{"id":148,"date":"2026-05-01T10:51:10","date_gmt":"2026-05-01T10:51:10","guid":{"rendered":"http:\/\/200okconsulting.com\/?p=148"},"modified":"2026-05-01T10:51:10","modified_gmt":"2026-05-01T10:51:10","slug":"all-pdpn-positive-cells-were-restricted-to-the-basal-layer-of-the-epithelial-lining-with-a-small-amount-of-extension-23-layers-of-cells-toward-the-parabasal-or-lower-middle-layers-the-upp","status":"publish","type":"post","link":"https:\/\/200okconsulting.com\/?p=148","title":{"rendered":"\ufeffAll PDPN-positive cells were restricted to the basal layer of the epithelial lining, with a small amount of extension (23 layers of cells) toward the parabasal or lower middle layers; the upper layers were negative for this protein (Fig"},"content":{"rendered":"

\ufeffAll PDPN-positive cells were restricted to the basal layer of the epithelial lining, with a small amount of extension (23 layers of cells) toward the parabasal or lower middle layers; the upper layers were negative for this protein (Fig. single basal layer. The expression level of PDPN was significantly decreased (P<0.05) and a significant loss or reduction of PDPN expression was observed in KCOTs following decompression. Larger sample groups are required to further verify this result. Keywords:keratocystic odontogenic tumour, decompression, podoplanin, immunohistochemistry == Introduction == According to the 2005 World Health Organization classification, keratocystic odontogenic tumour (KCOT), which was previously termed odontogenic keratocyst, is usually categorised as a benign odontogenic tumour (1). Several factors justified this decision (2), including the following: i) Clinically, KCOT behaves as a locally destructive and highly recurrent lesion; ii) histopathologically, it is typical to observe the basal epithelial layer budding into the connective tissue and the absence of mitotic figures in the suprabasal layer; and iii) genetically, mutations of the tumour suppressor gene, Patched 1, in systemic or sporadic KCOT were successively reported by Lenchet al(3) and Barretoet al(4), indicating that dysregulation of the Hedgehog signalling pathway is usually involved in the molecular pathogenesis. At present, marsupialisation or decompression combined with two-stage curettage or enucleation is usually a common treatment for large KCOT. This treatment has the advantage of minimal invasiveness and the preservation of appearance and function (1). This procedure decreases the size of the lesion (5) and in specific circumstances, leads to a lower recurrence rate (1), although a final conclusion has not been reached Farampator<\/a> with regard Rabbit polyclonal to Ki67<\/a> to this potential benefit (2). To improve the outcome of decompression, it is necessary to elucidate the underlying molecular mechanisms of this therapy. Podoplanin (PDPN), a 3643-kDa mucin-like transmembrane glycoprotein, is usually widely used as a marker for lymphatic endothelial cells (6). However, recent studies have shown that this protein is also expressed in a variety of normal tissues, as well as neoplastic tissues in pathological and physiological settings (6,7). This molecule has diverse functions, including regulation of organ development, cell motility, tumourigenesis and metastasis (6,8,9). Previous studies (7,10) have reported Farampator that Farampator PDPN is usually markedly expressed in KCOTs, as in the cases of ameloblastoma and adenomatoid odontogenic and calcifying cystic odontogenic tumours, but unfavorable in orthokeratinised odontogenic cysts (OOCs) and dentigerous cysts, suggestive of its neoplastic nature. It is likely that this upregulated expression of PDPN has a role in the processes of tumour proliferation and invasion. Following decompression, the intracystic environment of KCOTs change. Furthermore, several previous studies found that the typical histological features were lost (11,12) and that a variety of biomarkers associated with proliferation (12), invasion, cell differentiation (13) or apoptosis (14) were downregulated following the therapy. To the best of our knowledge, the manner in which the expression of PDPN changes following decompression has not been previously reported. Through the immunochemical detection of 16 cases, the present study is the first to report that this PDPN expression in KCOTs is usually notably downregulated following this therapy. == Materials and methods == == Patients == The presents study analysed the cases of 16 patients with histologically confirmed KCOTs from the Stomatology Hospital of Jiangsu Province (Nanjing, China) and the Shanghai Ninth Peoples Hospital (Shanghai, China). Recurrent cases or those associated with nevoid basal cell carcinoma syndrome were excluded. All patients underwent decompression surgery followed by two-stage cyst enucleation. The clinical information of the patients is usually shown inTable I. Post-operative follow-up was comprised of clinical and radiographic examinations between January 2004 and September 2012. The average duration of draining and irrigation prior to the two-stage surgery was 19.5 months (range, 6.544.0 months). == Table I. == Patient clinical information and intensity of PDPN expression. Group I samples were obtained at the time of decompression and group II samples were obtained at the time of two-stage enucleation. Immunohistochemical activity was Farampator measured as follows: 2, strongly positive; 1, weakly to moderately positive; and 0, unfavorable. PDPN, podoplanin; M, male; F, female; Ant, anterior region; Ang, angular region; Mol, molar region; Ram, mandibular ramus. Paraffin specimens of the tissue samples that were obtained at the time of decompression and enucleation were gathered from the Division of Oral Pathology of the Stomatology Hospital of Jiangsu Province and the Shanghai Ninth Peoples Hospital. All patients provided signed.<\/p>\n","protected":false},"excerpt":{"rendered":"

\ufeffAll PDPN-positive cells were restricted to the basal layer of the epithelial lining, with a small amount of extension (23 layers of cells) toward the…<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[18],"tags":[],"class_list":["post-148","post","type-post","status-publish","format-standard","hentry","category-mapk"],"_links":{"self":[{"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/posts\/148","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=148"}],"version-history":[{"count":1,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/posts\/148\/revisions"}],"predecessor-version":[{"id":149,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=\/wp\/v2\/posts\/148\/revisions\/149"}],"wp:attachment":[{"href":"https:\/\/200okconsulting.com\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=148"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=148"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/200okconsulting.com\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=148"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}