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Schwannomas are relatively slow-growing benign tumors of the nerve sheath. Schwannomas are relatively rare in occurrence. The head and neck region is the least affected site. The clinical features of intraoral schwannoma are not adequately tackled in the literature. The paper underpins the literature for similar cases. This manuscript reports also a rare case of a palatal schwannoma in a 33-year-old female and reviews the challenges of diagnosis and prognosis of hard palate schwannoma.

Sjogren syndrome (SS) is an autoimmune epithelitis characterized by lymphocytic glandular infiltration and various extraglandular manifestations. SS is usually encountered in middle-aged females (>50 years). Immunological, viral, hereditary, environmental and hormonal etiologic factors are controversially proposed with regard to the pathogenesis of SS with no upper hand given. The present study reports an atypical case of SS in a 25-year-old female who was closely followed up for three years. Being pregnant in 2015, SS ran a total remission course but did relapse more aggressively after delivery. Immunologically implicating, the possible interpretation, which may account for such a pathological fluctuation, is also tackled.

Quite rarely, major salivary glands tend to display neural tumors. Intraparotid facial nerve schwannoma, when encountered, is often confusing given the similarity of the histological pictures of such tumors with other primary salivary variants and phenotypes as well as the lack of definitive histological findings of fine needle biopsies. Therefore, the final decision is usually made, at the surgical setting. There, the lesional intimacy to the nerve and the frozen biopsy of the safety margins determine, quite correctly, the best treatment option. This paper reports a rare case of intraparotid facial nerve schwannoma and focuses light on such a diagnostic challenge.

This study aims at investigating the pathogenesis and oncogenesis of ameloblastoma. Being the commonest odontogenic tumor with idiopathic nature, ameloblastoma poses a fierce controversy about its oncogenesis. Immunohistochemical markers, over years, have highlighted specific pathways which are inherently undertaken in the tumorigenic process of ameloblastoma. Besides the recently pronounced clue of BRAF V600E mutant gene, this study introduces a new marker with its outstanding impact on our contemporary knowledge about ameloblastoma. Extrapolating from the systematic review of medical literature and recruiting a novel immunohistochemical marker, ameloblastoma enacts a new scenario supporting the approved involvement of MAPK by overexpressing WT1 a total of 37 archival cases, regardless of the histological variant in study. There evinces a significant contribution of Wilm's tumor gene, as an oncogene rather than a suppressor gene, to the pathogenesis of the ameloblastomatous tumorigenesis. Moreover, no ameloblastomatous histological phenotype has established, given the literature underpinned, a concrete impact on the clinical behavior. Immunohistochemical research papers which investigated tumorigenesis - although they do not quantitatively measure much- had the most significant impact on the diagnostic and prognostic levels. WT1 may play, therefore, a remarkable role in the oncogenesis of ameloblastoma.

Bizarre parosteal osteochondromatous proliferation (BPOP), or eponymically Nora's lesion, is a rare growing, to a certain extent, exophytic lesion usually emanating from the periosteum or its adjacent layers. BPOP is idiopathically painful . Given its cartilage-producing nature and pain, BPOP is viewed with great suspicion. Regular post-surgical radiographs and clinical follow-up are mandatory. In the gnathic bones, the lesion is extremely rare. To the author's best knowledge, this paper reports the sophomoric appearance of BPOP in the anterior maxilla, in an adult female.

Adenoid ameloblastoma (AA) is a very rare subtype of solid/multicystic ameloblastoma. It demonstrates areas of typical or atypical adenomatoid odontogenic tumor along with the ameloblastic content. To date, there are 17 reported cases of AA. This paper reports, however, the first introduced adenoid variant in a peripheral ameloblastoma. It also depicts an unusual appreciation of cellular atypia and nuclear pleomorphism. This find may promote a new pathogenetic scenario to the current nosology of this debatable lesion and to the WHO taxonomy of benign ameloblastomas in 2005.

Caliber persistent artery is a rarely reported lesion which prefers, given the underpinned literature, the labial arteries. This paper reports a very rare case of an isolated palatal ulcerative lesion in a non-insulin dependent diabetic patient. The patient refused to run any radiological tests, other than the periapical radiograph, but consented the incisional biopsy. Therefore, histochemical and immunohsitochemical stains were ushered to establish, non-invasively, a diagnosis. Accordingly, this paper explores the diagnostics and differential diagnosis of caliber persistent artery and reviews briefly the previously reported cases.

Adenomatoid odontogenic tumor (AOT) is always a benign tumor with rare incidence of recurrence while ameloblastoma is the commonest gnathic tumor, which is always aggressive. Although co-occurrence of these lesions has been reported, this paper describes a homogenous combination of atypical AOT and ameloblastomatous proliferation with some malignant microscopic features. To date, A dozen cases or slightly more of this uncommon composite odontogenic tumor have been, quite correctly, reported in the literature under the designation of adenoid ameloblastoma. Of these, neither cellular atypia nor pleomorphism has been revealed. This extremely rare ameloblastomatous variant can pose a significant diagnostic challenge. Moreover, there were some findings of severe nuclear vacuolization, mitotic figures, cellular pleomorphism and nuclear hyperchromatism and chromatin peripheralization. However, the scattered occurrence of these was not sufficient for claiming a malignancy. To confirm, two immunohistochemical markers - Calretinin and p53 - were recruited. Rendering itself to be suspicious, a rapt attention should be paid toward well interrogating this lesion histologically and immunohistochemically.