FEH is a rare but potentially serious disease of the mucosa. In 1965, Archard et al. [1
]. described Inuit and Indian children from North and South America suffering from verruciform papules and nodules on the oral mucosa, sometimes also affecting the anal and/or genital mucosa. Today it is known to exist in numerous populations and ethnic groups such as Eskimos, North, South, and Central American Indians [1
]. Although people of other races may be affected, there are relatively few reports of Caucasians with FEH [2
]. A comprehensive study was conducted in Sweden [5
] and a total of 17 cases (0.11% of the population) were found, with uncertain geographical or familial distribution. A series of 17 cases in Norwegian Caucasians had also been described [3
FEH is clinically characterized by multiple circumscribed, sessile, soft elevated nodules of the oral mucosa which sometimes form clusters. They are reddish or whitish or like the adjoining oral mucosa [1
]. In our case the clinical manifestations were similar to those usually reported. The condition usually occurs in children and has familial predilection, may last for several months, or years, before running its course [1
]. There is not a certain explanation for this feature but some authors proposed that the less developed immunologic system in children can be related with the beginning of the disease and later, developing of immunity is responsible for vanishing of the lesions. This may explain why no lesions are found in adults.
Setting the diagnosis of FEH is extremely important because of the need for the differential diagnosis with other conditions, namely inflammatory fibrous hyperplasia, inflammatory papillary hyperplasia, verruciforme xanthoma, verrucous carcinoma, Cowden’s disease, condyloma acuminatum, and focal dermal hypoplasia syndrome (Goltz–Gorlin syndrome) [2
]. The diagnosis of FEH can be made on the basis of clinical observations, but histological examination may show characteristics of viral infection, as reported here. Microscopically epithelial hyperplasia in FEH presents as an abrupt and considerable focal acanthosis. Koilocyte changes and mitosoid bodies are present in the superficial keratinocytes. Histopathologically, FEH was differentiated from papilloma and viral warts by its lack of pronounced surface projections and presence of mitosoid bodies [4
PCR is a rapid, sensitive and useful tool to identify the viral etiology of FEH lesions [7
]. An additional advantage of PCR using consensus primers to HPV detection is the range of viral diversity that can be identified. Once the presence of HPV was detected in the case presented in this paper, sequencing of PCR products was important to establish which viral type was actually the etiologic agent of FEH (in this case, HPV subtype 32).
FEH is described in the literature as a benign condition that heals spontaneously and therefore requires no treatment, except in some cases of functional (e.g., lesions that are constantly traumatized on biting) or aesthetic impairment [8
]. Several treatment modalities have been proposed for FEH like cryotherapy, electrocoagulation, treatment with carbon dioxide laser or systemic treatment with interferon-α or topical treatment of interferon-β and retinoic acid [9
]. In the case presented, the lesion on the left buccal mucosa was traumatized on biting and excised under local anaesthesia to arrive at a definitive diagnosis. Recurrence and the site of new lesions are unpredictable, and continued review of the patient is often necessary. The patient described here has been followed for 18 months without recurrences or changes in the aspect of the remaining lesions.
Hyperplasias are often mistaken in clinical experiences. There are many underlying factors for FEH such as genetic predisposition and a viral factor may be pointed out. Recent reports have indicated the presence of FEH in HIV infected patients. Supression of the immune system leaves the patient vulnurable to opportunistic infections, including HPV infections [9
]. The early detection of associated oral disease should, in many cases result in earlier diagnosis of HIV infection. Although many immunocompromised patients do develop many HPV lesions, some of which are caused by HPV subtypes with so called high-risk for malignancy (such as 18, 31, 33, 35 and 51). Recent research has shown no malignant potential for HPV 13 and 32 subtypes [10
There are many underlying factors for FEH such as genetic predisposition and a viral factor may be pointed out. The early detection of associated oral disease should, in many cases result in earlier diagnosis of HIV infection. Dental staff should be aware of these kind of lesions and histopathological examination together with a careful clinical observation should be carried out for a definitive diagnosis.