Could scalp pain be a type of unclassified headache? / A dor no couro cabeludo poderia ser um tipo de dor de cabeça não classificada?

The scalp is the structure that covers the skull. It is commonly affected by painful processes resulting from infestations, infectious or inflammatory diseases. This pain located in the scalp does not have well-defined clinical characteristics and is not yet included in the ICHD-3 diagnostic criteria. The authors suggest including this pain in the next classification of headaches as a headache attributed to a scalp disorder.

O couro cabeludo é a estrutura que cobre o crânio. É comumente acometida por processos dolorosos decorrentes de infestações, doenças infecciosas ou inflamatórias. Essa dor localizada no couro cabeludo não possui características clínicas bem definidas e ainda não está incluída nos critérios diagnósticos da ICHD-3. Os autores sugerem incluir esta dor na próxima classificação de dores de cabeça como dor de cabeça atribuída a um distúrbio do couro cabeludo.

Final results of a prospective study of scalp cooling in preventing chemotherapy-induced alopecia.

Aim: Alopecia is a distressing effect of cancer treatments. Our study examined efficacy and safety of scalp cooling to prevent chemotherapy-induced alopecia. Materials & methods: Early breast cancer patients candidate to anthracycline and/or taxane were eligible. Dean's alopecia scale was used to classify alopecia. Results: From February 2016 to November 2018, 127 women were enrolled; 55 (43.3%) received epirubicin/cyclophosphamide (4 EC 3 weeks) followed by paclitaxel (12 P weeks); 50 (39.4%) received 4 EC 3 weeks; 20 (15.7%) received 12 P weeks/trastuzumab and 2 docetaxel/cyclophosphamide (4 TC 3 weeks). The success rate was 71.7% (G0 21.3%, G1 31.5%, G2 18.9%). Frequent side effects were: coldness, headache, scalp pain and head heaviness. Conclusion: In our study, scalp cooling can prevent alopecia thus supporting the wider use in early breast cancer.

Chondrogenic differentiation of human scalp adipose-derived stem cells in Polycaprolactone scaffold and using Freeze Thaw Freeze method.

Human adipose tissue has been identified as a viable alternative source for mesenchymal stem cells. SADSCs were isolated from human scalp biopsy and then were characterized by Flow cytometry. SADSCS expressed CD90, CD44, and CD105 but did not express CD45 surface marker. Growth factors were used for chondrogenesis induction. Histology and immunohistology methods and gene expression by real-time PCR 14 days after induced cells have shown the feature of chondrocytes in their morphology and extracellular matrix in both inducing patterns of combination and cycling induction. Moreover, the expression of gene markers of chondrogenesis for example collagen type II aggrecan and SOX9 has shown by real-time PCR assay. Then, SADSCs were seeded alone on polycaprolatone (PCL) and with Freeze thaw Freeze (PCL+FTF) scaffolds and SADSCs differentiated toward the chondrogenic lineage and chondrogenesis induction were evaluated using scanning electron microcopy (SEM) and MTT assay. Our results showed that SADSCs were also similar to the other adipose-derived stem cells. Using TGF-beta3 and BMP-6 were effective for chondrogenesis induction. Therefore using of TGF-beta3 and BMP-6 growth factors may be the important key for in vitro chondrogenesis induction. The bio-composite of PCL+FTF nanofibrous scaffolds enhance the chondroblast differentiation and proliferation compared to PCL scaffolds .Therefore, our model will make it possible to study the mechanism of transition from chondroblast to chondrocyte.

The walking dead: sequential nuclear and organelle destruction during hair development.

BACKGROUND: Transition of hair shaft keratinocytes from actively respiring, nucleated cells to structural cells devoid of nucleus and cytoplasm is key to hair production. This form of cell 'death', or cornification, requires cellular organelle removal to allow the cytoplasm to become packed with keratin filament bundles that further require cross-linking to create a strong hair fibre. Although these processes are well described in epidermal keratinocytes, there is a lack of understanding of such mechanisms, specifically in the hair follicle. OBJECTIVES: To gain insights into cornification mechanisms within the hair follicle and thus improve our understanding of normal hair physiology. METHODS: Scalp biopsies and hair-pluck samples were obtained from healthy human donors and analysed microscopically after immunohistochemical staining. RESULTS: A focal point of respiratory activity was evident in keratogenous zone cells within the hair shaft, which also exhibited nuclear damage. Nuclear degradation occurred via both caspase-dependent and caspase-independent pathways. Conversely, mitophagy was driven by Bnip3L and restricted to the boundary of the keratogenous zone at Adamson's Fringe. CONCLUSIONS: We propose a model of stepwise living-dead transition within the first 1 mm of hair formation, whereby fully functional, nucleated cells first consolidate required functions by degrading nuclear DNA, yet continue to respire and provide the source of reactive oxygen species required for keratin cross-linking. Finally, as the cells become packed with keratin bundles, Bnip3L expression triggers mitophagy to rid the cells of the last remaining 'living' characteristic, thus completing the march from 'living' to 'dead' within the hair follicle.

Alterations in Hair Follicle Morphology and Hair Shaft Production After Follicular Unit Transplantation.

Follicular unit transplantation is the most commonly performed technique in modern restorative hair transplantation surgery. It relies on the acquisition of intact follicular units from microdissected scalp skin strips and their subsequent transplantation into the recipient regions affected by alopecia. Ideally, the translocation of follicular units from the balding-resistant areas of the scalp (usually the occipital region) to the recipient site should not result in any morphological change in the grafts. Nevertheless, the insults associated with surgical intervention present grafted follicles to mechanical and chemical cues differently from those of the physiological steady-state conditions in undamaged skin. This disruption of the normal follicular microenvironment might alter important aspects of hair biology in grafts, for example, hair cycle and pigmentation, and, in turn, could lead to differences in hair appearance, eventually culminating in a diminished esthetical outcome of the surgery. In this study, the authors analyzed native and grafted scalp hair follicles (HFs) from 2 patients who had undergone follicular unit transplantation surgeries formerly. Scanning electron microscopy and light microscopy-based histomorphometry revealed a marked enlargement of follicular structures in the grafts with a concomitant increase in hair shaft diameter. Immunohistological staining confirmed a thickening of the dermal sheath in transplanted HFs that also harbored a denser vascular network. Taken together, these results show that the grafted HFs analyzed were subjected to marked morphological changes during their residence in the recipient site and that this phenomenon is associated with a modulation of follicular vascularization.

Therapeutic efficacy of autologous platelet-rich plasma and polydeoxyribonucleotide on female pattern hair loss.

Autologous platelet-rich plasma (PRP) exerts positive therapeutic effects on hair thickness and density in patients with pattern hair loss. The aim of our study was to evaluate the efficacy of intra-perifollicular autologous PRP and polydeoxyribonucleotide (PDRN) injections in treating female pattern hair loss (FPHL). Twenty FPHL patients were treated with a single session of PRP injection, followed by 12 sessions of PDRN intra-perifollicular injection, along the scalp at weekly intervals. Additionally, another 20 FPHL patients were treated with 12 sessions of PDRN injection only. Meanwhile, one half of the backs of two rabbits was injected with the PRP preparation, while the other half was injected with phosphate buffered saline as a control. Tissue samples from the rabbits were analyzed by real-time polymerase chain reaction and Western blotting. Compared with baseline values, patients treated with PRP and PDRN injections exhibited clinical improvement in mean hair counts (23.2 ± 15.5%; p < 0.001) and mean hair thickness (16.8 ± 10.8%; p < 0.001). In addition, patients treated with the 12 sessions of intra-perifollicular PDRN injection alone also showed clinical improvement in mean hair counts (17.9 ± 13.2%; p < 0.001) and mean hair thickness (13.5 ± 10.7%; p < 0.001). Comparison analyses between the two groups revealed that combined therapy with PRP and PDRN induces greater improvement in hair thickness than treatment with PDRN therapy alone (p = 0.031), but not in hair counts (p > 0.05). The pilot animal study revealed significant up-regulation of WNT, platelet-derived growth factor, and fibroblast growth factor expression in rabbit skin treated with the PRP preparation, compared with control skin. In conclusion, intra-perifollicular injections of autologous PRP and/or PDRN generate improvements in hair thickness and density in FPHL patients.

The effect of autologous activated platelet rich plasma (AA-PRP) injection on pattern hair loss: clinical and histomorphometric evaluation.

To investigate the safety and clinical efficacy of AA-PRP injections for pattern hair loss. AA-PRP, prepared from a small volume of blood, was injected on half of the selected patients' scalps with pattern hair loss. The other half was treated with placebo. Three treatments were given for each patient, with intervals of 1 month. The endpoints were hair re-growth, hair dystrophy as measured by dermoscopy, burning or itching sensation, and cell proliferation as measured by Ki-67 evaluation. At the end of the 3 cycles of treatment, the patients presented clinical improvement in the mean number of hairs, with a mean increase of 18.0 hairs in the target area, and a mean increase in total hair density of 27.7 ( number of hairs/cm(2)) compared with baseline values. Microscopic evaluation showed the increase of epidermis thickness and of the number of hair follicles two weeks after the last AA-PRP treatment compared to baseline value (P < 0.05). We also observed an increase of Ki67(+) keratinocytes of epidermis and of hair follicular bulge cells and a slight increase of small blood vessels around hair follicles in the treated skin compared to baseline (P < 0.05).

A meeting of two chronobiological systems: circadian proteins Period1 and BMAL1 modulate the human hair cycle clock.

The hair follicle (HF) is a continuously remodeled mini organ that cycles between growth (anagen), regression (catagen), and relative quiescence (telogen). As the anagen-to-catagen transformation of microdissected human scalp HFs can be observed in organ culture, it permits the study of the unknown controls of autonomous, rhythmic tissue remodeling of the HF, which intersects developmental, chronobiological, and growth-regulatory mechanisms. The hypothesis that the peripheral clock system is involved in hair cycle control, i.e., the anagen-to-catagen transformation, was tested. Here we show that in the absence of central clock influences, isolated, organ-cultured human HFs show circadian changes in the gene and protein expression of core clock genes (CLOCK, BMAL1, and Period1) and clock-controlled genes (c-Myc, NR1D1, and CDKN1A), with Period1 expression being hair cycle dependent. Knockdown of either BMAL1 or Period1 in human anagen HFs significantly prolonged anagen. This provides evidence that peripheral core clock genes modulate human HF cycling and are an integral component of the human hair cycle clock. Specifically, our study identifies BMAL1 and Period1 as potential therapeutic targets for modulating human hair growth.

BMS1 is mutated in aplasia cutis congenita.

Aplasia cutis congenita (ACC) manifests with localized skin defects at birth of unknown cause, mostly affecting the scalp vertex. Here, genome-wide linkage analysis and exome sequencing was used to identify the causative mutation in autosomal dominant ACC. A heterozygous Arg-to-His missense mutation (p.R930H) in the ribosomal GTPase BMS1 is identified in ACC that is associated with a delay in 18S rRNA maturation, consistent with a role of BMS1 in processing of pre-rRNAs of the small ribosomal subunit. Mutations that affect ribosomal function can result in a cell cycle defect and ACC skin fibroblasts with the BMS1 p.R930H mutation show a reduced cell proliferation rate due to a p21-mediated G1/S phase transition delay. Unbiased comparative global transcript and proteomic analyses of ACC fibroblasts with this mutation confirm a central role of increased p21 levels for the ACC phenotype, which are associated with downregulation of heterogenous nuclear ribonucleoproteins (hnRNPs) and serine/arginine-rich splicing factors (SRSFs). Functional enrichment analysis of the proteomic data confirmed a defect in RNA post-transcriptional modification as the top-ranked cellular process altered in ACC fibroblasts. The data provide a novel link between BMS1, the cell cycle, and skin morphogenesis.

Histopathology of scarring and nonscarring hair loss.

This article reviews the histologic findings of alopecia, preceded by a brief discussion of biopsy and processing techniques, the normal follicular anatomy and cycle, and expected findings in transverse sections. Subtle histologic abnormalities will be missed unless the normal follicular anatomy and follicular cycle, when viewed in transverse sections, are understood.

Hair through the female life cycle.

At a population level female scalp hair growth shows features of regression with chronological ageing, although there is wide interindividual variation in timing and degree. The subjective assessment of hair loss is classically determined by hair density but it is apparent that other factors contribute to the clinical picture. Changes can occur in hair cycling, hair density, hair diameter and pigmentation, and possibly in structural qualities of the hair fibre. These changes are most pronounced in female pattern hair loss. Although conventionally considered as the female counterpart of male androgenetic alopecia the evidence that female pattern hair loss is androgen dependent is less clear cut than in men and it probably has a multifactorial basis. The emerging evidence implicating environmental factors is of particular interest as, unlike genes, such factors may be amenable to intervention. The clinical signs in women complaining of hair loss may be variable. In evaluating the patient complaining of hair loss, while true pathology must always be considered, the clinician needs to be aware of how age affects hair growth. These changes form the focus of this article.

The developmental trajectory of brain-scalp distance from birth through childhood: implications for functional neuroimaging.

Measurements of human brain function in children are of increasing interest in cognitive neuroscience. Many techniques for brain mapping used in children, including functional near-infrared spectroscopy (fNIRS), electroencephalography (EEG), magnetoencephalography (MEG) and transcranial magnetic stimulation (TMS), use probes placed on or near the scalp. The distance between the scalp and the brain is a key variable for these techniques because optical, electrical and magnetic signals are attenuated by distance. However, little is known about how scalp-brain distance differs between different cortical regions in children or how it changes with development. We investigated scalp-brain distance in 71 children, from newborn to age 12 years, using structural T1-weighted MRI scans of the whole head. Three-dimensional reconstructions were created from the scalp surface to allow for accurate calculation of brain-scalp distance. Nine brain landmarks in different cortical regions were manually selected in each subject based on the published fNIRS literature. Significant effects were found for age, cortical region and hemisphere. Brain-scalp distances were lowest in young children, and increased with age to up to double the newborn distance. There were also dramatic differences between brain regions, with up to 50% differences between landmarks. In frontal and temporal regions, scalp-brain distances were significantly greater in the right hemisphere than in the left hemisphere. The largest contributors to developmental changes in brain-scalp distance were increases in the corticospinal fluid (CSF) and inner table of the cranium. These results have important implications for functional imaging studies of children: age and brain-region related differences in fNIRS signals could be due to the confounding factor of brain-scalp distance and not true differences in brain activity.

A case of extensive aplasia cutis congenita: a conservative approach.

Aplasia cutis congenita is a rare, sporadic congenital malformation characterized by skin defects, sometimes extending to the underlying bone. We report a case of a boy born with a large rhomboid scalp and skull defect measuring 8 × 12 cm with no other anomalies. Conservative treatment led to the complete epithelization of the skin defect with secondary closure of the cranial vault without need for surgical intervention.

Validity of methyl mercury hair analysis: mercury monitoring in human scalp/nude mouse model.

OBJECTIVE: The grafting of human scalp hair was used as a new application of this method to explore methyl mercury incorporation into human hair and to validate this model for mercury monitoring in hair. METHODS: Human scalp grafts were transplanted to athymic BALB/c nude mice. The animals were exposed to methyl mercury either as a single dose i.p. or continuously for 4 months, using ALZET osmotic pumps. The mercury concentration in hair was determined using x-ray fluorescence (XRF) spectrometry by segmental (2 mm) analysis of a single strand, and tissue concentrations were measured by cold vapor atomic absorption analysis. RESULTS: Human scalp hair grown in nude mice showed long-term persistence of human features including the expression of histocompatibility antigens (KAB 3, W 6/32, SF 1-1.1.1) and normal hair morphometry. The disposition of methyl mercury in nude mice followed a one-compartment model with a whole body elimination half-life of 6.7 days (elimination constant, k = 0.1/day). Autoradiographic studies revealed that methyl mercury was rapidly incorporated into areas of the hair follicle undergoing active keratinization. Methyl mercury concentrations in human hair transplanted onto nude mice were two orders of magnitude higher than in blood and attained a mean hair: blood ratio of 217 : 1, similar to ratios reported only in human studies. CONCLUSIONS: This study demonstrated that human hair grown on nude mice can record the level of exposure to methyl mercury and can serve as a valuable research tool to study mercury incorporation into human hair.

Primary essential cutis verticis gyrata in an adult female patient: a case report.

Cutis verticis gyrata (CVG) is a very rare morphological condition of the scalp characterized by ridges and furrows resembling the surface of the brain. Primary or idiopathic CVG occurs in the absence of underlying soft-tissue abnormalities and is often associated with neuropsychiatric disorders. Secondary CVG occurs as a result of a local inflammatory or neoplastic process of the scalp or a systemic illness that produce pathologic changes in the scalp structure. The choice of treatment of CVG is surgical repair which depends on the size and location of the lesion, the underlying disorder, and the wishes of the patient, including primary repair, serial excision, skin grafting, local flaps and tissue expansion. In this case report, we describe the first female patient in the published work with primary essential CVG that appeared at 30 years of age. Because the patient had no cosmetic or functional complaint, no surgical intervention was attempted. Primary essential CVG, a very uncommon disorder, may be encountered in females after the third decade. The classification of CVG is essential to properly diagnose and treat patients who present with these unusual scalp lesions.

Complete osseous regeneration of a large skull defect in a patient with cutis aplasia: a conservative approach.

Cutis aplasia (or aplasia cutis congenita) is a congenital absence of all skin layers, often extending through bone. This defect usually occurs in the scalp and can be extensive, exposing the dura mater, and deeper meninges. Treatment regimens for cutis aplasia have included early operative intervention, including skin and bone grafts, local scalp flaps, or free flaps to close the defect. In addition to the significant perioperative risks, these invasive procedures may inhibit the osteogenic potential of the dura to initiate and sustain bony closure of the defect. We report a case of an infant with Adams-Oliver syndrome and cutis aplasia involving a large portion of the skull that was treated conservatively with topical Silvadene dressings. No surgical treatment of bone or soft tissue reconstruction was necessary. This case report is the first to our knowledge to document complete bony restoration of the cranial vault through serial three-dimensional CT scans. The intensive therapeutic intervention in this case report allowed early discharge from the hospital, a gradual amelioration of the patient's alopecia as the hair-bearing scalp slowly covered the defect, and precluded the need for any subsequent bony reconstruction of the cranial vault. We hypothesize that conservative treatment of cutis aplasia maintains dural induction of osseous regeneration, and any treatment plan for bony defects of cutis aplasia should consider maintenance of dural integrity. Although further investigation is warranted, an initial trial of antimicrobial dressing care might optimally promote secondary closure of the cranial vault without the need for surgical intervention.

Human scalp hair follicle development from birth to adulthood: statistical study with special regard to putative stem cells in the bulge and proliferating cells in the matrix.

The depths of hair follicle compartments, and in particular of the bulge, the putative site of hair follicle stem cells, have not yet been determined in human scalp skin from infants, children or adolescents. This information is necessary in order to use the scalp safely as a donor site for skin grafts. We therefore investigated the development of the infundibulum, the bulge, Adamson's fringe, the B-fringe and the matrix by measuring the depths of these five follicular compartments in parietal scalp biopsy specimens from 100 patients ranging in age from 2 weeks to 21 years. The thickness of the epidermis and the dermis were also assessed. The correlations of these measurements with age were determined by regression analysis. The regression equation for the bulge was found to be b (microns) = 683.3 + 30.8y (r = 0.73; SEM = 145.5) where y is the age in years, and for the matrix it was m (microns) = 1616.2 + 90.4y (r = 0.76; SEM = 406.5); P < 0.0001 for the null hypothesis. The growth of the inferior portion below the bulge was not parallel but proportional to that of the superior portion. The relative position of the bulge in the dermis was stable, whereas the inferior portion moved progressively more deeply into the subcutis. These findings provide evidence for the postulated biologically advantageous localization of the bulge, and thus is a further argument in favour of the bulge as the site of follicular stem cells.

Matrilysin (PUMP) correlates with dermal invasion during appendageal development and cutaneous neoplasia.

Matrix-degrading metalloproteinases play a major role in tissue remodeling. Recent studies have shown that enzymes of this class are constitutively expressed primarily by stromal cells and not by epithelium. Here we present immunohistochemical evidence that matrilysin is localized within epidermal cells in developing skin and in tumor cells of cutaneous malignancies. The expression of matrilysin protein in developing fetal skin (6-15 weeks) is localized primarily to the germinative basal cell layer of fetal epidermis and early appendageal buds. The buds continue to express matrilysin during mesenchymal invasion. As development progresses (15-19 weeks) matrilysin is concentrated only in cells at the distal portion of the invading follicular and sweat gland appendageal cords. In adult skin, matrilysin was localized specifically to the outer root sheath of the hair follicles and the secretory cells of the eccrine glands but was absent in the epidermis. Nodulocystic, keratotic, adenoid basal cell carcinomas (BCCs) did not express matrilysin. In contrast, in the more aggressive morpheaform (infiltrative) BCCs and recurrent BCCs, matrilysin was localized at the tumor-stromal interface. In squamous cell carcinomas matrilysin was present in tumor cells at the stromal interface surrounding the tumor nests. The demonstration of matrilysin protein in germinal basal cells during fetal skin development and its presence in tumor cells at the stromal junction suggests that this enzyme may contribute to the proteolytic activity associated with cell-extracellular matrix interactions during appendageal development and tumor invasion.