The U.S. black population is prone to developing benign fibro-osseous lesions of various types. They range from localized lesions, such as focal cemento-osseous dysplasia, usually involving the apex of a mandibular molar, to periapical cemento-osseous dysplasia, usually involving the mandibular anterior teeth, to florid (multi-focal) cemento-osseous dysplasia, involving all four quadrants. The term cemento-osseous is preferred to cemental because a combination of cementum droplets and woven bone are usually present (Fig. 4-1).

Fibrous dysplasia, a malformation of bone, is of unknown cause and is not premalignant, although a gene (GNAS) has been identified for this condition. The monostotic form often affects the maxilla unilaterally. The polyostotic form is associated with various other abnormalities, such as skin pigmentations and endocrine dysfunction (Albright and Jaffe-Lichtenstein syndromes). Cherubism, which used to be termed familial fibrous dysplasia, is probably not a form of fibrous dysplasia and is associated with a different gene mutation (SH3BP2). In the past, fibrous dysplasia was treated with radiation, which sometimes caused the development of osteosarcoma. The best way to treat cherubism is by recontouring the bone after the teenage growth spurt and when lesions become quiescent.

False. Historically, the globulomaxillary cyst was classified as a nonodontogenic or fissural cyst thought to result from the entrapment of epithelial rests along the line of fusion between the lateral maxillary and nasomedial processes. Current thinking puts it into the category of odontogenic cysts of a) developmental origin, and possibly related to the development of the lateral incisor or canine (if the teeth are vital), or of b) inflammatory origin (radicular cyst) if the teeth are nonvital. The two embryonic processes mentioned do not fuse. The fold between them fills in and becomes erased by mesodermal invasion so that there is no opportunity for trapping of epithelial rests. This cyst occurs between the roots of the maxillary lateral incisor and cuspid.

True. The epithelium of this intrabony cyst arises from proliferation of entrapped epithelium when the right and left palatal shelves fuse in the midline. This should be distinguished from a nasopalatine duct cyst, which arises from remnants of the duct in the area of the nasopalatine foramen. The soft tissue counterpart, which also occurs in the midline of the palate and is known as the palatal cyst of the newborn (Epstein pearl), is congenital and exteriorizes on its own.

They are most likely dental lamina cysts of the newborn (Bohn nodules). The epithelium of these cysts arises from remnants of dental lamina on the alveolar ridge after odontogenesis. Sometimes they appear at the junction of the hard and soft palate. Dental lamina cysts of the newborn tend to involute and do not require treatment.

The boy most likely has the bifid rib–basal cell nevus syndrome, which is inherited as an autosomal dominant trait. The cysts are odontogenic keratocysts, which have a higher incidence of recurrence than other odontogenic cysts. The new name for keratocyst is keratocystic odontogenic tumor because they are now considered to be cystic neoplasms. Other findings include palmar pitting, palmar and plantar keratosis, calcification of the falx cerebri, hypertelorism, ovarian tumors, and neurologic manifestations, such as mental retardation and medulloblastomas. Mutation in the PTCH gene is responsible for this condition.

No. The odontogenic keratocyst–keratocystic odontogenic tumor is a specific histologic entity. There is some controversy as to whether this is a cyst or cystic tumor, with the new terminology favoring the latter. The epithelial lining exhibits corrugated parakeratosis, uniform thinness (unless altered by inflammation), and palisading of the basal cell nuclei. The recurrence rate is high, and the condition is associated with the basal cell carcinoma–bifid rib (Gorlin-Goltz) syndrome. Odontogenic cysts that produce orthokeratin do not show the basal cell nuclei changes, do not have the same tendency to recur, and are not associated with the syndrome. These cysts are referred to as orthokeratinized odontogenic cyst. The histologic distinctions are important because they have clinical and prognostic implications.

Ameloblastoma, mucoepidermoid carcinoma and, least commonly, squamous cell carcinoma may arise in a dentigerous cyst. Odontogenic tumors that may arise in a dentigerous relationship, although not within a dentigerous cyst, include adenomatoid odontogenic tumor, calcifying cystic odontogenic tumor (Gorlin cyst) and calcifying epithelial odontogenic tumor (Pindborg tumor). The odontogenic keratocyst or keratocystic odontogenic tumor, formerly classified as a cyst and now as a cystic neoplasm, are often seen in a dentigerous relationship with an impacted tooth (Fig. 4-2).

A lateral radicular cyst is an inflammatory cyst in which the epithelium is derived from rests of Malassez (like a periapical or apical radicular cyst). It is in a lateral rather than an apical location because the inflammatory stimulus is emanating from a lateral accessory canal. The associated tooth is always nonvital. The lateral periodontal cyst is a developmental cyst in which the epithelium probably is derived from rests of dental lamina. It is usually located between the mandibular premolars, which are vital.

Cleft lip and cleft palate should be considered as two entities, (1) cleft palate alone and (2) cleft lip, with or without cleft palate. The former is more common in females and the latter in males. The incidence of cleft palate alone is 1 in 2000 to 3000 births, whereas the incidence of cleft lip with or without cleft palate is 1 in 700 to 1000 births (highest in Asians and Native Americans). Of all cases, 25% are cleft palate alone and 75% are cleft lip with or without cleft palate.

Most cases of benign migratory glossitis are associated with atopy (history of hay fever, asthma, and eczema) and some human leukocyte antigen (HLA) types. Some cases have been associated with fissured tongue and patients with psoriasis, especially generalized pustular psoriasis, have a higher incidence of benign migratory glossitis. (Fig. 4-3).

Hairy tongue is not a developmental lesion but a benign reactive condition. It is caused by reduced shedding and increased buildup of the keratin of the filiform papillae of the tongue. Factors that predispose to this include dehydration, smoking, and reduced intake of coarse foods, fresh foods, and vegetables. Most patients have a history of a recent illness and have been on antibiotics, systemic steroids, and oxygenating mouth rinses. The papillae are putatively colonized by chromogenic bacteria, so the tongue may appear black, brown, or even green. It does not represent candidiasis.

Predisposing factors include the following: (1) poor immune function, which may be related to age (very young and very old), malignancies, immunomodulating medications (topical or systemic), endocrine dysfunction, or human immunodeficiency virus (HIV) infection; (2) malnutrition; (3) antibiotics that upset the normal balance of flora; (4) dental prostheses, especially dentures that act as fomites; and (5) alteration in saliva flow and constituents.

No. Approximately one-quarter to one-third of the adult population harbors Candida spp. in the mouth. Swabs from patients who are carriers for candida who do not have candidiasis, will grow candida.

False. Actinomycetes is a gram-positive bacteria. Do not be fooled by the suffix -mycosis.

These yellowish granules (hence the name) are seen within the pus of lesions of actinomycosis. They represent aggregates of Actinomyces (usually A. israelii), which are invariably surrounded by neutrophils.

Aspergillosis and zygomycosis tend to infect immunocompromised hosts; the latter causes rhinocerebral infections in patients with diabetes mellitus.

Histoplasmosis (caused by Histoplasma capsulatum) is endemic in the Ohio-Mississippi basin, coccidioidomycosis (caused by Coccidioides immitis) is endemic in the San Joaquin Valley in California, and blastomycosis (caused by Blastomyces) dermatitidis is endemic from the Great Lakes basin to the Mississippi valley.

False. The herpes viruses are unique in that they exhibit latency. Once a person has been infected by HSV-1, the virus remains latent within the sensory ganglia (e.g., trigeminal ganglion) for life. When conditions are favorable (for the virus, not the patient), HSV travels along nerve fibers and causes a mucocutaneous lesion at a peripheral site, such as a cold sore on the lip. A positive antibody titer (immunoglobulin G [IgG]) indicates that the patient has been previously exposed, and at the time of reactivation the titer may rise. Hypersensitivity to recurrent HSV infections may lead to an ulcerative condition called erythema multiforme.

Clinically, recurrent aphthous ulcers (minor) occur only on the nonkeratinized mucosae of the labial mucosa, buccal mucosa, sulci, ventral tongue, soft palate, and faucial pillars. Recurrent herpetic ulcers occur on the vermilion border of the lips (cold sores or fever blisters) and on the keratinized mucosae of the palate and attached gingiva in immunocompetent individuals. A culture confirms the presence of virus. In immunocompromised hosts, however, recurrent herpetic lesions may occur on the keratinized and nonkeratinized mucosae and may mimic aphthous ulcers (Fig. 4-5).

The patient has herpes zoster infection, which typically is unilateral. The patient also has Ramsay-Hunt syndrome, which is caused by infection of cranial nerves VII and VIII with herpes zoster, leading to facial paralysis, tinnitus, deafness, and vertigo.

Infectious mononucleosis usually presents as multiple, painful, punctate ulcers of the posterior hard palate and soft palate in young adults or adolescents. It is often associated with regional lymphadenopathy and constitutional signs of a viral illness, such as fever and malaise.

The benign conditions are usually associated with HPV-6 and -11; the malignant ones are usually associated with HPV-16 and -18. Heck’s disease is associated with HPV-13 and HPV-32.

Herpangina and hand-foot-and-mouth disease are caused by the type A coxsackievirus and generally affect children, who then develop oral ulcers associated with an upper respiratory tract viral prodrome. Lymphonodular pharyngitis is also caused by coxsackievirus.

Koplik spots are early manifestations of measles or rubeola (hence they also are called herald spots). They are 1- to 2-mm, yellow-white ulcers with surrounding erythema that occur on the buccal mucosa, usually a few days before the body rash of measles is seen. Koplik spots are not usually seen in German measles.

Noma, which is a gangrenous stomatitis resulting in severe destruction of the orofacial tissues, is usually encountered in areas in which malnutrition is rampant. The bacteria are similar to those associated with acute necrotizing ulcerative gingivitis—namely, spirochetes, fusiform bacteria, and others. It is sometimes seen in patients with AIDS.

Strictly speaking, a granuloma is a collection of epithelioid histiocytes that is often associated with multinucleated giant cells such as the Langhans-type giant cells seen in granulomas of tuberculosis (caused by Mycobacterium tuberculosis). Many infectious agents, including fungi (e.g., Histoplasma spp.) and those causing tertiary syphilis (Treponema pallidum) and cat scratch disease (Bartonella henselae), can produce granulomatous reactions. Foreign body reactions are often granulomatous. Orofacial granulomatosis may be related to hypersensitivity to foods, flavorings, and preservatives. Crohn’s disease and sarcoidosis are granulomatous diseases of unclear etiology (Fig. 4-6).

Langhans cells are multinucleated giant cells seen in granulomas, usually those caused by M. tuberculosis. Their nuclei have a characteristic horseshoe distribution. Do not confuse them with Langerhans cells, which are antigen-processing cells.

False. The periapical granuloma is a tumor-like (-oma) proliferation of granulation tissue found around the apex of a nonvital tooth. It is associated with chronic inflammation from pulp devitalization. The inflammation can stimulate proliferation of the epithelial rests of Malassez to form an apical radicular or periapical cyst (Fig. 4-7).

Condensing osteitis, a relatively common condition, manifests as an area of radiopacity in the bone, usually adjacent to a tooth that has a large restoration or endodontic therapy, although occasionally it may lie adjacent to what appears to be a sound tooth. It is asymptomatic. Histologically, condensing osteitis consists of dense bone, with little or no inflammation. It probably arises as a bony reaction to a low-grade inflammatory stimulus from the adjacent tooth. Idiopathic osteosclerosi, bone scar and dense bone island are terms used for similar bone lesions unassociated with teeth.

False, but with reservations. A traumatic ulcer is the most common form of oral ulcer and, as its name suggests, occurs at the site of trauma, such as the buccal mucosa, lateral tongue, lower labial mucosa, or sulci. It follows a history of trauma, such as mastication or toothbrush injury. An aphthous ulcer may occur at the same sites, but often with no history of trauma. However, patients prone to developing aphthae tend to do so after episodes of minor trauma (Fig. 4-8).

This is a factitial injury. Children may inadvertently chew their tongues and buccal mucosae while tissues are numb from local anesthesia because the tissues feel strange to the child. Children and parents should be advised to be alert for such behavior.

It depends. The term mucocele refers loosely to a cystlike lesion that contains mucus and usually occurs on the lower lip, ventral tongue, or floor of the mouth. However, it may occur wherever mucous glands are present. In most cases, it is not a true cyst because it is not lined by epithelium. It is caused by escape of mucus into the connective tissue when an excretory salivary duct is traumatized. Therefore, the mucocele is lined by fibrous and granulation tissue. In a few cases, it is caused by distention of the excretory duct because of a distal obstruction or the presence of a sialolith; the preferred term is salivary duct cyst.

This painless ulcer usually develops on the hard palate but may occur wherever salivary glands are present. It represents vascular compromise and subsequent infarction of the salivary gland tissue, with reactive squamous metaplasia of the salivary duct epithelium that may mimic squamous cell carcinoma. The lesion resolves on its own.

The first thing is to rule out chronic atrophic candidiasis (denture stomatitis or denture sore mouth) because this much more common. The patient should be treated with fluconazole (much more effective than nystatin or clotrimazole) or Mycostatin–triamcinolone cream applied directly to the denture to be worn by the patient; the denture must also be soaked in an antifungal agent overnight because it is a fomite. If these measures are taken and there is no response, the patient should be patch-tested by an allergist or dermatologist to a panel of denture base materials, which include metals and acrylic polymerization products. Usually, the lesions resolve with topical steroids.