A correlation of immunohistochemical expression of TP53 and severity of inflammation with varying grades of oral squamous cell carcinoma.

PURPOSE: Epithelial cells exposed to carcinogens and genetic damage, once surpass reversible cell damage, either undergo apoptosis or transform into malignancy, chiefly oral squamous cell carcinoma (OSCC). Progressive accumulation of genetic errors in TP53 results in tumorigenesis. Inflammation is also a modulator in this process. The present study attempted to correlate the immunohistochemical expression of TP53 with increased aggressiveness of OSCC, to determine how these immune cells regulate the path of carcinogenesis and to define the role of inflammation in TP53 immunoexpression. MATERIALS AND METHODS: Tissue sections from 24 biopsy-proven cases of OSCC were stained with anti-TP53 antibody. Five hundred neoplastic epithelial cells and inflammatory cells, each, were counted at invasive tumor front. Two hundred peritumoral neutrophils were counted based on nuclear lobes present. RESULTS: The least TP53 expression was seen in well-differentiated OSCC (P < 0.001), whereas neutrophil count and plasma cell count were found to be least in well-differentiated OSCC (P < 0.001), whereas the number of lymphocytes and macrophages decreased with increased grading of OSCC (P < 0.001). Four- and five-lobed neutrophils were found to be highest in poorly differentiated OSCC (P < 0.001), whereas two-lobed neutrophil count was seen to be maximum in well-differentiated OSCC (P < 0.001). CONCLUSION: TP53 plays a significant role in the initiation and progression of OSCC. Inflammation plays a role of friend and a foe simultaneously, and little modification in the present treatment modalities for OSCC can bring a favorable change in the life of cancer survivors.

A correlation of immunohistochemical expression of TP53 and CDKN1A in oral epithelial dysplasia and oral squamous cell carcinoma.

PURPOSE: Oral epithelial dysplasia (OED) occurs on exposure of epithelial cells to carcinogens and genetic alteration. Once the reversible cell damage is surpassed, cells either undergo apoptosis or transform into malignancy, chiefly oral squamous cell carcinoma (OSCC). Progressive accumulation of genetic errors (including mutations in TP53 and CDKN1A) is associated with the initiation and progression of potentially malignant oral lesions toward frank malignancy. The present study attempted to correlate the immunohistochemical expression of CDKN1A and TP53 with increasing severity of OED along with increased aggressiveness of OSCC as reflected in the clinicopathologic variables. MATERIALS AND METHODS: Tissue sections from forty biopsy-proven cases of OED and OSCC were stained with anti-TP53 and anti-CDKN1A mouse monoclonal antibodies. One hundred cells in each case were counted under high power magnification. RESULTS: Poorly differentiated OSCC showed the highest TP53 expression (mean = 70.285), with least expression seen in mild dysplasia (mean = 22.125) (P < 0.001). Higher TP53 count was seen in cases with margin involvement, without recurrence and lymph node involvement and in cases which died of disease. CDKN1A expression was seen only in five cases and that too focally in the cytoplasm, thereby warranting removal of analysis of CDKN1A positivity from the study. CONCLUSION: The expression of TP53 in OED highlights its role in initial carcinogenesis. Although the role of CDKN1A in the cell cycle has been documented, its relationship to various clinical and pathological variables of OSCC and its different treatment modalities could not be adequately assessed.

Driving the Mineral out Faster: Simple Modifications of the Decalcification Technique.

INTRODUCTION: Quicker decalcification is essential for faster diagnosis of hard tissue pathology. Heat and mechanical agitation are known to hasten decalcification. AIM: To compare the rate of decalcification, cellular and staining characteristics of decalcified specimens of bone and teeth by using the conventional method (10% formal formic acid), heating to 45(o)C and by physical agitation with magnetic stirrer. MATERIALS AND METHODS: Weight-matched samples of caprine-origin bone (n=15) and teeth (n=15) were decalcified using three methods namely: a) Gooding and Stewart's fluid; b) Gooding and Stewart's fluid heated to 45(o)C for 6 hours daily; and c) Gooding and Stewart's fluid agitated using a magnetic stirrer for 6 hours daily. Non-lesional skin tissue samples were placed along with each specimen. End point of decalcification (chemical test) was noted; 4 micron sections were taken and stained with H&E. STATISTICAL ANALYSIS: Differences in rate of decalcification and staining characteristics were assessed by Kruskal Wallis test and chi-square test respectively. RESULTS: Hard tissues decalcified faster with stirring and heating methods. The amount of osteocyte retraction noted in bone was significantly reduced in the stirring method. In tooth specimens, modified techniques resulted in poorer nuclear-cytoplasmic contrast of pulp cells. Heating affected the odontoblast layer. Soft tissues exhibited higher eosinophilia in stirring and conventional methods, whereas nuclear-cytoplasmic contrast and chromatin staining was poorest in heating and conventional methods. CONCLUSION: Physical agitation of decalcifying fluid may be recommended while maintaining satisfactory quality of tissue morphology and staining.

Post-radiation changes in oral tissues - An analysis of cancer irradiation cases.

INTRODUCTION: Radiation, commonly employed as neoadjuvant, primary, and adjuvant therapy for head and neck cancer causes numerous epithelial and stromal changes, prominent among which is fibrosis with its early and late consequences. Very little is known about the true nature of the fibrosed tissue and the type of fibers accumulated. Radiotherapy affects the supporting tumor stroma often resulting in a worsening grade of tumor post-radiation. AIM: To study epithelial, neoplastic, stromal, and glandular changes in oral cavity induced by radiation therapy for oral squamous cell carcinoma (OSCC) using special stains. MATERIALS AND METHODS: The study included 27 samples of recurrent OSCC following completion of radiotherapy (recurrence within an average span of 11 months), and 26 non-irradiated cases of OSCC. Patients with a history of combined radiotherapy and chemotherapy were not included in the study. The epithelial changes assessed included epithelial atrophy, apoptosis, necrosis, dysplasia, and neoplasia. The connective tissue was evaluated for amount of fibrosis, quality of fibers (using picrosirius red staining), fibrinous exudate, necrosis, pattern of invasion, vessel wall thickening, and salivary gland changes. The aforementioned changes were assessed using light and polarizing microscopy and tabulated. STATISTICAL ANALYSIS: Epithelial and connective tissue parameters were compared between the irradiated and non-irradiated cases using chi square and t-tests. RESULTS: Epithelial and connective tissue parameters were found to be increased in irradiated patients. Pattern of invasion by tumor cells varied from strands and  cords between the two groups studied. The effect of radiation was seen to reflect on the maturity of fibers and the regularity of their distribution.