Tips Of Rete Ridges Research Articles

Hypertrophic Lichen Planus: An Up-to-Date Review and Differential Diagnosis.

Hypertrophic lichen planus (HLP) is a variant of lichen planus that can be difficult to diagnose based on histopathologic features alone. Thus, patient clinical history and clinicopathologic correlation are essential considerations to make the correct diagnosis. To discuss the clinical and histologic presentation of HLP and provide a thorough review of commonly encountered mimickers in the differential diagnosis. Data were derived from a literature review, personal clinical and research experiences, and a review of cases in the archives of a tertiary care referral center. In general, HLP involves the lower extremities and is characterized by thickened, scaly nodules and plaques that are often pruritic and chronic in nature. HLP affects both males and females and is most common in adults 50 to 75 years of age. Unlike conventional lichen planus, HLP tends to have eosinophils and classically displays a lymphocytic infiltrate most concentrated around the tips of rete ridges. The differential diagnosis for HLP is broad and encompasses numerous entities in many different categories, including premalignant and malignant neoplasms, reactive squamoproliferative tumors, benign epidermal neoplasms, connective tissue disease, autoimmune bullous disease, infection, and drug-related reactions. Therefore, a high index of suspicion must be maintained to avoid a misdiagnosis and potential inappropriate treatments.

Annular Lichenoid Dermatitis (of Youth).

About 20 years after its first description, Annular Lichenoid Dermatitis of Youth (ALDY) is recognized as a distinctive lichenoid dermatosis with specific clinical and histological features. The disease occurs mostly in young persons all over the world, runs a chronic course, and has an obscure etiopathogenesis. Clinically, lesions consist of persistent, asymptomatic erythematous macules and round-oval annular patches with a red-violaceous non-scaling border and central hypopigmentation, mostly localized on the groin and flanks. Histology shows a peculiar lichenoid dermatitis characterized by irregular epidermal hyperplasia with an alternation of thinned and quadrangular rete ridges and a dense band-like lichenoid infiltrate of lymphocytes in the papillary dermis. Typically, there is infiltration of lymphocytes into the lower epidermal layers with massive necrosis/apoptosis of keratinocytes, which is limited to the tips of rete ridges. Dermal lymphocytes are usually CD3+, CD4+, while most of the intraepidermal T cells are CD8+. Analysis of TCR-γ-chain gene rearrangement displayed polyclonality in all cases examined. Differential diagnosis mainly includes morphea, mycosis fungoides, annular erythemas and inflammatory lesions of vitiligo. Topical corticosteroids and topical tacrolimus represent the most effective drugs for ALDY treatment.

Clinico-pathological correlation of localised Dowling-Degos disease

A 26-years-old young man came with complaints of abnormally dark skin coloring (hyperpigmentation), particularly in the back of the hands and intertriginous folds between digits, progressively spreading since last 5 years without any family history of the same. He was diagnosed with clinical diagnosis of hyper-pigmented disorder under evaluation most probably medication induced. He had no personal and family history of such skin disease or diabetes mellitus. We received a skin biopsy of 0.3 × 0.3 cm which was totally embedded for histopathology reporting. Section studied through skin reveals epidermis, dermis and subcutaneous tissue. Epidermis shows hyperkeratosis, irregular acanthosis with focal filliform down growth of epidermis. Multiple keratin horn cysts were seen in the down growth. The tips of rete ridges showed pronounced hyperpigmentation. Histopathological impression was given as Dowling-Degos disease (DDD). DDD is a rare genetic skin condition without definite cure, although its prevalence is unknown. So we report a DDD case in a young man with clinico-pathological correlation.

Localized Dowling-Degos disease

A 26-year-old young man came with complaints of abnormally dark skin coloring, particularly in the back of the hands and intertriginous folds between digits, progressively spreading in the last 5 years. There was no family history of the same. He had no personal and family history of skin disease or diabetes mellitus. A clinical diagnosis of drug-induced hyperpigmentation disorder was made. A skin biopsy of 0.3 cm × 0.3 cm which was totally embedded for histopathology reporting was obtained. The section revealed epidermis, dermis, and subcutaneous tissue. Epidermis shows hyperkeratosis, irregular acanthosis with focal filliform down growth of the epidermis. Multiple keratin horn cysts were seen in the down growth. The tips of rete ridges showed pronounced hyperpigmentation. The histopathological impression was Dowling-Degos disease (DDD). DDD is a rare genetic skin condition without a definite cure, although its prevalence is unknown. We report a DDD case in a young man.

Differential expression of p63 isoforms in normal skin and hyperproliferative conditions

The p63 is regarded as a potential stem cell marker. Expression of p63 isoforms was examined in normal skin and hyperproliferative conditions including psoriasis and artificial skin equivalents (SEs). Rapidly adhering (RA) and slowly adhering (SA) cells were isolated, and Western blotting was performed. Expression of p63 (4A4) and p63 (H-137) is similar in all conditions, although there is some variation in psoriasis. However, expression of p63alpha (C-12) is markedly different. In normal skin, p63alpha (C-12)-positive cells were scattered in whole epidermis. But in psoriasis, p63alpha (C-12)-positive cells were observed at the tips of rete ridges. In SEs, p63alpha (C-12)-positive cells were not well observed. Western blot results showed that the RA cells express p63 (4A4) and p63 (H-137) strongly compared with SA or nonadhering (NA) cells. In contrast, SA or NA cells strongly express p63alpha (C-12). Results suggest that both p63 (4A4) and p63 (H-137) can detect epidermal stem cells. But, p63 (H-137) seemed to be a better marker because p63 (H-137)-positive cells were more localized at basal layer. In addition, it can be said that p63alpha (C-12) can detect TAp63, which is important in differentiation of epidermis. Furthermore, it is concluded that molecular control of TAp63 is especially disorganized in hyperproliferative condition including psoriasis and SEs.

An immunohistochemical analysis of human Merkel cell density in gingival epithelium from dentate and edentulous subjects

To investigate whether there is a difference in the density of Merkel cells between the gingiva of dentate and edentate subjects. One hundred and two blocks of human mandibular (n=55) and maxillary (n=47) gingiva from 69 white skinned individuals (44 males, 25 females, mean age 70.1 years, range 42--92 years) were analysed. Twenty-six individuals had teeth remaining in at least one jaw (mean age of dentate 64.5 years, edentate 72.1 years), of which 15 were dentate in both jaws. Overall, 24/55 mandibles and 17/47 maxillae were dentate. Five micrometer sections were stained with a monoclonal antibody to cytokeratin 20 (CK 20) using standard immunoperoxidase or immunoalkaline phosphatase methods. Positive cells were counted in 20 consecutive high power fields using the x 40 objective in three sections from each biopsy, and the results analysed for differences related to age, sex, site and presence of teeth. CK 20-positive Merkel cells were present either singly or in clusters in the basal epithelial layers, particularly at the tips of rete ridges. Numbers of gingival Merkel cells were significantly higher (p<0.005, Mann-Whitney) in edentate (cells per field mean, median, standard deviation, respectively: 1.39, 0.64, and 1.85) when compared to dentate (0.67, 0.20, and 1.21) specimens. The differences were not statistically significant for any other variable. The data raise the possibility that reduced perception following loss of teeth may be compensated for by an increase in the local Merkel cell population.