1997 Volume 43 Issue 2 Pages 62-70
Among 221 patients with primary oral SCCs, 18 (8.1%) had late recurrence at the primary site from 36 to 175 months after the initial treatment. Late recurrence of oral carcinomas was evaluated clinicopathologically, and the following results were obtained:
1) Late recurrence occurred at a significantly higher incidence in T 1 tumors than T 2-4 tumors.
2) As for the clinical growth pattern, superficial type primary tumors were more likely to have late recurrence than exophytic or endophytic type (p>0.05).
3) There was no difference in late recurrence rate between patients who received chemotherapy and those who received no chemotherapy. Among 69 patients who received radiation, radiation-induced oral carcinoma occurred in 1 patient (1.4%), 11 years after radiotherapy.
4) Histopathologically, the degree of differentiation and mode of invasion, were similar for primary and recurrent lesions.
5) Late recurrence occurred in tumors associated with epithelial dysplasia (13/71 cases, 18.3%) at a significantly higher rate than those lacking epithelial dysplasia (3 /105 cases, 2.9%). Epithelial dysplasia adjacent to carcinoma was also observes in 93.8% of primary lesions with late recurrence.
6) Margin status was an important factor affecting lacal recurrence rate but not late recurrence rate.
7) Among the 18 primary tumors with late recurrence, tumor suppressor gene, p53, was detected in 50% of primary carcinomas, 26.7% of dysplasia, and 11.1% of normal epithelium.
These results suggest that late recurrence is a de novo carcinoma caused by field cancerization. Epithelial dysplasia adjacent to cancer is an important factor in predicting late recurrence of oral carcinomas. Thus, long-term follow-up is necessary for such patients, even when primary tumors are small and completely resected.
