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A histological study of 74 vitiligo cases revealed inflammatory and degenerative changes in the epidermis, papillation, blood vessels, sweat glands and ducts, sebaceous glands and hair follicles, dermis (connective tissue), and dermal nerves and nerve endings.
Solar-induced cutaneous changes are more prevalent and profound in older persons and, thus, are often inappropriately attributed to the aging process, per se. Structural and functional alterations caused by intrinsic aging and independent of environmental insults are now recognized in the skin of elderly individuals. Structurally the aged epidermis likely becomes thinner, the corneocytes become less adherent to one another, and there is flattening of the dermoepidermal interface. The number of melanocytes and Langerhans cells is decreased. The dermis becomes atrophic and it is relatively acellular and avascular. Dermal collagen, elastin, and glycosaminoglycans are altered. The subcutaneous tissue is diminished in some areas, especially the face, shins, hands, and feet, while in others, particularly the abdomen in men and the thighs in women, it is increased. The number of eccrine glands is reduced and both the eccrine and apocrine glands undergo attenuation. Sebaceous glands tend to increase in size but paradoxically their secretory output is lessened. The nail plate is generally thinned, the surface ridged and lusterless, and the lunula decreased in size. There is a progressive reduction in the density of hair follicles per unit area on the face and scalp, independent of male-pattern alopecia. The hair shaft diameter is generally reduced but in some areas, especially the ears, nose, and eyebrows of men and the upper lip and chin in women, it is increased as vellus hairs convert to cosmetically compromising terminal hairs. Functional alterations noted in the skin of elderly persons include a decreased growth rate of the epidermis, hair, and nails, delayed wound healing, reduced dermal clearance of fluids and foreign materials, and compromised vascular responsiveness. Eccrine and apocrine secretions are diminished. The cutaneous immune and inflammatory responses are impaired, particularly cell-mediated immunity. Clinical correlates of these intrinsic aging changes of the skin include alopecia, pallor, xerosis, an increased number of benign and malignant epidermal neoplasms, increased susceptibility to blister formation, predisposition to injury of the dermis and underlying tissues, delayed onset and resolution of blisters and wheals, persistent contact dermatitis, impaired tanning response to ultraviolet light, increased risk for wound infections, prolongation of therapy necessary for onychomycosis, and thermoregulatory disturbances.
Alkanes are widely distributed in nature and impaired alkane synthesis was implicated in certain neurological disorders. However, the mechanism of synthesis of alkanes in animals is unknown. Our search to find a convenient animal tissue to study alkane biosynthesis resulted in the finding that the uropygial gland (a modified sebaceous gland) of the eared grebe (Podiceps nigricollis) produces large amounts of alkanes. These alkanes, which constitute 35-41% of the total lipid produced, are mainly C21, C23, C25, and C27 n-alkanes. Cell free homogenates of this tissue synthesized alkanes from both fatty acid and aldehyde in the absence of O2. Differential centrifugation of the homogenates indicated that this activity was located in the microsomal fraction. With isolated microsomes conversion of fatty acid to alkane required CoA, ATP, and NADH whereas conversion of an aldehyde to alkane did not require the addition of cofactors. That the final step in alkane synthesis is a decarbonylation was shown by the stoichiometric production of heptadecane and CO from octadecanal. CO was identified by adsorption to RhCl [(C6H6)3P]3 and oxidation of the trapped CO to CO2 by watergas shift reaction. The enzyme preparation also catalyzed incorporation of 14C from 14CO into octadecanal showing the reversible nature of the decarbonylase. This decarbonylase had a sharp pH optimum at 7.0, a Kapp of 180 microM and a V1/2 of 90 rho mol/min/mg protein for octadecanal. The enzyme was inhibited by the metal chelators EDTA, O-phenanthroline, and 8-hydroxyquinoline, but not by KCN. It was stimulated nearly 3-fold by 5 microM 2-mercaptoethanol and inhibited by the presence of O2. During the conversion of [1-3H]octadecanal to heptadecane, 3H was lost to water and 3H from 3H2O was incorporated into the alkane generated from unlabeled octadecanal. The mechanism of the decarbonylation and the nature of the enzyme remain to be elucidated.
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Muir-Torre syndrome (MTS) is a rare autosomal-dominant disorder characterized by the predisposition to both sebaceous skin tumors (or multiple keratoacanthomas) and internal malignancies. A subtype of MTS is allelic to hereditary nonpolyposis colorectal cancer and is caused by germline mutations in the DNA mismatch repair genes MSH2 or MLH1. In these cases both internal and skin tumors show characteristic microsatellite instability (MSI). The aim of the present study was to determine whether immunohistochemical examination of MSH2 or MLH1 protein expression in MTS-associated skin tumors can be used as a diagnostic screening tool to identify patients with germline mutations in MSH2 or MLH1. In the present study 28 skin lesions from 17 patients (20 sebaceous gland tumors, 4 sebaceous hyperplasias, 3 keratoacanthomas, and 1 squamous cell carcinoma) were tested immunohistochemically with antibodies against MSH2 and MLH1. Eighteen of these tumors were from eight patients with known MSH2 germline mutations, two tumors were from a patient with a germline mutation in MLH1, and eight microsatellite stable sporadic skin tumors served as controls. One sample had to be excluded because of a lack of immunoreactivity. All eight microsatellite stable tumors expressed both DNA repair proteins. In 15 of the tumors from MSH2 germline mutation carriers, loss of MSH2 expression was observed, one tumor showed reduced MSH2 expression, and one tumor displayed positive immunoreactivity to MSH2. Both tumors of the MLH1 germline mutation carrier showed loss of the MLH1 protein. In conclusion, our findings demonstrate that immunohistochemical testing of MTS-related skin tumors is a reliable screening method with high predictive value for the diagnosis of the DNA mismatch repair-deficient MTS.
Although the usual size of senile sebaceous hyperplasia is 2 to 3 mm in diameter, we report one "giant" nodular case on the face. The patient is a 75-year-old Japanese man with a dome-shaped, skin-colored nodule on his right cheek. The lesion was 10 mm in diameter and had multiple small umbilications on its surface. He also had several small, yellow-colored, asymptomatic papules with central umbilication on his cheeks. Histologically, the giant nodule and the papule on the right cheek showed the same architectural pattern, a sharply demarcated hyperplasia of grouped mature sebaceous glands with a sebaceous converging duct, whose opening to the surface epithelium corresponded to the clinical umbilication. The reason for the giant growth of this senile sebaceous hyperplasia in our case is obscure; the patient had not been stressed by inductive agents or factors such as systemic corticosteroid and hemodialysis except for electrocoagulation on the lesion. In spite of the extraordinarily large size of the nodule, the conservative proliferating pattern seemed to show the benign hyperplastic character of senile sebaceous hyperplasia.
Three cases of an extremely rare occurrence of sebaceous glands in the cervix have been reported. Our findings suggest that these glands develop by sebaceous metaplasia in the regenerative epithelium of ectocervical origin.
Sebaceous glands on the vermilion border of the lips and the oral mucosa are common in adults. Only pathologic sebaceous glands visible through the epithelium should be regarded as Fordyce's granules. The incidence of Fordyce's granules increases from childhood to adulthood, and is slightly higher in men. The most prevalent sites are the vermilion border of the lips and the buccal mucosa. Fordyce's granules usually have the same histological features as cutaneous sebaceous glands. Pathologic alterations are rare. There is no significant correlation between Fordyce's granules and systemic diseases.
A case of keratoacanthoma of the maxillary gingiva in a 12-year-old white boy has been presented. This is only the fourth case of solitary intraoral keratoacanthoma reported in the English-language literature. A review of the literature on solitary and multiple mucosal keratoacanthomas and the incidence of ectopic sebaceous glands has been included. In all mucous membrane locations where keratoacanthomas have arisen, there have been other reported cases of ectopic sebaceous glands in these areas. These findings have led us to consider that intraoral and perhaps all mucous membrane keratoacanthomas arise i, sebaceous glands or their ducts, whether they be normal in their location, as in the buccal mucosa, or ectopic.
BACKGROUND: Smallpox is notorious for leaving its survivors with disfiguring scars, but it is unclear how these scars are produced. Modern dermatopathology textbooks report that smallpox produced epidermal lesions, yet the process of scarring requires dermal involvement. OBJECTIVES: Our goal was to uncover past theories on the mechanism of smallpox scarring. METHODS: We conducted a comprehensive review of English-language textbooks and English-translations of textbooks in general medicine, dermatology, pathology, and dermatopathology from the past 150 years as well as relevant journal publications for the same time period. RESULTS: We identified five different theories to explain the scarring of smallpox. The five proposals are that scarring resulted from: the extension of suppuration into the dermis; the extension of suppuration into the dermis along with inappropriate treatment and scratching; secondary bacterial ecthyma; the destruction of elastic fibers; or the destruction of sebaceous glands. CONCLUSION: The theory that best fits clinical and histological observations is that smallpox caused scars through the destruction of sebaceous glands, first proposed by Gerrit Bras in 1952. Although this explanation is not found in any dermatopathology text, it is supported by today's leading authorities on smallpox. However, since variola virions have never actually been identified in sebaceous glands, or even in the dermis, further study of preserved tissue is warranted. Until then, the mechanism of scar formation remains speculative.
In vivo light microscopic radioautography was used to demonstrate the distribution of taurine in adult and newborn mice at 30 min. and 3 hrs. after the injection of 3H-taurine. This study showed that the injected taurine was present in free form in the skin. Radioautographically, it was found that in the adult a very high density of taurine was found over the epidermis and external root sheaths near the opening of the hair follicles. The external root sheath just below the insertion of the sebaceous glands and the peripheral part of the sebaceous glands showed a high taurine distribution. Connective tissue in the dermis, however, showed low uptake of taurine. In the neonate mouse, the density of injected taurine in both the epidermis and the external root sheath was lower than that the density in the connective tissue in the dermis. We report these findings in detail and discuss some of the functional roles of taurine in the skin.
The activity of 3 beta-hydroxysteroid dehydrogenase delta 4-5 isomerase (3 beta-HSD) was assayed in various tissues microdissected from the freeze-dried human skin of 13 subjects. The sebaceous gland possessed the highest activity of 3 beta-HSD in the skin, while the apocrine sweat gland showed only one fourth of that activity. The vellus hair follicle showed nearly one half of the activity of the sebaceous gland, whereas the terminal hair follicle exhibited much lower activity. The activity of the epidermis and of the dermis were negligible. Incubation of fresh whole skin of the forehead with 7 alpha-3H-DHA and subsequent isolation of various tissues revealed that the metabolites identified in the sebaceous gland were androstanedione and androstenedione, whereas testosterone and/or dihydrotestosterone were not detected.
Both testosterone and dihydrotestosterone may be able to stimulate sebaceous glands, and the glandular function may continue under direct testosterone control in the presence of 5 alpha-reductase blockade. Antagonism of sebaceous gland hypertrophy, induced by exogenous testosterone or dihydrotestosterone, has been studied in the hairless hamster using established and experimental drugs applied topically. The results support the proposition that testosterone plays a direct role in mediating sebaceous gland response. This suggests possibilities for the design of sebum inhibitory drugs with minimal systemic anti-androgenic side effects.
Transdermal pathways and targets in the skin for estradiol were investigated using dry-mount autoradiography. 3H-estradiol-17 beta was applied at doses of 30.1 pmol, 120.4 pmol and 301 pmol/cm2 to shaved rat skin in the dorsal neck region. Vehicles were DMSO, ethylene glycol or sesame oil. After 2 h of topical treatment with 30.1 pmol 3H-estradiol x cm-2 dissolved in DMSO a distinct cellular distribution was apparent. Target cells with concentrations of radioactivity were found in epidermis, sebaceous glands, dermal papillae of hair and fibroblasts. After treatment with 120.4 and 301 pmol/cm2, a penetration gradient of radioactivity was recognizable however it masked specific cellular and subcellular uptake. The stratum corneum accumulated and retained radioactivity, apparently forming a depot for the hormone. Strong concentration and retention of the hormone was conspicuous in sebaceous glands for more than 24 h, suggesting that sebaceous glands serve as a second storage site for the hormone. In all autoradiograms two penetration pathways to the dermis were visible: one through the stratum corneum and epidermis, the other through the hair canals and hair sheaths.
The Muir-Torre syndrome is an autosomal dominant genodermatosis characterized by the occurrence of one or more sebaceous gland tumors (either adenoma, epithelioma, or carcinoma) and a single malignant internal neoplasm. To date, 133 cases of Muir-Torre syndrome have been described. Colorectal (49%) and genitourinary (21%) carcinomas are the most common initial neoplasms. The case of a man with a history of recurrent ocular sebaceous carcinoma who subsequently had seminoma is described, and previously published reports of men with Muir-Torre syndrome and genitourinary tumors are discussed. Including this report, an associated genitourinary tumor was the initial malignant internal neoplasm in 11 men with Muir-Torre syndrome. The detection of a genitourinary neoplasm preceded diagnosis of the patient's Muir-Torre syndrome-associated sebaceous gland tumor in five patients (45%). All patients with sebaceous gland tumors of the type associated with Muir-Torre syndrome warrant consideration of Muir-Torre syndrome and appropriate workup to detect asymptomatic malignant visceral neoplasms.
Juxta-clavicular beaded lines (JCBL) are unique malformations of sebaceous glands or a variant of sebaceous hyperplasia with characteristic clinical features (1, 2). We describe a patient with JCBL, who received immunosuppressants following kidney transplantation. To our knowledge, our patient is the first case of JCBL in a kidney transplant recipient.
Microcystic adnexal carcinoma (MAC) in a 48-year-old Japanese male was studied. A firm nodule had appeared on the right side of his upper lip at the age of 38 years and then had gradually enlarged. Light microscopic examinations revealed numerous strands and islands of basaloid cells and keratinous cysts with desmoplastic stroma in the dermis and subcutaneous tissue. Some keratinous cysts showed early calcification and some contained pilar structures. Clear cells resembling sebaceous gland cells were observed in the strands of tumor cells connecting the keratinous cysts. In the middle dermis, there were small ductal structures containing amorphous eosinophilic material. Immunoperoxidase staining for carcinoembryonic antigen was focally positive in the lumina of small ducts, on the ductal lining surface of tumor cells, and in the contents of keratinous cysts. Electron microscopic examinations revealed tumor cells resembling non-keratotic keratinocytes, and containing tonofilaments, mitochondria, and vacuoles. In some parts, tumors were differentiated to various types of sebaceous gland, sweat duct, or sweat secretary segments. Sebaceous gland cells contained lipid droplets and glycogen. Tumors differentiated to sweat duct had a marked similarity to embryo eccrine duct in the lower epidermis because of the presence of multivesicular dense bodies and periluminal filamentous zones and the absence of myoepithelial cells. Tumors differentiated to sweat secretary segments had a similarity to embryo eccrine secretary segments because of the absence of multivesicular dense bodies, periluminal filamentous zones and myoepithelial cells.
The migration of epithelial cells from dermal appendages toward the wound surface is essential for re-epithelialization of partial thickness burn injuries. This study provides evidence that these cells in vivo synthesize a mitogenic and fibrogenic factor, insulin-like growth factor-1 (IGF-1), which may promote the development of the post-burn fibroproliferative disorder, hypertrophic scarring (HSc). An evaluation of 7 post-burn hypertrophic scars, 7 normal skin samples obtained from the same patients and 4 mature scars revealed that IGF-1 expressing cells from the disrupted sweat glands tend to reform small sweat glands of 4-10 cells/gland in post-burn HSc. The number of these cells increases with time and the glands become larger in mature scar. Other epithelial cells such as those found in sebaceous glands and basal and suprabasal keratinocytes, also express IGF-1 protein and mRNA as detected by Northern and RT-PCR analysis of RNA obtained from whole skin and separated epidermis and dermis. However, cultured keratinocytes did not express mRNA for IGF-1. Histological comparisons between normal and HSc sections show no mature sebaceous glands in dermal fibrotic tissues but the number of IGF-1 producing cells including infiltrated immune cells was markedly higher in the dermis of hypertrophic scar tissues relative to that of the normal control. In these tissues, but not in normal dermis, IGF-1 protein was found associated with the extracellular matrix. By in situ hybridization, IGF-1 mRNA was localized to both epithelial and infiltrated immune cells. Collectively, these findings suggest that in normal skin, fibroblasts have little or no access to diffusible IGF-1 expressed by epithelial cells of the epidermis, sweat and sebaceous glands; while following dermal injury when these structures are disrupted, IGF-1 may contribute to the development of fibrosis through its fibrogenic and mitogenic functions. Reformation of sweat glands during the later stages of healing may, therefore, limit this accessibility, and lead to scar maturation.