The skin of the nose shows several specific anatomical and histological peculiarities that should be considered when evaluating skin lesions on the nose or when planning the reconstruction of surgical defects [7]. The skin in the areas of the dorsum, columella and sidewalls is thin, loose, compliant and relatively less sebaceous [8, 9]. The skin in the areas of the nasal tip and alae is thicker, more sebaceous, more adherent and less flexible [4]. Surgical procedures on the skin of the nose have to respect these different qualities and the nasal topography, including the nasal aesthetic subunits, to achieve the best possible result. The different aesthetic subunits are the tip subunit, columella subunit, dorsal subunit, right and left alar base subunits, right and left alar side wall subunits and right and left dorsal side wall subunits [10]. The anatomical nasal subunits include the dorsum, sidewalls, lobule, soft triangles, alae and columella. The concept of subunits of the external tissue of the nose has proven useful for planning reconstruction. If more than 50% of the subunit is lost it is favorable to replace the whole subunit with regional tissue or a transplant from a donor site [11]. The most important skin diseases on the nose that can require surgical consultation or successfully undergo laser therapy are described below. The description of all dermatoses that can involve the nose would extend beyond the scope of this review. Therefore, our description is limited to those calling for laser or surgical therapy and to those that are clinically most important in the daily practice of a dermatologic surgeon.
Rosacea is a multiphasic inflammatory condition that typically affects the skin of the face and nose. Clinically, rosacea has been classified in four different stages. Stage I, also called rosacea erythematosa telangiectasia (pre-rosacea), shows facial flushing and telangiectasia. Stage II, rosacea papulopustulosa (vascular rosacea), is characterized by persistent facial erythema, telangiectasia, thickened skin, papules and pustules (Fig 9). Stage III, glandular-hypertrophic or inflammatory rosacea, shows erythematous papules and pustules, telangiectasias, edema, connective tissue and sebaceous gland hyperplasia. Stage IV, or rhinophyma, shows dermal and sebaceous gland hyperplasia, and dilated and cystic sebaceous glands. Most individuals affected by rosacea are of northern European origin, and up to one-third have a family history of the disorder [91]. Clinical signs include facial flushing, erythema, telangiectasia and papulopustular efflorescence similar to acne as described previously. Women are three times more likely to be affected than men, with the reported prevalence between 0.5 and 10% [92, 93]. The pathophysiology has been poorly understood, and there have been only limited descriptions of factors that exacerbate or improve this disease [94]. Recent molecular studies suggest that an altered innate immune response is involved in the pathogenesis of vascular and inflammatory disease and is responsible for the observed clinical findings in patients with rosacea [95].
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First described in 1889 by Hutchinson as a "crateriform ulcer of the face", keratoacanthoma is a fast-growing, epithelial tumor that develops from hair follicles or the surface epithelium of the skin. It can occur solitarily (frequent) or with multiple lesions (rare). The lesion consists of a firm, cone-shaped nodule (1-3 cm in diameter) with a central horn-filled crater. It shows rapid growth within weeks or months followed by spontaneous resolution over 4-6 months in most cases. Histologically and clinically it often resembles SCC. There is debate about whether it undergoes transformation into SCC or is SCC from the beginning [108, 109]. Nevertheless, as SCC can masquerade as keratoacanthoma, surgical excision with an excision margin of 2-3 mm is recommended [106]. Because the histologic changes at the base of the lesion are important for histologic differentiation, a shave biopsy should be avoided and an excision of the lesion in its entirety should be performed [110]. Immunocompromised patients and those with Muir-Torre syndrome (the combined occurrence of at least one sebaceous skin tumor and one internal malignancy in the same patient) show an increased incidence of keratoacanthoma [111, 112].
Byrd et al. [3] reported the top ten bacterial species found on the skin through site area surveys in healthy volunteers based on high-throughput gene sequencing analysis. Human skin samples were found to be dominated by gram-positive bacteria belonging to the genera Staphylococcus spp., Corynebacterium spp., Enhydrobacter spp., Micrococcus spp., Cutibacterium spp., and Veillonella spp. A culture-based study by Myles et al. [7] that focused on the culturable fraction of gram-negative bacteria (GNB) from the human skin identified Roseomonas mucosa, Pseudomonas spp., Acinetobacter spp., Pantoea septica, and Moraxella osloensis as commensal residents. Other studies have verified that gram-negative bacteria (GNB), including Enterobacteriaceae, nonfermenting GNB, and anaerobes, are underestimated skin commensal organisms but are also part of the transient fraction of the skin microbiota [8, 9].
Within the viral fraction found on the skin, bacteriophages are predominant. The lytic activity of bacteriophages has been linked to the modulation of bacterial populations, and thus, bacteriophages participate in the homeostasis of the skin microbiota. Through culture-based approaches and genomic analysis of skin samples, Liu et al. [17] revealed an increased frequency of C. acnes phages isolated from healthy individuals compared to patients with Acne vulgaris and suggested that phages may play a role in modulating skin bacterial populations. Metagenomic shotgun sequencing analysis suggests that Cutibacterium and Staphylococcus phages are the most abundant skin phages, while other phages, such as Streptococcus and Corynebacterium phages, are also present but at lower relative abundances [18]. Byrd et al. [3] reported the top ten viruses found on the skin. Phages were identified as well as Acheta domestica; Densovirus; Alphapapillomavirus; Human papillomavirus (β), (γ) and (μ); Merkel cell polyomavirus; Molluscum contagiosum virus; Polyomavirus HPyV7; Polyomavirus; HpyV6 RD114 retrovirus; and Simian virus. Papillomaviruses and Molluscum contagiosum are known to cause dermatological lesions, such as warts. Merkel cell polyomavirus is implicated in the development of carcinoma. The question of the underappreciated abundance of phages was discussed recently by Hannigan et al. [19]. Whether the presence of these phages plays a role in skin microbiota dysbiosis or the expression of virulence or antibacterial genes needs to be further studied.
The culture of microorganisms is a historical method for studying their characteristics and properties. With recent advances in molecular biology, this fundamental tool has been shelved in favor of next-generation sequencing methods, which are more sensitive and faster than culture. However, next-generation sequencing does not provide all the information needed to understand the habits of microorganisms in vivo; for example, it provides no information about the viability of the detected organisms [98]. A goal that is as important as the improvement of sampling and storage methods is the improvement of culture parameters in efforts aimed at isolating the viable and culturable fraction of the skin microbiome, which presents its own particularities and shows certain consistent traits [64]. For example, Myles et al. [7] showed that when using a low-nutrient culture medium (R2A), inhibition of the gram-positive fraction by treating the sample with vancomycin and a reduced incubation temperature led to the isolation of the gram-negative fraction of the skin microbiota. Moreover, other parameters of the protocol could be adjusted to obtain more efficient culture media for the growth of diverse skin microorganisms and to improve the methods of colony identification [101, 102]. In these efforts, the culturomics method was improved by Lagier et al. [103], which allowed the discovery of multiple unknown bacteria. By using these methods (i.e., the combination of multiple culture media and conditions), Timm et al. [104] collected more than 800 strains, including more than 30 bacterial genera and 14 fungal genera. However, because this technique requires fastidious and time-consuming work, an increasing number of scientific teams have reinstated this method uniquely or with the use of complementary metagenomic tools [30, 105, 106].
The democratization of metagenomic technologies has induced a shift in interest related to human-associated microorganisms. The skin microbiota has been largely underestimated in terms of diversity, which has persisted because of culture techniques that induce bias due to the growth of microbes in artificial settings [106]. To apply this kind of method for skin microbiome analyses, particular attention is needed at each step of the protocol, including the DNA extraction method, library construction, sequencing step (e.g., primer selection, the chosen platform [88], and the use of blanks and controls), and subsequent analysis (e.g., the selected database and software) [27, 106,107,108]. Furthermore, advanced methods to isolate and cultivate difficult strains by reverse genomics have been recently proposed [109].
Many biological models have been produced in an attempt to reconstitute the skin-microbiome interaction with different complexity levels. The first studies consisted of culturing human skin cells, mainly keratinocytes or sebocytes, with bacteria or their metabolites. The main goal of these studies was to understand the pathways involved in pathogen infections or commensal benefits for the skin. Keratinocytes incubated with sterile filtered Staphylococcus aureus medium showed increased production of proteolytic enzymes, followed by the degradation of skin barrier proteins, such as desmoglein-1 and filaggrin [110]. In contrast, some metabolites produced by S. epidermidis could increase the keratinocyte production of antimicrobial peptides via Toll-like receptor 2 activation [36]. 2ff7e9595c
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