Higher expressions of p53 and proliferating cell nuclear antigen (PCNA) in atrophic oral lichen planus and patients with areca quid chewing.
OBJECTIVE
The aim of the study was to examine the expressions of p53 and proliferating cell nuclear antigen (PCNA) in oral lichen planus (OLP) in relation to its clinical behavior and the patients' oral habits.


METHODS
Immunohistochemical study was carried out to investigate the expressions of p53 and PCNA in 56 OLP specimens. The results were correlated with the clinical behavior of the disease and the patients' oral habits. The expression rates were further compared with those of normal oral mucosa (NOM), epithelial hyperkeratosis (EH), epithelial dysplasia (ED), and squamous cell carcinoma (SCC).


RESULTS
The staining rate of p53 (28.6%) and PCNA labeling index (LI) (27.6 +/- 8.8%) in OLP were similar to those in EH ( P = .868, .074, respectively), but higher than those of NOM and lower than those of ED and SCC (all P < .05). In OLP, no significant correlations were found between p53 or PCNA expression and the patients' age, gender, lesion duration, location, size, number of site, presence of pain, presence of local irritant, and the habits of alcohol drinking and cigarette smoking (all P > .05). In addition, the mean PCNA LI of p53+ cases was close to that of p53- cases (P = .38). However, the staining rate of p53 in OLP was higher in areca quid (AQ) chewers compared to abstainers (P = .001), and the mean PCNA LI in atrophic cases was higher than that in hypertrophic cases (P = .029). Interestingly, the staining rate of p53 and mean PCNA LI were significantly increased in AQ chewers with atrophic OLP (100%, 36.7% +/- 9.0%, respectively), which were similar to those in ED and SCC (all P > .05).


CONCLUSIONS
Although this study could not confirm the precancerous nature of OLP by the relatively low p53 and PCNA expression, the results do suggest that atrophic form OLP and patients with AQ chewing habit may have a higher disease activity in view of higher expression rates of p53 and PCNA in the lesions.
Lee
Jang-Jaer
JJ
Department of Dentistry, National Taiwan University Medical Center, Taipei, Taiwan, 10016.
Kuo
Mark-Yenping
MY
Cheng
Shi-Jung
SJ
Chiang
Chun-Pin
CP
Jeng
Jiiang-Huei
JH
Chang
Hao-Hueng
HH
Kuo
Ying-Shiung
YS
Lan
Wan-Hong
WH
Kok
Sang-Heng
SH
D000293:Adolescent; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D001114:Areca / Q000009:adverse effects*; D002294:Carcinoma, Squamous Cell / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D017676:Lichen Planus, Oral / Q000150:complications / Q000378:metabolism* / Q000473:pathology; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D009061:Mouth Mucosa / Q000378:metabolism; D009062:Mouth Neoplasms / Q000378:metabolism; D011230:Precancerous Conditions / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis / Q000096:biosynthesis*; D019966:Substance-Related Disorders / Q000150:complications* / Q000209:etiology / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000096:biosynthesis*
D018809:Proliferating Cell Nuclear Antigen; D016159:Tumor Suppressor Protein p53