Verrucous Hyperplasia

considerable acanthosis with broadened rete ridges causes deprivation of distant epithelial cells from blood supply and appearance becomes edematous and swollen. These necrotic cells undergo desquamation. Also leaving cleft in the surface of the epithelium. Verrucous projections are formed in this way in between clefts. At a later stage both the verrucous projections and the clefts undergo keratinization [5].
This is a case of verrucous hyperplasia with candidal superinfection in a background of early oral submucous fibrosis. OSF is a precancerous condition associated with chronic betel and areca nut chewing. A clear dose dependent relationship was observed for both frequency and duration of chewing areca nut in development of OSF [10]. Fibrosis is resulted by increased collagen synthesis or reduced collagen degradation. Development of squamous cell carcinoma
is seen in one-third of the OSF patients, but the development of verrucous hyperplasia is rarely reported. According to clinico pathological study done by Hazarey VK et al. [6] there is a One of cases verrucous hyperplasia in a background of submucous fibrosis. That has been showed adjacent atrophic epithelium and juxtaepithelial hyalinization, showing features of OSF.
Diagnosis of lesions can be confirm by biopsy. The most reliable way is routine haematoxylin-eosin stained tissue sections to recognize the exophytic growth patterns of oral verrucous hyperplasia. C-erb B-3 protein expression was an index of malignancy during progression from Verrucous Hyperplasia to Verrucous Carcinoma and Squamous cell carcinoma[11]. Expression of P53 and EGFR levels could be used as marker while differentiating verrucous hyperplasia from verrucous carcinoma and squamous cell carcinoma [12].
Many reports have considered oral verrucous hyperplasia as a potentially malignant disorder [5]. However, it has not been listed as potentially malignant disorder by the WHO [5]]. Verrucous carcinoma is consider as a low grade malignancy. It has recognized as a forerunner of verrucous carcinoma. Therefor these two lesions should be managed identically [5].
In a hospital based follow-up study from Taiwan where oral verrucous hyperplasia is very common, the malignant transformation rate was estimated at 20% in a cohort of forty-four male subjects with verrucous hyperplasia [1].
Verrucous carcinoma has been treated with different modalities such as excision with
ORAL VERRUCOUS HYPERPLASIA
7 | P a g e or without radical surgery, chemotherapy, radiation, or a combination of these modalities [13].
Surgery is the most common treatment modality. The use of radiotherapy is controversial. The conventional treatment of oral verrucous hyperplasia is total surgical excision.
Recurrence and/or transformation of oral verrucous hyperplasia to either verrucous carcinoma or conventional SCC have been report after surgical intervention. Shear and Pindborg had reported recurrence in four of their patients with lesions showing both verrucous hyperplasia and verrucous carcinoma [4]. According to clinico pathological study done by HazareyVK et al. 13 cases were treated with surgical excision. Two cases were treated with lasers. Few showed evidence of recurrence after excision. Laser operated two cases showed recurrence within one year of follow-up [9]. Wide surgical excision of the primary verrucous lesion with adequate mucosal and soft-tissue margin is necessary to avoid local recurrence [5].
Conclusion.
Oral verrucous hyperplasia was reported as a premalignant lesion by many researchers, although WHO is not still reported. The clinical diagnosis of this condition is difficult and histological features are essential for separate this from similarly appearing conditions. Therefor correct diagnosis, adequate, surgical intervention and follow up care are essential for good prognosis of this condition.