This article by S. Burt Wolbach and Percy R. Howe describes the histopathological changes in white rats following a diet deficient in fat-soluble vitamin A. The study highlights the widespread keratinization of epithelial tissues as the primary pathological feature, which is not limited to the eyes but affects multiple organs, including the respiratory and genitourinary tracts, various glands, and the skin. The authors emphasize that the condition, termed fat-soluble A avitaminosis, is characterized by epithelial keratinization, glandular atrophy, and growth arrest, rather than the previously assumed eye-specific changes like xerophthalmia and keratomalacia. The study analyzed the effects of vitamin A deficiency on various tissues, including the respiratory tract, alimentary tract, genitourinary tract, eyes, and paraocular glands. The histopathology revealed that keratinization of epithelial cells occurs in the respiratory tract, salivary glands, and other organs, often preceded by atrophy of the original epithelium. The process is not directly caused by infection but is a result of the deficiency itself. The authors also observed that the keratinization is a widespread phenomenon, affecting multiple organs and tissues, and that the severity of the changes varies depending on the age and weight of the rats. The study also discusses the effects of vitamin A deficiency on the skeletal system, the integumentary system, and the nervous system. The authors found no significant changes in the skeletal system, and no evidence of rachitic or scurvy changes in the rats. The nervous system showed no signs of lesions, and the peripheral nerves were not affected. The study concludes that the primary pathological change in vitamin A deficiency is the widespread keratinization of epithelial tissues, which is not directly caused by infection but is a result of the deficiency itself. The study also highlights the importance of proper diet composition and duration of the experiment in accurately diagnosing the effects of vitamin A deficiency.This article by S. Burt Wolbach and Percy R. Howe describes the histopathological changes in white rats following a diet deficient in fat-soluble vitamin A. The study highlights the widespread keratinization of epithelial tissues as the primary pathological feature, which is not limited to the eyes but affects multiple organs, including the respiratory and genitourinary tracts, various glands, and the skin. The authors emphasize that the condition, termed fat-soluble A avitaminosis, is characterized by epithelial keratinization, glandular atrophy, and growth arrest, rather than the previously assumed eye-specific changes like xerophthalmia and keratomalacia. The study analyzed the effects of vitamin A deficiency on various tissues, including the respiratory tract, alimentary tract, genitourinary tract, eyes, and paraocular glands. The histopathology revealed that keratinization of epithelial cells occurs in the respiratory tract, salivary glands, and other organs, often preceded by atrophy of the original epithelium. The process is not directly caused by infection but is a result of the deficiency itself. The authors also observed that the keratinization is a widespread phenomenon, affecting multiple organs and tissues, and that the severity of the changes varies depending on the age and weight of the rats. The study also discusses the effects of vitamin A deficiency on the skeletal system, the integumentary system, and the nervous system. The authors found no significant changes in the skeletal system, and no evidence of rachitic or scurvy changes in the rats. The nervous system showed no signs of lesions, and the peripheral nerves were not affected. The study concludes that the primary pathological change in vitamin A deficiency is the widespread keratinization of epithelial tissues, which is not directly caused by infection but is a result of the deficiency itself. The study also highlights the importance of proper diet composition and duration of the experiment in accurately diagnosing the effects of vitamin A deficiency.