One type of soft tissue lesions of the oral cavity is lipoma, which is a kind of benign tumor composed of mature lipid cells. Although the lipoma presents as one of the most common mesenchymal neoplasms, most tend to develop on the trunk and proximal portions of the extremities. However, lipomas in the oral and maxillofacial region are much less frequent. Here we present a case of an intraoral lipoma in a six year-old child.
Child ; Diagnosis, Differential ; Humans ; Lipoma ; pathology ; surgery ; Male ; Mouth Mucosa ; pathology ; surgery ; Mouth Neoplasms ; pathology ; surgery

OBJECTIVEIt is currently considered that the defect of mitotic spindle caused by centrosome abnormalities may be one of the reasons for the development of aneuploidy in tumors. This study attempted to elucidate the possible role of centrosome defects in the development and progression of OSCC by investigating the frequency of centrosome amplification in oral precancerous lesions and OSCC.

METHODSFormalin-fixed, paraffin-embedded tissues of 12 cases of normal oral epithelium, 22 case of dysplasia with different degree epithelium dysplasia and 32 cases of OSCC with different differentiation were investigated for centrosome status by using indirect immunofluorescence double staining with antibodies to centrosome protein gamma-tubulin and cytokeratin. The differences and the change trend of centrosome status in these groups were statistically analyzed by SPSS10.0.

RESULTSNormal oral epithelium showed normal centrosomes in epithelium cells, while 16 of 22 cases (72.73%) of dysplasia (DYS) and 27 of 32 cases (84.38%) of OSCC showed the evidence of centrosome amplification and morphological abnormalities characterized by huge size, clump or supernumerary centrosomes in a fraction of epithelium or tumor cells. The percentage of cells with abnormal centrosomes increased gradually from mild-dysplasia epithelium to poorly differentiated OSCC, which positively correlated with the histologicalcytologic grade of oral precancerous lesions and OSCC (P < 0.01).

CONCLUSIONCentrosome amplification was an early event and that might play a role in the establishment and perhaps the progression of OSCC. There might be some direct relationship between centrosome defects and the cellular morphological phenotype characteristics of dysplasia and OSCC. Centrosome amplification could be served as an alternative diagnostic indicator of dysplasia and the intervention of centrosome cycle might serve as a particular way for the prevention and treatment of OSCC in the future.

Carcinoma, Squamous Cell ; genetics ; pathology ; Centrosome ; pathology ; Humans ; Mouth Mucosa ; pathology ; Mouth Neoplasms ; genetics ; pathology ; Precancerous Conditions ; pathology

Facial Neoplasms ; classification ; pathology ; Humans ; Jaw Neoplasms ; classification ; pathology ; Mouth Neoplasms ; classification ; pathology

OBJECTIVETo investigate the relationship between centrosome abnormalities and aneuploidy in oral squamous cell carcinoma (OSCC) and elucidate the possible underlying mechanisms of chromosome instability (CIN) in OSCC.

METHODSFormalin-fixed, paraffin-embedded tissues of 8 cases of normal oral epithelium and 32 cases of OSCC were examined for centrosome status by using indirect immunofluorescence staining, and chromosome instability (aneuploidy) in some tissues were detected by flow cytometry. The correlation between centrosome abnormalities and aneuploidy in OSCC was statistically analyzed by SPSS12.0.

RESULTSNormal oral epithelium showed normal size and number of centrosomes in epithelium cells, while 25 out of 32 cases of OSCC showed the evident centrosome amplification characterized by huge size and/or supernumerary centrosomes in a fraction of tumor cells, and 21 out of 32 cases were aneuploidy. The percentage of cases with abnormal centrosomes in aneuploid OSCC (19/21) was significantly higher than that in diploid OSCC(6/11) (P =0.032). Centrosome abnormality was significantly correlated with aneuploidy (Spearman r = 0.413, P = 0.047), and a positive correlation was found between the degree of centrosome amplification and the degree of DNA ploidy abnormality (Pearson r = 0.364, P = 0.041).

CONCLUSIONSCentrosome abnormality may be a contributing factor for chromosome instability in OSCC.

Aneuploidy ; Carcinoma, Squamous Cell ; genetics ; pathology ; Centrosome ; pathology ; Chromosomal Instability ; Humans ; Mouth Mucosa ; pathology ; Mouth Neoplasms ; genetics ; pathology

Humans ; Jaw Neoplasms ; pathology ; surgery ; Mouth Neoplasms ; pathology ; surgery ; Pharyngeal Neoplasms ; pathology ; surgery ; Skull Base ; pathology ; surgery

Humans ; Lichen Planus, Oral ; pathology ; Mouth Neoplasms ; pathology ; Precancerous Conditions ; pathology

The apoptosis in primary oral squamous cell carcinomas (OSCCs) without lymph node (IN) metastases and its relation with clinical stages and pathological grades was investigated. The terminal deoxynucleotidyl trasferase (TdT)-mediated dUTP nick end labeling (TUNEL) was used to detect the apoptotic cells in 15 cases of OSCCs. The percentage of apoptotic cells among tumor cells were calculated as apoptotic index (AI). The results showed that in all 15 cases of OSCCs, apoptotic cells could be visualized by TUNEL with AI ranging from 0.03 to 0.92 (average 0.32). AI was significantly negatively correlated with pathological grades (P < 0.05). It was concluded that the apoptotic rate was related to the malignant degree of OSCCs without LN metastases.
Apoptosis/*physiology ; Carcinoma, Squamous Cell/*pathology ; Lymph Nodes/pathology ; Lymphatic Metastasis ; Mouth Neoplasms/*pathology

Cancers of the upper aerodigestive tract (UADT) constitute 3.5-4% of all malignancies. Since the majority of cases are squamous cell carcinomas which are related with epidemiologic factors, a different pattern of UADT cancer might be present between the Western and Asian populations. We performed a pathology based statistical study on UADT cancers in Korean patients. Cases from Korea Cancer Center Hospital, from January 1, 1988 through December 31, 1998, were subjected to the study. Among 2,842 cases, epithelial malignancies accounted for 87.8%, with squamous cell carcinoma as the major type (76.5%). The larynx was the most commonly affected site (26%), followed by the oral cavity (25.1%), oropharynx (13%), nasopharynx (9%), hypopharynx (8.4%), paranasal sinuses (6.4%), nasal cavity (6%) and salivary glands (6.1%). The percentage of squamous cell carcinoma was highest (98.7%) at the hypopharynx, and lowest at the nasal cavity (42.3%), which showed the most diverse tumor entities. Korean patients with UADT cancers presented with a higher incidence of non-epidermoid malignancy including sarcoma (1.5%) and malignant melanoma (1.4%), and a higher frequency of involvement of the sinonasal tract, compared with the Western patients.
Head and Neck Neoplasms/classification/*pathology ; Humans ; Hypopharyngeal Neoplasms/classification/pathology ; Korea ; Laryngeal Neoplasms/classification/pathology ; Mouth Neoplasms/classification/pathology ; Nasal Cavity ; Nasopharyngeal Neoplasms/classification/pathology ; Oropharyngeal Neoplasms/classification/pathology ; Paranasal Sinus Neoplasms/classification/pathology ; Salivary Gland Neoplasms/classification/pathology

The integrity of the basal stem cell layer is critical for epithelial homoeostasis. In this paper, we review the expression of oral mucosal stem cell markers (OM-SCMs) in oral submucous fibrosis (OSF), oral potentially malignant disorders (OPMDs) and oral squamous cell carcinoma (OSCC) to understand the role of basal cells in potentiating cancer stem cell behaviour in OSF. While the loss of basal cell clonogenicity triggers epithelial atrophy in OSF, the transition of the epithelium from atrophic to hyperplastic and eventually neoplastic involves the reactivation of basal stemness. The vacillating expression patterns of OM-SCMs confirm the role of keratins 5, 14, 19, CD44, β1-integrin, p63, sex-determining region Y box (SOX2), octamer-binding transcription factor 4 (Oct-4), c-MYC, B-cell-specific Moloney murine leukaemia virus integration site 1 (Bmi-1) and aldehyde dehydrogenase 1 (ALDH1) in OSF, OPMDs and OSCC. The downregulation of OM-SCMs in the atrophic epithelium of OSF and their upregulation during malignant transformation are illustrated with relevant literature in this review.
Animals ; Carcinoma, Squamous Cell ; pathology ; Cell Transformation, Neoplastic ; pathology ; Mice ; Mouth Mucosa ; Mouth Neoplasms ; pathology ; Oral Submucous Fibrosis ; pathology ; Stem Cells

OBJECTIVETo investigate the expression and significance of integrin-beta1 in oral leukoplakia and early invasive carcinoma.

METHODSThe expression of integrin-beta1 and Ki-67 was examined in 12 normal oral mucosa, 10 simple hyperplasia, 24 epithelial dysplasia and 14 early invasive carcinoma by immunohistochemistry.

RESULTSIn normal and simple hyperplasia epithelium, integrin-beta1 was mostly expressed in the basal cell membrane, and Ki-67 in the nuclei of basal and the parabasal layers. In dysplasia epithelium and early invasive carcinoma, integrin-beta1 showed membrane staining and Ki-67 showed nuclear staining in dysplastic basal cells, sprinkle cells and SCC cells. Integrin-beta1 and Ki-67 were overexpressed in 7 and 10 of 24 dysplasia cases and in 8 of 14 early invasive carcinoma cases respectively. There was a significant difference in integrin-beta1 and Ki-67 expression among the four groups (chi2 = 10.651, P = 0.014; chi2 = 14.831, P = 0.002), in integrin-beta1 expression among normal oral mucosa, simple hyperplasia and early invasive carcinoma (P = 0.008, P = 0.013) and in Ki-67 expression among normal oral mucosa and dysplasia, early invasive carcinoma (P = 0.026, P = 0.001), and among simple hyperplasia and early invasive carcinoma (P = 0.005). A significant correlation between integrin-beta1 and Ki-67 (R = 0.442, P < 0.01) was found.

CONCLUSIONSIntegrin-beta1 showed increased staining in dysplasia epithelium cells and SCC cells, and may correlate to the proliferation of the dysplasia cells.

Carcinoma, Squamous Cell ; metabolism ; pathology ; Cell Proliferation ; Humans ; Integrin beta1 ; metabolism ; Ki-67 Antigen ; metabolism ; Leukoplakia, Oral ; metabolism ; pathology ; Mouth Mucosa ; pathology ; Mouth Neoplasms ; metabolism ; pathology