Publications by authors named "Kandarkar S"

Giant cell tumor of the bone (GCTB) is a benign bone tumor that can occasionally progress to malignancy, usually in chronic cases. It is a common benign and aggressive bone tumor that affects patients aged between 20 and 45 years. The most common location is the knee joint.

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Giant cell tumors (GCTs) are rare, benign, and locally invasive tumors, typically found in the epiphysis of long bones, most commonly at the distal femur and proximal tibia. To date, GCTs of the distal end of the ulna have been very rare. We document a case of a 38-year-old female with a distal ulna GCT, managed with en-bloc resection of the tumor with flexor carpi ulnaris and extensor carpi ulnaris tendon stabilization.

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Introduction: Anterior cruciate ligament (ACL) reconstruction using hamstring tendon graft is a commonly performed orthopedic surgery. Lateral femoral condyle fracture through the femoral tunnel is a rare complication following ACL reconstruction. These cases are reported to be managed in two stages, fracture fixation by open reduction and internal fixation with bone grafting of the femoral tunnel, followed by revision ACL reconstruction after the fracture union.

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Objective: To evaluate the role of vitamins C and E as chemopreventive agents in oral carcinogenesis by optical and ultrastructural studies.

Materials And Methods: The cheek pouch of male hamsters was treated with the oral carcinogen, dimethylbenz(a)anthracene (DMBA), to induce multiple tumour formation. Vitamins C and E were applied either singly or in combination as a chemopreventive agent.

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Oral mucosal neoplastic disease in rodents has been induced by various chemical carcinogens, including water soluble 4-nitroquinoline-1-oxide (4NQO). It has been suggested that vitamin C can inhibit, delay or prevent the development of neoplasms, as well as enhance the induction of neoplasia. In this investigation, 4NQO was used to produce a high yield of carcinomas of the palatal mucosa of rats in a relatively short period of time and topical vitamin C was applied to delay the neoplastic transformation.

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Vitamin C is an essential nutrient whose protective influence is carcinogenesis has been reported frequently, suggesting that vitamin C inhibits the formation of some carcinogens and decreases the incidence and delays of the neoplastic lesions. However, the mechanisms by which this occurs are unknown. In this study, the water soluble carcinogen 4-nitroquinoline-1-oxide (4NQO) has been used to induce a high yield of tumours in the oral cavity either singly or in combination with tobacco.

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Clinical evaluation, upper gastrointestinal endoscopy and electron microscopy of mucosal biopsies from antrum, body and fundus of stomach were performed in three control subjects and 17 habitual tobacco chewers. Electron microscopic abnormalities such as discontinuous, fragmented basement membrane with reduction in hemidesmosomes, and widened intercellular spaces filled with clusters of desmosomes were found in the gastric mucosa of habitual tobacco chewers; these were similar to those reported in experimental carcinogenesis and leukoplakia. It is concluded that habitual chewing of tobacco produces electron microscopic alterations in the human gastric mucosa which may be important precursors for gastric malignancy.

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Seventeen chronic tobacco chewers and three control subjects underwent clinical evaluation, upper gastrointestinal endoscopy and esophageal mucosal biopsies. The esophageal biopsies were processed and examined under the electron microscope. A large number of ultrastructural abnormalities such as discontinuous, fragmented basement membrane, with reduction in hemidesmosomes, widened intercellular spaces were found in the esophageal mucosa of chronic tobacco chewers which resembled the ultrastructural features of experimental carcinogenesis and leukoplakia.

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This study reports the mechanism of involvement of vitamin C in the pathogenesis of induced oral carcinogenesis in the hamster cheek pouch epithelium. This site was exposed to either DMBA singly or in combination with vitamin C or DMBA for 7 weeks followed by only vitamin C till tumour induction. Macroscopically, vitamin C reduces the epithelial tumour incidence in the hamster cheek pouch.

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Vitamin C is an essential nutrient whose protective influence in carcinogenesis has been reported frequently. In general, evidence suggests that vitamin C inhibits the formation of some carcinogens and decreases the incidence and delays the onset of neoplastic lesions but the mechanisms by which this occurs are not known. In 1973, Wallenius and Lekholm induced intra-oral palatal squamous cell carcinomas by the use of the water soluble carcinogen 4-nitroquinoline-1-oxide (4NQO) applied thrice weekly to the palatal mucosa of rats.

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Experiments were performed to study the early and late ultrastructural changes during hamster cheek pouch carcinogenesis using a regimen of topical application of 9,10 dimethyl-1-1-2 benzanthracene (DMBA) twice a week in liquid paraffin oil. The DMBA was administered for a period of 2 and 4 1/2 months. Hamsters exposed to DMBA for 2 months developed moderate precancerous changes, whereas the hamsters treated with DMBA for 4 1/2 months developed frank and multiple oral tumors with a cauliflower appearance.

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In this study initially a precancerous condition, leukoplakia, was develop at 6 weeks treatment of DMBA whereas in the animals treated both DMBA + Vit. A, leukoplakia was seen at 10 weeks followed by papilloma or nodules at 12 weeks. Tumours induced by DMBA were more in number than DMBA + Vit.

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The present study reports light and electron microscopic observations of hamster cheek pouch epithelium exposed to 25 micrograms DMBA (DMBA = 9,10 Dimethyl, 1,2 Benz(a)-nthracene, RA = Retinoic Acid) and 25 micrograms DMBA along with 25 micrograms, 50 micrograms and 100 micrograms retinoic acid. Significant delay in tumour induction was observed in the animals treated with DMBA + retinoic acid. DMBA + retinoic acid treated cheek pouch developed papillary epidermoid carcinomas which were less invasive and less keratinized than only DMBA treated animals.

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The utility of hamster cheek pouch model for studies on oral carcinogenesis has been explored using 9,10-dimethyl-1-2-benzanthracene as a carcinogen. Based on the morphological, histopathological and electron microscopic observations the hamster cheek pouch carcinogenesis can be separated into different stages starting from the normal to the fully grown carcinomas. This system is reliable, precise, consistent and can be used for the evaluation of different agents for initiating or promoting effects and as well as for the studies on mechanism of oral carcinogenesis.

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The altered pattern in the expression of keratin proteins as a function of tumour progression was studied in the hamster cheek pouch and compared the changes with electron microscopic observations using DMBA as a carcinogen. In the case of hyperplasia and well developed tumours a conspicuous loss of 67 K and an increase in 46 K was observed compared to the controls. The increased expression of low molecular weight keratins during tumour growth is well supported by the enhanced expression of tonofilament bundles, electron microscopically.

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The objective of this study was to provide a detailed account of the morphogenesis and early cytodifferentiation of the hamster cheek pouch. Although the newborn "cheek pouch" is used for in vitro studies of the effects of retinoids and carcinogens, its rudimentary structure has not been adequately described. Complete paraffin serial sections of the heads of 14- and 15-day fetuses were cut in three planes to determine the location and shape of the earliest pouch rudiments.

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The role of vitamin A in the induction and growth of chemically induced tumors is still controversial. While in some studies vitamin A influenced inhibition of chemically induced tumors was observed, other studies report on an enhancing influence of this substance on tumor induction. The cheek pouch epithelium of sixty five Syrian golden hamsters was exposed to DMBA and different doses of retinyl acetate, singly and in combination with DMBA.

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This paper reports a study on the influence of excess of vitamin A palmitate on the induction and maintenance of oral tumors. Sixty four weanling Syrian hamsters were divided in four groups and painted three times a week, either with 0.5% DMBA or 15% vitamin A palmitate, singly or in combination.

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