ABSTRACT
Gastroesophageal reflux disease [GERD] is a major public health problem that may cause erosive or nonerosive esophagitis in symptomatic patients. The severity of esophagitis in GERD seems to be correlated not only to the amount of reflux and altered motor activity but also to the ability of the mucosa to resist injury and repair the damage. This study aimed to evaluate the cell proliferation status of esophageal epithelium in both normal individuals and patients with GERD with or without erosions and its correlation with the degree of inflammation of the esophagus. This study was carried out on 33 individuals; their ages ranged between 17 and 74 years. All participants were subjected to a clinical assessment and an endoscopic evaluation. Four biopsies were taken using an endoscope at 5 cm from the Z-line; histological esophagitis was identified and graded. Cell proliferation was evaluated by Ki-67 immunostaining. The prevalence of GERD was the highest in the 15-29 years age group [46.43%] and decreased with age. Cell proliferation [estimated by the Ki-67-labeling index [Ki-67 LI]] was reduced in esophageal epithelium in erosive [13.44%] and nonerosive [36.83%] reflux disease in relation to normal individuals [68%]. There was a statistically significant positive correlation between cell proliferation [Ki-67 LI] and the endoscopic grade of esophagitis among patients with erosive disease. However, there was no significant correlation between cell proliferation [Ki-67 LI] and the histological grade of esophagitis in both erosive and nonerosive reflux disease. The ability of the mucosa to resist injury and to repair the damage should be considered a key factor in the development of GERD. Esophageal mucosa exposed to chronic acid insult show reduced cell replication, estimated by the Ki-67 LI. Erosive esophagitis in GERD seems to be related to a low cell proliferation rate of esophageal epithelium rather than the amount of reflux
ABSTRACT
Background/Aims: Differential diagnosis between aggressive osteoblastoma and low grade osteosarcoma may be very diffi cult or even impossible on a small biopsy. This study was designed to assess the usefulness of immunoexpression of COX-2 and osteocalcin in the differential diagnosis of the two tumour types. Methods: Immunostaining of COX 2 and osteocalcin were studied in 9 osteoblastomas and 30 osteosarcomas. Results: All osteoblastomas and 11/20 (55%) high-grade osteosarcomas showed COX-2 immunoreactivity. All low grade osteosarcomas were COX-2 negative. COX-2 was signifi cantly higher (p<0.002) in osteoblastomas 9/9 (100%) than in osteosarcomas 13/30 (43%) and in aggressive osteoblastomas versus low grade osteosarcomas (p<0.01). Osteocalcin was found in tumour cells of all osteosarcomas and osteoblastomas and in the osteoid matrix of 84% of osteosarcomas and 78% of osteoblastomas. Strong osteocalcin was signifi cantly higher (p<0.02) in osteoblastomas (78%) than in osteosarcomas (27%). Conclusion: COX-2 is a valuable marker in distinction between osteosarcoma and osteoblastoma. Negative COX-2 could confi rm the diagnosis of low grade osteosarcoma versus aggressive osteoblastoma. Intensity and distribution of osteocalcin may indicate the degree of osteoblastic differentiation.