Detection of epidermal growth factor receptor in inflammatory periapical lesions

Abstract

Epithelial cell proliferation is often observed in periapical lesions of endodontic origin. The mechanisms which stimulate the epithelial cell rests of Malassez to proliferate are not understood fully. Fifteen inflammatory periapical lesions (10 granulomas and five cysts) obtained from periapical surgery and six additional periapical lesions (four granulomas and two cysts) collected from extracted teeth were examined using immunohistochemical staining and 125I-EGF (epidermal growth factor) binding assay to detect the presence of epidermal growth factor receptor. The results indicated that the periapical lesions without epithelial cell proliferation had a weak immunoperoxidase staining or low specific binding of 125I-EGF. In contrast, the periapical lesions with epithelial cell proliferation and cyst formation exhibited a strong immunoperoxidase staining in the epithelial cells or high specific binding of 125I-EGF.

Area of Rests of Malassez in Young and Adult Rat Molars: Evidences in the Formation of Large Rests

“…It has been demonstrated that the cells of RM express epidermal growth factor (EGF), which participates in the proliferation and differentiation of these epithelial cells (Thesleff, 1987;Nordlund et al, 1991). Furthermore, the proliferative activity of epithelial cells is modulated by growth factors, inflammatory mediators, and cytokines such as tumor necrosis factor (TNF), transforming growth factor-a (TGF-a), prostaglandins (PGE 2 ), and interleukin-1 and interleukin-6 (Lin et al, 1996). The cervical region is usually susceptible to inflammatory processes (Rincon et al, 2006) and, then, several cytokines can be released.…”

Immunohistochemical Expression of Notch Signaling in the Lining Epithelium of Periapical Cysts

“…Epithelial cell proliferation in periapical cyst has been demonstrated by the expression of proliferation markers, eg, ki67, in the lining epithelium (38). Considering the established role of Notch signaling in stem/progenitor cell maintenance, differentiation, and proliferation, the activation of Notch pathway in the epithelial cells of periapical cysts as well as the reported expression of other endogenous regulatory mediators and growth factors (4)(5)(6)(7)(8) in periapical cystic wall indicate that periapical cysts are in dynamic state, and the growth and expansion of cysts might be related to epithelial cell proliferation caused by those factors. In addition, Notch has been shown to affect cell cycle kinetics (39), and in particular, Notch 1 has antiapoptotic properties in T cells by preventing death by neglect and/or negative selection in cells destined to die Basic Research-Biology (40).…”

“…Their pathogenesis has been attributed to persistent microbial infection within the root canal system of a tooth (1), but the molecular mechanisms that stimulate proliferation of epithelial cells considered crucial in generating the cyst have not been clarified. Several endogenous regulatory mediators such as cytokines, prostaglandins, interleukins (4)(5)(6), the keratinocyte growth factor (KGF) (7) and the epidermal growth factor (EGF) receptor (8), expressed in cystic wall, might be involved.…”

Experimental evidence supports the abscess theory of development of radicular cysts

“…But, none of the control cages that received only epithelial cells showed the development of cyst-like pathology, an observation that would with limitations discredit the theory of central epithelial necrosis. (10,11) This means that the establishment and proliferation of epithelium was more successful in trial cages, probably due to the influence inflammatory mediators and growth factors released during the inflammation (16,18,19) as a consequence of the bacterial inoculation. Our additional, limited data (not included here) showed that pure cultures of Actinomyces israelii or a mixture Porphyromonas endodontalis and…”

“…(7)(8)(9)(10)(11)(12)(13)(14) The formation of the cysts has been described as taking place in three stages. (15) During the first phase the dormant epithelial cell-rests proliferate, probably under the influence of inflammatory cytokines and growth factors (16)(17)(18)(19) that are released by various cells residing in the apical lesion. During the second phase an epithelium-lined cavity comes into existence, the mechanism of which is unknown.…”