Search

The Fourier transform infrared (FTIR) imaging technique was used in a transmission model for the evaluation of twelve oral hyperkeratosis (HK), eleven oral epithelial dysplasia (OED), and eleven oral squamous cell carcinoma (OSCC) biopsy samples in the fingerprint region of 1800–950 cm−1. A series of 100 µm × 100 µm FTIR imaging areas were defined in each sample section in reference to the hematoxylin and eosin staining image of an adjacent section of the same sample. After outlier removal, signal preprocessing, and cluster analysis, a representative spectrum was generated for only the epithelial tissue in each area. Two representative spectra were selected from each sample to reflect intra-sample heterogeneity, which resulted in a total of 68 representative spectra from 34 samples for further analysis. Exploratory analyses using Principal component analysis and hierarchical cluster analysis showed good separation between the HK and OSCC spectra and overlaps of OED spectra with either HK or OSCC spectra. Three machine learning discriminant models based on partial least squares discriminant analysis (PLSDA), support vector machines discriminant analysis (SVMDA), and extreme gradient boosting discriminant analysis (XGBDA) were trained using 46 representative spectra from 12 HK and 11 OSCC samples. The PLSDA model achieved 100% sensitivity and 100% specificity, while both SVM and XGBDA models generated 95% sensitivity and 96% specificity, respectively. The PLSDA discriminant model was further used to classify the 11 OED samples into HK-grade (6), OSCC-grade (4), or borderline case (1) based on their FTIR spectral similarity to either HK or OSCC cases, providing a potential risk stratification strategy for the precancerous OED samples. The results of the current study support the application of the FTIR-machine learning technique in early oral cancer detection. [ABSTRACT FROM AUTHOR]

Cairns L, Naidu A, Robinson C M, Sloan P, Wright J M & Hunter K D (2010) Histopathology 57, 544-548 CD56 (NCAM) expression in ameloblastomas and other odontogenic lesions Aims: Ameloblastomas recapitulate certain elements of tooth formation. CD56 is expressed by a variety of cells and is used in tumour diagnosis, but is also expressed in the enamel organ during tooth development. The aim of this study was to describe the expression of CD56 in odontogenic lesions with particular reference to the differential diagnosis of ameloblastoma and odontogenic keratocyst. Methods: Cases were selected from the pathology archives at Glasgow Royal Infirmary, Glasgow, Royal Victoria Infirmary, Newcastle and Department of Diagnostic Sciences, Texas A&M Health Science Center Baylor College of Dentistry, Dallas. The study population included 38 ameloblastomas, 19 odontogenic keratocysts and a number of other odontogenic lesions, including nine compound odontomes. All sections were examined for CD56 immunoreactivity and the extent of staining was recorded. Results: Thirty-seven of 38 (97%) ameloblastomas expressed CD56 on the cell membrane of peripheral cells in tumour nests (16 extensively, 21 focally). Immunoreactivity was lost in areas of inflammation, acanthomatous differentiation, in areas of cystic change and upon fusion with overlying surface epithelium. One odontogenic keratocyst expressed CD56 (5%, P < 0.0001). CD56 was expressed very focally in two odontomes, exclusively in stratum intermedium-like cells. Conclusions: CD56 expression in odontogenic epithelium is highly suggestive of ameloblastoma and can help in differentiating this from odontogenic keratocyst. [ABSTRACT FROM AUTHOR]

Aims To immunohistochemically evaluate the cytokeratin ( CK) pattern of expression in localized juvenile spongiotic gingival hyperplasia ( LJSGH) as compared with the gingival epithelium ( GE). Methods and results Ten cases of LJSGH were semiquantitatively evaluated for the immunohistochemical pattern of CK1/10, CK4, CK8/18, and CK19. GE controls were taken from 10 cases of reactive gingival fibroepithelial hyperplasia. GEs showed mean positivity rates of 80% for both CK1/10 and CK4, and 5% for both CK8/18 and CK19. LJSGHs showed mean positivity rates of 65% for CK19, 60% for CK8/18, 30% for CK4, and 5% for CK1/10. The differences between LJSGHs and GEs were statistically significant ( P < 0.01). Conclusions The LJSGH pattern of CK expression is reminiscent of the profile described in the literature for the junctional epithelium ( JE). Possibly, JE exteriorized from the gingival sulcus would be more prone to irritation from a variety of sources, resulting in inflammation and hyperplasia, with the subsequent development of LJSGH. [ABSTRACT FROM AUTHOR]