Receptor activator NFκB-ligand and osteoprotegerin protein expression in human periapical cysts and granulomas

Menezes, Renato; Bramante, Clóvis Monteiro; Paiva, Katiúcia Batista Silva; Letra, Ariadne; Carneiro, Everdan; Zambuzzi, Willian Fernando; Granjeiro, José Mauro

doi:10.1016/j.tripleo.2005.10.054

Cited by 59 publications

(63 citation statements)

References 40 publications

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“…Recent studies have focused on the etiopathogenesis of chronic periapical lesions, odontogenic cysts and tumors, using immunohistochemistry to investigate the role of cytokines, growth factors, cellular differentiation factors, tumor suppressor genes and oncogenes in the initiation, development, and progression of these lesions (4,6,(12)(13)(14)(15)(16)(17).…”

Section: Discussionmentioning

confidence: 99%

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Immunohistochemical expression of p63, epidermal growth factor receptor (EGFR) and notch-1 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors

et al. 2012

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The aim of this study was to assess the immunohistochemical expression of p63 protein, epidermal growth factor receptor (EGFR) and Notch-1 in the epithelial lining of radicular cysts (RC), dentigerous cysts (DC) and keratocystic odontogenic tumors (KOT). For this study, 35 RC, 22 DC and 17 KOT were used. The clinical and epidemiological data were collected from the patient charts filed in the Oral Pathology Laboratory, University of Ribeirão Preto, Brazil. Immunohistochemical reactions against the p63, EGFR and Notch-1 were performed in 3-µm-thick histological sections. The slides were evaluated according to the following criteria: negative: <5% of positive cells, low expression: 5-50% of positive cells, and high expression: >50% of positive cells. Moreover, the intensity of EGFR and Notch-1 expressions was also evaluated. Fisher's exact test and Spearman's correlation coefficients were used for statistical analysis, considering a significance level of 5%. Almost all cases demonstrated p63, EGFR and Notch-1 expressions. The p63 expression was significantly higher in KOT (p<0.001). Positive correlation between these immunomarkers was observed. These findings suggest the participation of p63, EGFR and Notch-1 in the development, maintenance and integrity of cystic odontogenic epithelial lining, favoring lesion persistence. The high expression of p63 in KOT suggests that it may be related to their more aggressive biological behavior and marked tendency to recurrence.

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Section: Discussionmentioning

confidence: 99%

“…Several growth factors and other endogenous regulator mediators have been identified in RC, DC and KOT (3)(4)(5)12,13,15). The association of these mediators with the Notch-1 expression might induce the epithelial cell proliferation, with consequent growth of the lesions.…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical expression of p63, epidermal growth factor receptor (EGFR) and notch-1 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors

et al. 2012

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“…More recent studies have shown expression of RANK, RANKL, and OPG in the lining epithelium and walls of odontogenic cysts, including periapical cysts and granulomas [25]. Da Silva et al [9] evaluated these bone resorption regulators in odontogenic lesions.…”

Section: Discussionmentioning

confidence: 99%

The Role of RANK/RANKL/OPG Signalling Pathways in Osteoclastogenesis in Odontogenic Keratocysts, Radicular Cysts, and Ameloblastomas

Tekkeşın

Mutlu

Olgaç

2011

Head and Neck Pathol

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The aim of this study was to evaluate the immunohistochemical expression of molecules involved in osteoclastogenesis, including the receptor activator of nuclear factor kappa B (RANK), RANK ligand (RANKL) and osteoprotegerin (OPG) in odontogenic keratocysts (OKCs), which has been named as a keratocystic odontogenic tumour by the WHO, and compare their expression with radicular cysts and ameloblastomas. RANK is a member of tumour necrosis factor receptor family and it is activated by RANK ligand. OPG binds to RANKL and inactivates it. The imbalance of these factors could cause the differential bone resorption activity in some diseases and tumours. The expression of these molecules was evaluated in ameloblastomas (n = 20), OKCs (n = 20), and radicular cysts (n = 20) by immunohistochemistry. Immunohistochemical reactivity for RANK, RANKL, and OPG was detected in neoplastic and nonneoplastic epithelium and connective tissue cells. RANK showed the greatest expression in OKCs followed by ameloblastomas, with the lowest expression seen in radicular cysts. Expression of RANKL was detected in all lesions and no significant differences were observed between groups. OPG was expressed very low in all groups. In the stroma, the number of RANK positive cells was higher in OKCs when compared with ameloblastomas and radicular cysts but radicular cyst had higher numbers of RANKL positive cells in the stroma than ameloblastomas. The molecular system of RANK/RANKL/OPG is variably expressed in OKCs, radicular cysts, and ameloblastomas and this system may be involved in the osteoclastogenic mechanisms in OKCs and ameloblastomas. Advanced studies could further clarify the role of RANK, RANKL, and OPG in mediating tumour associated bone osteolysis.

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“…The slides were dried overnight at 37°C, the paraffin was removed in xylene, and re-hydration was achieved with consecutive ethanol washes (100%, 95%, 70%). Endogenous peroxidase was blocked in 3% hydrogen peroxide for 45 min, antigenic retrieval was performed in phosphate-citrate buffer (pH 6.0 at 96°C; P4809, Sigma-Aldrich, Mo., USA) for 20 min, and non-specific binding was blocked by incubation with 4% non-fat milk solution for 20 min, as described elsewhere (Accorsi-Mendonça et al 2005;Menezes et al 2006;Corotti et al 2009;Zambuzzi et al 2009b). Sections were incubated overnight at 4°C with polyclonal primary antibodies, namely goat anti-human MMP-2 (sc 6838), goat anti-human MMP-3 (sc 6839), goat anti-mouse MMP-9 (sc 6841), and goat anti-mouse RECK (sc 9689).…”

Section: Immunohistochemistrymentioning

confidence: 99%

Development of secondary palate requires strict regulation of ECM remodeling: sequential distribution of RECK, MMP-2, MMP-3, and MMP-9

et al. 2010

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We have evaluated RECK (reversion-inducing-cysteine-rich protein with Kazal motifs), MMP-2 (matrix metalloproteinase-2), MMP-3, and MMP-9 involvement during palate development in mice by using various techniques. Immunohistochemical features revealed the distribution of RECK, MMP-2, and MMP-3 in the mesenchymal tissue and in the midline epithelial seam at embryonic day 13 (E13), MMPs-2, -3, and -9 being particularly expressed at E14 and E14.5. In contrast, RECK was weakly immunostained at these times. Involvement of MMPs was validated by measuring not only their protein expression, but also their activity (zymograms). In situ hybridization signal (ISH) for RECK transcript was distributed in mesenchymal and epithelial regions within palatal shelves at all periods evaluated. Importantly, the results from ISH analysis were in accord with those obtained by real-time polymerase chain reaction. The expression of RECK was found to be temporally regulated, which suggested possible roles in palatal ontogeny. Taken together, our results clearly show that remodeling of the extracellular matrix is finely modulated during secondary palate development and occurs in a sequential manner.

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Receptor activator NFκB-ligand and osteoprotegerin protein expression in human periapical cysts and granulomas

Cited by 59 publications

References 40 publications

Immunohistochemical expression of p63, epidermal growth factor receptor (EGFR) and notch-1 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors

Immunohistochemical expression of p63, epidermal growth factor receptor (EGFR) and notch-1 in radicular cysts, dentigerous cysts and keratocystic odontogenic tumors

The Role of RANK/RANKL/OPG Signalling Pathways in Osteoclastogenesis in Odontogenic Keratocysts, Radicular Cysts, and Ameloblastomas

Development of secondary palate requires strict regulation of ECM remodeling: sequential distribution of RECK, MMP-2, MMP-3, and MMP-9

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