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By P. Goose. University of North Dakota--Lake Region. 2018.

Outer Root Sheath The outer root sheath 1mg anastrozole with amex women's health center tampa florida, or trichilemma discount anastrozole 1 mg line pregnancy cramps, has no granular layer and is glycogen rich, accounting for the pale cytoplasm. It appears at the base of the bulb as a thin lining becoming thicker as it extends upward to the level of the isthmus where it shows trichilemmal keratinization (Figs. The outer root sheath is covered by the hyaline or vitreous membrane, which is continuous with epidermal basement membrane surrounding the dermal papilla. Folds or corrugations of the hyaline membrane are sometimes seen projecting into the underlying trichilemmal layer. The hyaline membrane is surrounded by the fibrous dermal sheath of the hair follicle, which is continuous with the dermal papilla at the base of the hair bulb. Inner Root Sheath The inner root sheath starts from mid-isthmus extending to the base of the bulb. It expands and thickens as it continues upward (left) and is replaced at the level of the isthmus where it shows trichilemmel keratinization (right). Henle’s layer keratinizes first with the appearance of trichohya- line granules near the hair bulb, forming a distinct pinkish keratinized band higher up from the bulb (Fig. The cuticle of the inner root sheath is the next to keratinize, synchronizing with keratinization of the cuticle of the hair shaft (Fig. Finally, trichohyaline granules appear in Huxley’s layer, signaling impending keratinization (Fig. Keratinization of the inner root sheath is completed halfway up the lower follicle. The keratinized inner root sheath occupies the upper half of the lower follicle (Fig. The inner root sheath is surrounded by one or more layers of cells of the outer root sheath or trichilemma. The potential space between inner and outer root sheaths is named the companion layer and it allows the inner root sheath to slide upward over the outer root sheath during hair growth. Hair Shaft The hair shaft consists of the cuticle, cortex, and medulla (present in terminal hairs) (Fig. The hair fiber cortex is cylindrical and consists of keratin filaments embedded in a sulfur-rich matrix, enclosing the medulla and surrounded by the cuticle of the hair shaft. Henle’s layer, the outermost of the three layers of the inner root sheath, is beginning to keratinize (hematoxylin and eosin stain, original magnification 200x). The hair shaft is generated by transit amplifying matrix cells in the hair bulb, which surround the dermal papilla. The hair fiber diameter remains uniform during a single growth phase under normal conditions. Hair shaft and inner root sheath cuticles interlock to stabilize the growing hair and to ensure that the inner root sheath and hair shaft grow upward together. A comparative electron microscopic analysis of the cuticular structures of Asian and white hair revealed Asian hair has more cuticlar layers that are thicker and more densely packed than white hair. This may account for susceptibility of white hair to damage during daily grooming (23). Follicular Units Horizontal sections at the sebaceous duct level show follicular units. Follicular units are roughly hexagonal in shape and are surrounded by a loose network of collagen; they contain several termi- nal and vellus follicles with sebaceous ducts and glands and arector pili muscles (Figs.

Oral Lesions due to Drugs Gold-induced Stomatitis Stomatitis Medicamentosa Gold compounds are used selectively in patients Systemic administration of medications may with rheumatoid disorders purchase anastrozole 1mg with amex women's health center greensburg pa. Gold is stored in the induce hypersensitivity reactions in the oral tissues and is excreted slowly through the kidneys order 1mg anastrozole free shipping women's health problems brown discharge. Gold A plethora of drugs may cause stomatitis toxicity may be manifested with fever, headache, medicamentosa, including antipyretics, non- proteinuria, skin rashes, oral lesions, thrombocy- steroid anti-inflammatory drugs, sulfonamides, topenia, agranulocytosis, or aplastic anemia. Clinically, the condi- oral mucosa is red, with painful erosions covered tion is characterized by diffuse erythema of the with a yellowish membrane (Fig. There is an oral mucosa, purpuric patches, vesicles or bullae, intense burning sensation and increased saliva- painful erosions, ulcers, etc. The differential diagnosis includes stomatitis medicamentosa, erythema multiforme, pemphi- The differential diagnosis includes erythema mul- gus vulgaris, cicatricial pemphigoid, bullous pem- tiforme, pemphigus, bullous pemphigoid, cicatri- phigoid, and erosive lichen planus. Antibiotic-induced Stomatitis Systemic long-term administration of broad-spec- trum antibiotics, such as tetracycline, may cause a form of stomatitis. Clinically, it is characterized by a nonspecific diffuse erythema of the oral mucosa. The tongue is extremely red and painful, with desquamation of the filiform papillae (Fig. Hairy tongue and candidosis may also occur as a result of changes in the oral microbial flora. The differential diagnosis includes stomatitis medicamentosa, erythema multiforme, pellagra, and ariboflavinosis. Antibiotic-induced stomatitis, diffuse erythema and desquamation of the filiform papillae of the tongue. Oral Lesions due to Drugs Ulcerations due to Methotrexate Pen icillamine-induced Oral Lesions Methotrexate is a folic acid antimetabolite that is D-penicillamine, a heavy metal chelator used in used in the treatment of leukemias, solid cancers, the treatment of hepatolenticular degeneration psoriasis, etc. The most common side effects are cystinuria, and heavy metal intoxication), may be alopecia, liver and gastrointestinal disorders, etc. The noncutaneous side effects include terized by redness and painful erosions or ulcers hematologic, pulmonary, gastrointestinal, renal, (Fig. The most lips, and buccal mucosa, although they may occur common cutaneous manifestations are autoim- anywhere in the oral cavity. The most common oral manifestation is penicillamine-induced pemphigus, which is The differential diagnosis includes traumatic characterized by vesiculobullous lesions and ero- ulcer, thermal and chemical burn, and stomatitis sions of the oral mucosa, clinically, histopatholog- medicamentosa. Penicillamine-induced pemphigus usually appears Ulceration due to Azathioprine within 6 to 12 months after initiation of the drug and may resolve within several weeks after with- Azathioprine is an antimetabolite widely used as drawal of the drug. Alopecia, gastroin- aphthous stomatitis, and taste loss are also oral testinal disorders, and bone marrow toxicity are complications of the drug. Rarely, limited cial pemphigoid lesions are frequently seen in erosions or ulcers of the oral mucosa may develop penicillamine-treated patients with rheumatoid after long-term and high-dose administration (Fig. Lowering the dose of the drug, and B- classic pemphigus, cicatricial pemphigoid, bullous complex vitamin administration. Oral Lesions due to Drugs Phenytoin-induced Gingival The differential diagnosis includes fibrous gingival hyperplasia due to phenytoin, and nifedipine, gin- Hyperplasia gival fibromatosis, gingivitis, periodontitis, and Phenytoin is an antiepileptic agent widely used in leukemia. The lesions are usually A common side effect is fibrous gingival hyper- reversible after cessation of the drug.

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Some disorders (hypothyroidism cheap anastrozole 1 mg with mastercard breast cancer hormone therapy, chronic ill health) may retard skeletal development buy anastrozole 1mg overnight delivery breast cancer 65 years old. Bone formation (osteoblastic activity) and bone resorp- Skeletal maturation is assessed radiologically from a tion (osteoclastic activity) constitute bone turnover, a hand radiograph (including wrists) which is then com- process that takes place on bone surfaces and continues pared with an atlas of hand radiographs of normal throughout life [2]. Bone sesses changes in presence, size, and shape of certain formation and bone resorption are linked in a consistent bones with age. Precursor bone suming; both methods provide comparable results and cells are activated at a particular skeletal site to form os- reproducibility [6]. Automated, computer-based tech- teoclasts, which erode a fairly constant amount of bone. Following attainment of skeletal matu- teoblasts are recruited to fill the eroded space with new rity, there then follows a period of consolidation during bone tissue. Although the long bones grow teoclastic resorption or defective osteoblastic function re- in length at the metaphyses, they are remodeled in shape sult in a net loss of bone (osteoporosis). If there is both during development by endosteal resorption and pe- increased bone resorption and formation, this constitutes riosteal apposition. Woven immature, instead of ma- The size and shape of the skeleton and its individual ture lamellar, bone is laid down in Paget’s disease of bones are determined by genetic factors, but are influ- bone. Increased activation frequency of resorption units enced by endocrine and local growth factors, nutrition also results in a high turnover state (hyperparathyroidism, and physical activity [8]. Bisphosphonate therapy re- ton to adjust to those mechanical forces to which it is ex- duces the activation of resorption units by inhibiting os- posed. Black races Bones grow in length by enchondral ossification and have larger and heavier bones than whites, and Chinese remodel by periosteal apposition of bone, endosteal re- have a small skeletal mass and size. Although genetic sorption, and osteoclastic resorption along the periosteal factors are important, they are modified by environ- surface of the metaphysis. Defective osteoclastic function mental differences such as diet and physical activity prevents this normal resorption of bone, which is essen- [10, 11, 12]. Defective osteoclastic function [3] in particularly of trabecular bone, is believed to occur some diseases (i. Generally, both men and Bone resorption by osteoclasts is a single-stage process women lose bone as they grow older, but women lose in which collagen and mineral are removed together, more than men. Women lose approximately 15-30% of whereas bone formation is a two-stage process: os- their total bone mass between maturity and the seventh teoblasts lay down osteoid, which subsequently becomes decade, whereas men lose only about half this amount. Pre-requisites for normal mineralization are Relatively more trabecular bone is lost (40-50%) than Metabolic Bone Disease 91 compact bone (5%). After the age of 35, women lose tients (familial hyperplasia, multiple endocrine neopla- bone at an annual rate of approximately 0. Carcinoma of the parathyroid is an infrequent cause of This loss affects both cortical and trabecular bone, but primary hyperparathyroidism (0. Cure may be cortical bone is well preserved until the fifth decade of obtained by adequate surgical excision and there is a 50% life, when there is a linear loss in both sexes, such that or greater 5-year survival rate. However, recurrence is men lose about 25% of their cortical bone whilst common (30%) and metastases to regional lymph nodes, women lose about 30%. Metastases, when solitary, may be resected with bolic disorders of bone are: benefit. Hyperparathyroidism, in which a tumor or hyperpla- sia of the parathyroid glands causes increase in Secondary Hyperparathyroidism parathormone production and stimulation of osteo- clasts.

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