Juxtaoral Organ of Chievitz

Chievitz's organ, or the bucco-temporal organ, is thought to be a vestigial neuroepithelial structure. It has also been suggested that the juxtaoral organ is an anlage of the parotid gland, or arises from Schwann cells that have undergone squamous metaplasia [132]. It has been demonstrated in neonates and children and can persist into adult life [16]. The organ is usually found between the temporalis muscle and the bucco-temporal fascia or pterygomandibular raphe, and is usually present bilaterally. It is seen fortuitously, generally in material taken from surgical resections, and is important as it can be misinterpreted as a squamous cell carcinoma. Very rare cases have presented as tumours in the infratemporal fossa [83]. It is usually only a few millimetres in size and microscopically forms a multilobulated mass of discrete cell nests that resemble squamous epithelium, but do not show obvious keratinisation. Occasionally, the cells have clear cytoplasm and form duct-like structures that may contain mucin-negative colloid. The cell nests are associated with nerve fibres, particularly at the periphery, and this may be mistakenly interpreted as a squamous carcinoma with perineural involvement, or sometimes mu-coepidermoid carcinoma and thyroid carcinoma [103]. The central areas of the epithelial cell nests are positive for cytokeratin 19 and most cell nests are positive for vimentin and weakly positive for epithelial membrane antigen. They are negative for S-100 protein, glial acidic fibrillary protein, and neuroendocrine markers such as chromogranin, synaptophysin and neurone-specific enolase [132]. A similar appearance to the juxtaoral organ has rarely been described elsewhere in the mouth, including intraosseous locations [47].

Herpes simplex is a common virus that often causes subclinical infections. It is, however, a cause of serious and sometimes fatal illnesses in immunocompromised patients. In the orofacial tissues, clinically apparent infections can be primary or recurrent. The majority of cases of oral infections are due to Herpes simplex type 1, but an increasing proportion is being attributed to Herpes simplex type 2, which is typically more closely associated with genital infections. The virus is transmitted by close contact. Although in the past primary herpes affected children most frequently, in Western societies it is seen increasingly in young and middle-aged adults.

Primary herpes infection (primary herpetic gingivo-stomatitis) is characterised by widespread vesicular lesions of the oral mucosa [183]. Any site may be involved, but the hard palate and the dorsum of the tongue are the most common locations. The vesicles quickly rupture to leave shallow, painful, sharply demarcated ulcers that are 1-2 mm in diameter and have an erythematous halo. Ulcers frequently coalesce to form more irregular lesions. Gingivitis is a very characteristic feature of primary herpes. The gingivae are swollen and often strikingly erythematous, even in the absence of frank ulceration. There is often conspicuous cervical lymphade-nopathy, together with mild fever and malaise. Oral lesions usually resolve spontaneously within 1-2 weeks. About a third of patients infected with Herpes simplex, either clinically or sub-clinically, are susceptible to recurrent infections.

It is uncommon for herpetic lesions to be biopsied (Fig 3.1). In the early stages there is intercellular oedema and ballooning and vacuolisation of keratinocytes due to intracellular oedema. This leads to intraepithe-lial vesiculation. Nuclei become enlarged, and occasionally basophilic or eosinophilic nuclear inclusions with a clear halo (Lipschutz bodies) can be identified. Cells may fuse to form multinucleated epithelial giant cells. The vesiculation is followed rapidly by epithelial necrosis and breakdown, leading to ulceration and more florid inflammatory infiltration.

Herpes simplex virus can persist in a latent form in the trigeminal ganglion and when re-activated causes recurrent infections. These are typically seen at the mucocutaneous junctions of the mouth or nasal cavity, and involvement of the lips, the most common site, is called herpes labialis. A variety of apparently disparate factors can trigger re-activation, including the common cold ("fever blister"), exposure to sunlight, menstruation, stress and others. There is usually a brief prodromal burning or prickling sensation in the affected area, followed by the formation of a localised cluster of vesicles. These rapidly break down, ulcerate and crust. The lesions usually heal spontaneously in 1-2 weeks. Occasionally there may be intraoral recurrences, particularly in the hard palate. These may be triggered by local anaesthetic injections. Persistently recurrent intraoral herpes, however, should always raise the possibility of immunosuppression. Atypical and often very severe forms of intraoral herpes infections can be seen in patients who are immunocompro-mised [21].

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