the PET scan is superimposed, localization of FDG uptake is possible. In this PET/CT of the neck, there is a single bright orange focus of uptake representing carcinoma metastasis to a lymph node, not otherwise detectable, and it represents persistence of the cancer requiring further treatment.



Figure 6.10


Squamous cell carcinoma of tongue, gross

The large fungating mass seen here involving the right posterior tongue has extensive surface ulceration. This large mass led to difficulty swallowing and progressive cachexia. Squamous cell carcinomas may progress from in situ lesions to invasive lesions over a variable time that can range from months to years. Smaller lesions discovered earlier have a less advanced stage, are more easily excised, and have a better prognosis, but most of these oropharyngeal cancers are discovered at a more advanced stage.



Figures 6.11 and 6.12


Ameloblastoma, gross and CT image

On the left , a coronal section through an excised portion of the mandible reveals a mass lesion (♦) that is below a molar tooth. This lesion is slow growing and locally invasive but has a benign course in most cases. The head CT scan in the “soft-tissue window” shows the mass lesion (♦) expanding the left mandibular ramus of a teenage boy. The histologic pattern of an ameloblastoma mimics the enamel organ of the tooth. Neoplasms of a related histologic appearance include craniopharyngiomas of the sella turcica and adamantinomas of long bone.





Figure 6.13


Odontogenic abscess, CT image

This head CT scan shows an abscess (♦) involving the first molar of the left mandible. Lack of dental care can lead to serious complications from dental caries. When the tooth enamel is breached, infection can reach the inner tooth pulp and extend down the tooth root to the tooth socket and the bone of the mandible or maxilla. One measure of the health of a society is directly proportional to the level of dental care.



Figure 6.14


Nasal polyps, CT image

These lobulated soft-tissue densities (♦) in the nasal cavities are inflammatory, or allergic, nasal polyps extending into paranasal sinuses. Although benign, they can obstruct the nasal passages and cause discomfort from difficulty breathing and mass effect. The polyps start as local inflammation with areas of edema and enlargement of the turbinates. Patients with such polyps may have a history of allergic rhinitis, or “hay fever,” from increased inflammatory reactivity with type I hypersensitivity to allergens such as plant pollens. The allergens contact and cross-link IgE bound to mast cells, causing degranulation with immediate release of vasoactive amines such as histamine, which cause vasodilation and fluid exudation. There is also mast cell synthesis of arachidonic acid metabolites, such as prostaglandins, which produce more vasodilation. Mast cell cytokines, such as tumor necrosis factor and interleukin-4, attract neutrophils and eosinophils. Only approximately 0.5% of atopic individuals develop nasal polyps. The polyps can reach 3 to 4 cm in length and produce nasal airway obstruction.



Figure 6.15


Allergic nasal polyp, microscopic

Recurrent attacks of rhinitis may lead to the development of nasal polyps, which may be multiple and measure a few millimeters to several centimeters in size. There is overlying respiratory mucosa at the left, an underlying edematous stroma with inflammatory cells, including the eosinophils, characteristic of an acute allergic response. Neutrophils, plasma cells, and occasional clusters of lymphocytes also can be seen here in the later inflammatory reaction. Such polyps are rare in children and are most often seen in individuals older than 30 years. Sometimes these polyps can become eroded and secondarily infected. Such polyps can be excised.



Figure 6.16


Sinonasal papilloma, microscopic

Note the respiratory pseudostratified epithelium overlying invaginations extending beneath the surface as an endophytic lesion. They may arise from human papillomavirus type 6 or 11 infection, typically in adult men from ages 30 to 60. These benign but locally aggressive lesions arise in the nose and paranasal sinuses and may recur if not completely excised. The exophytic form of sinonasal papilloma is covered by squamous epithelium.



Figure 6.17


Nasopharyngeal angiofibroma, CT image

Here is a mass (♦) filling and expanding the nasal cavity on the left. The maxillary sinuses are not involved. It can cause nosebleeds and nasal obstruction and sometimes proptosis or facial deformity. Angiofibromas arise at the sphenopalatine foramen in the posterolateral aspect of the nasal wall. This uncommon lesion is almost always seen in adolescent boys. Although initially circumscribed, it can slowly invade into surrounding bone. More invasive lesions can extend laterally into the pterygopalatine fossa and posterior nasal cavity or superiorly to the sphenoid sinus and orbit. Intracranial invasion can occur with involvement of the cavernous sinus, sella, and optic chiasm.



Figure 6.18


Nasopharyngeal angiofibroma, microscopic

The nasal angiofibroma is histologically benign but can produce a mass effect to block the nasal passages, erode adjacent structures, ulcerate, and bleed. The tumor is composed of a collagenous stroma with plump to spindled fibroblastic or myoblastic cells along with scattered capillaries but absent mitoses. Larger thin-walled staghorn-like vascular spaces may be present. They can recur following excision.

Dec 29, 2020 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Head and Neck
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