Magnetic scaffolds divided by composition, production, and MNPs embedded. Redrafted from [5].
\r\n\tVirtual Reality (VR) is a computer-created sensory experience that allows the user to believe in the apparent reality. The user is then either completely surrounded by this virtual world or partly included by listening and watching virtual reality applications. Thereby, the user's senses detect only virtual stimuli produced by a computer, and direct entry of the user's movement in the computer can be achieved.
\r\n\tVirtual Environments (VE) are based on objects defined in the computer's memory in such a way that a computer can later attach these items on the screen with the possibility of interaction. By combining elements of the unreal (imaginary) environment and the real environment (which can also be distant), the user creates a feeling of presence in the virtual environment.
\r\n\tVirtual reality is mostly applied in the following fields - medicine, military, education, entertainment, design and development, marketing.
\r\n\tMedicine is one of the strongest fields of VR’s application. VR is used in the field of surgery, both for training (practicing on virtual human models) and in surgery planning. In psychiatry, the virtual reality is used for treating various psychotic disorders, starting from the fear of flying, to post-traumatic stress disorder, where it marks very good results.
\r\n\tSimulations of various vehicles are among the most common applications of virtual reality. Many experts are trained in different simulators, but it is especially important to be able to rehearse situations that in reality rarely occur (for example, hostage rescue).
\r\n\tVirtual reality is ideal for the entertainment industry, because of the possibility to create an illusion. There are many amusement parks that have numerous attractions using virtual reality techniques.
\r\n\tVirtual reality can also, be used for the presentation of future projects in architecture and for creating prototypes of future products, as a successful tool for the promotion and marketing at exhibitions and fairs.
\r\n\tDespite the numerous areas of application, there are limitations as well. Although there has been considerable progress recently, the equipment is still impractical, large, expensive and complex. Certain types of virtual reality can cause nausea.
\r\n\tIn this book, we will discuss the key elements in terms of virtual reality, available technologies and resources (hardware and software), as well as the appropriate application of virtual reality, through training and entertainment, with a retrospective view of potential health problems, security, and privacy.
Palmoplantar keratosis or palmoplantar keratoderma (PPK) constitutes a heterogeneous group of disorders characterized by excessive epidermal thickening of the palms and soles of affected individuals [1]. PPK can be characterized as either inherited or acquired. Transgredient PPK extends beyond palmoplantar skin, contiguously or as callosities on pressure points on the fingers or knuckles, or elsewhere. Typical pathohistological findings of PPK are orthokeratotic hyperkeratosis, hyper- or hypogranulosis and acanthosis. These changes are non-specific and found in many types of PPK.
PPK is classified clinically as diffuse, focal, striate, or punctuate and develops either in isolation or in association with other cutaneous or extracutaneous manifestations. The diffuse type consists of uniform involvement of the palmoplantar surface. The focal type consists of localized areas of hyperkeratosis located mainly on pressure points and sites of recurrent friction. The striate type presents with linear hyperkeratosis on the palms and soles. The punctate type features multiple small, hyperkeratotic papules, spicules, or nodules on the palms and soles. These tiny keratoses may involve the entire palmoplantar surface or may be restricted to certain locations.
Unna-Thost PPK is inherited in an autosomally dominant manner without associated organ involvement. The condition may manifest in the first few months of life but is usually well developed by age 3-4 years. The disease develops in early childhood and persists throughout life. Clinically, there is hyperkeratosis on the palms and soles. Unna-Thost PPK is characterized by a well-demarcated, symmetric, often "waxy" hyperkeratosis involving the whole of the palms and soles. It is usually nontransgredient, with a sharp demarcation of the lesions at the wrists. Aberrant keratotic lesions may appear in the dorsum of the hands, feet, knees, and elbows. The dorsa of the fingers may be involved with a sclerodermalike thickening of the distal digit. A cobblestone hyperkeratosis of the knuckles may be seen. Nails may be thickened.
Histological findings include orthokeratotic hyperkeratosis associated with hypergranulosis or hypogranulosis and moderate acanthosis. Molecular biology features include linkage to type II keratin locus on band 12q11-13, corresponding to a keratin 1 gene mutation. Treatment includes salicylic acid, 50% propylene glycol in water under plastic occlusion several nights per week, and lactic acid- and urea-containing creams and lotions; all have been shown to be helpful. Mechanical debridement with a blade may also be useful. Oral retinoid therapy has had variable effects.
This type is inherited in an autosomal dominant fashion. It has an estimated prevalence of at least 4.4 cases per 100,000 population in Northern Ireland. Onset occurs in the first few months of life, but the disease is usually well developed by age 3-4 years. A well-demarcated, symmetric thick, yellow hyperkeratosis is present over the palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis [2]. An erythematous band is frequently present at the periphery of the keratosis. The surface is often uneven and verrucous. Finally, it is usually nontransgredient, with a sharp demarcation of the lesions at the wrists.
Histologically, keratinocytes show epidermolysis, hyperkeratosis, acanthosis, and papillomatosis. Perinuclear vacuolization and large keratohyalin granules are seen. Cellular breakdown in the spinous and granular cell layers sometimes leads to blister formation. Keratin 1 and keratin 9 mutations have also been reported. Treatment includes salicylic acid, 50% propylene glycol in water under plastic occlusion several nights per week, and lactic acid- and urea-containing creams and lotions; all have been shown to be helpful. Mechanical debridement with a blade also may be useful. Oral retinoid therapy has had variable effects and may not benefit patients with certain genotype profiles, such as K1 mutations.
Clinical features of Vörner PPK are very similiar to Unna-Thost PPK. Unna-Thost PPK may have a waxy appearance, compared with the dirty appearance of Vörner PPK. Hyperhidrosis and pitted keratolysis may be present with Unna-Thost PPK. Differentiation from Unna-Thost PPK can be made histopathologically, with the finding of epidermolysis. There is no epidermolysis or vacuolar changes in Unna-Thost PPK.
Mal de Meleda is characterized by a diffuse, thick hyperkeratosis with a prominent erythematous border. This disease is characterized by early infancy onset and follows a progressive course with extension to the dorsal surfaces of the hands and feet. This condition is inherited in an autosomal recessive fashion. The prevalence is 1 case per 100,000 population. The disease has its onset in early infancy and follows a progressive course. It was first described in inhabitants of the Adriatic Island of Meleda.
Mal de Meleda frequently presents with constrictive bands, perioral erythema, nail changes, and occasional brachydactyly, with a progressive clinical course throughout the patients’ lives. The main clinical characteristics are transgressive PPK, hyperhidrosis, and perioral erythema. Clinical dermatological features include diffuse, thick keratoderma with a prominent erythematous border. Lesions spread onto the dorsa of the hands and the feet (transgredient). Constricting bands are present around the digits and can result in spontaneous amputation. Well-circumscribed psoriasis-like plaques or lichenoid patches may be present on the knees and the elbows. Patients may have severe hyperhidrosis, possibly accompanied by malodor. Secondary bacterial and fungal infections are common. Other clinical features include: lingua plicata, syndactyly, hair on the palms and the soles, high-arched palate, and left-handedness.
Histologic findings include orthokeratosis and normogranulosis without epidermolysis. Mutations in the gene SLURP1 located on chromosome 8q24.3 were identified as the cause of Mal de Meleda. Molecular biology features include mutations in the gene encoding SLURP1 found on band 8q24.3.
Nagashima-type PPK is included in the diffuse autosomal recessive type of hereditary PPKs without associated features [3]. Nagashima-type PPK was first described in a report from Japan in 1977. Since then, more than 20 cases have been reported in Japan. Nagashima-type cases have been reported only in the Japanese literature; this type of PPK is not well known in Western countries, even though the existence of this disease is recognized. Therefore, the definition and characterization of this disease have not been well recognized globally.
Onset of disease occurs between birth and age 3 years (Figures 1, 2). Because its clinical manifestations are similar to but milder than those of mal de Meleda, it was originally described as a mild form of Mal de Meleda. Mal de Meleda is much more severe than Nagashima-type. It usually involves perioral erythema and occasionally exhibits brachydactyly, nail abnormalities, and lichenoid plaques. Unlike Mal de Meleda, spontaneous amputation has never been observed in Nagashima type PPK. Furthermore, there is no evidence of a SLURP1 mutation in patients with Nagashima-type PPK. The results of genetic study suggested that Nagashima-type PPK is distinct from Mal de Meleda.
Vohwinkel syndrome (mutilating and diffuse PPK) is associated with various extracutaneous features, including ichthyosis and deafness. Onset occurs in infancy. Clinically, this condition manifests in infants as a honeycomblike keratosis of the palms and the soles. It becomes transgredient during childhood. Later-forming, constricting, fibrous bands appear on the digits and can lead to progressive strangulation and autoamputation. Starfish-shaped keratosis may occur on the knuckles of the fingers and toes, which is a characteristic feature of this disorder. Alopecia, hearing loss, spastic paraplegia, myopathy, ichthyosiform dermatosis, and nail abnormalities are other associated manifestations. Other reported findings are deaf-mutism, congenital alopecia universalis, pseudopelade type alopecia, acanthosis nigricans, spastic paraplegia, myopathy, nail changes, mental retardation, bullous lesions on the soles, and seizures [4].
Nagashima-type PPK
Histological findings include hyperkeratosis, acanthosis, and a thickened granular cell layer with retained nuclei in the stratum corneum. Molecular biology studies have confirmed that the most common mutation is found in the gene encoding connexin 26. This subtype is associated with hearing loss. In contrast, a mutation in the gene for loricrin is associated with mutilating keratoderma and ichthyosis but not deafness. The mode of inheritance for mutation in the loricrin and connexin 26 genes is autosomal dominant. Treatment includes oral retinoids.
Bart-Pumphrey syndrome is an autosomal-dominant disorder characterized by knuckle pads, leukonychia, PPK and hearing loss. Onset occurs in infancy. PPK may be diffuse and striate, with accentuation of crease patterns and with a grainy surface [5]. Clinically, all neonates are hearing impaired from birth and develop diffuse PPK in childhood. Leukonychia and hyperkeratoses over the joints of the hand may also appear.
Knuckle pads are circumscribed, with hyperkeratotic or fibrous growths over the dorsal aspects of the small joints of the hands or feet. Leukonychia that may be seen in Bart-Pumphrey syndrome is defined as whiteness of nails that can occur either in patches or involving the total nail. Large keratohyaline granules are found in the keratinocytes, and the keratohyaline-containing cells reflected light, resulting in a white nail appearence. Molecular biology studies reveal a new mutation in the gene that encodes connexin 26, which explains the clinical overlap with Vohwinkel syndrome.
Nagashima-type PPK
The term “loricrin keratoderma” has been suggested to group patients with dominantly inherited PPK that has a different clinical presentation characterized by non-bullous congenital ichthyosiform erythroderma, progressive symmetric erythrokeratoderma, and the patients with Vohwinkel syndrome, carrying mutations in loricrin gene [6, 7]. In all loricrin keratoderma patients, the common signs are the palmoplantar honeycomb hyperkeratosis and ichthyosis. Collodion baby was sometimes reported independently from the clinical evolution of the patients. The originally described Vohwinkel syndrome, because of mutations in connexin 26 gene, shows: palmoplantar honeycomb hyperkeratosis; constricting fibrous bands encircling fingers or toes, characterized as pseudoainhum, leading to autoamputation of the fifth finger due to circulatory impairment; starfish-shaped hyperkeratotic lesions on the extensor surfaces; and high-tone deafness. By contrast, in loricrin keratoderma, the hearing impairment and starfish-shaped hyperkeratosis are absent and a generalized non-erythrodermic ichthyosis is described.
Clouston syndrome (hidrotic ectodermal dysplasia) is an autosomal dominant ectodermal dysplasia characterized by hypotrichosis, severe nail dystrophy, and PPK as well as hyperpigmentation of the skin over the large joints. Clinical features include diffuse papillomatous PPK (especially over pressure points of the palms and soles), dystrophic nails, and hypotrichosis. Thickened, hyperpigmented skin may also appear over the small and large joints, including the knuckles, elbows, and knees. Thickened, severely dystrophic nails develop, but they may be normal at birth. Universal sparsity of hair involves the scalp, eyebrows, eyelashes, and axillary and genital regions. Sensorineural deafness, polydactyly, syndactyly, clubbing of the fingers, mental retardation, dwarfism, photophobia, and strabismus are associated manifestations.
Clouston syndrome reveals orthohyperkeratosis with a normal granular layer based on histopathological analysis of PPK. Ultrastructural studies of the hair of these patients demonstrate disorganization of hair fibrils with loss of the cuticular cortex. Positional cloning identifies GJB6 on chromosome 13q12 as the causative gene for Clouston syndrome [8].1GJB6 encodes connexin 30 (Cx30), which belongs to a family of cell membrane proteins, the connexins, which form gap junctions between neighbouring cells.
Olmsted syndrome is an uncommon genetic disorder with symmetrical, diffuse, transgredient, mutilating PPK and periorificial hyperkeratosis [9]. Most cases of this condition are sporadic, with the exception of one report of an autosomal dominant pattern of inheritance. Onset occurs in the first year of life. Clinically, PPK begins focally in infancy and then becomes diffuse and severe. Later findings include flexion deformities and constriction of the digits, sometimes leading to spontaneous amputation. Progressive, well-defined perioral, perianal, and perineal hyperkeratotic plaques are present, as is onychodystrophy. Alopecia, deafness, nail dystrophy, and dental loss may be associated. Squamous cell carcinoma and malignant melanoma are also known to develop in the affected areas. Rare findings include large joint laxity, ichthyotic lesions, absent premolar teeth, hearing loss for high frequencies, and sclerosing cholangitis.
Histological findings include hyperkeratosis without parakeratosis and mild acanthosis. Abnormal expression of keratin 5 and 14 has been reported. Treatment includes oral and topical retinoids. Full-thickness excision and skin grafting has also been reported to result in clinical improvement.
Huriez syndrome is an autosomal dominant genodermatosis, characterized by the triad of congenital scleroatrophy of the distal extremities, PPK, and hypoplastic nail changes. The soles are not commonly involved. It was first described in two large pedigrees from northern France [10]. In addition to its occurrence in French patients, it has also been reported in Tunisia, Germany and Italy [11]. Onset occurs in infancy. Clinical features include red, atrophic skin on the dorsal hands and feet at birth. Diffuse, mild keratoderma is more marked on the palms than the soles. Other clinical features are sclerodactyly and nail abnormalities (hypoplasia, fissuring, ridging, koilonychia). The age at the onset of skin cancer is much lower than in the general population, and tumors arise in the areas of the affected skin. Affected individuals carry a more than 100-fold higher risk for the development of aggressive squamous cell carcinoma of the skin.
Histological findings include acanthosis, accentuation of the granular layer, and orthokeratosis. Langerhans cells are almost completely absent in the affected skin. Electron microscopy reveals normal dermoepidermal junctions and desmosomes; however, dense bundles of tonofilaments are seen in the epidermal layer. The granular layer shows large, coarse, clumped keratohyalin. Molecular biology findings include a mutation in the gene mapped to 4q23.
Papillon-Lefèvre syndrome is a rare disease characterized by skin lesions, which include PPK and hyperhidrosis with severe periodontal destruction involving both the primary and the permanent dentitions [12]. It is transmitted as an autosomal-recessive condition, and consanguinity of parents is evident in about one-third of the cases. This disease usually has its onset between the ages of 1 to 4 years. The male to female ratio is roughly equal. Its prevalence is estimated to be 1 to 4 per million in the general population with a carrier rate of 2 to 4 per 1000.
Clinically, diffuse transgredient PPK may be observed, typically developing within the first 3 years of life. Punctiform accentuation, particularly along the palmoplantar creases, may be seen. Unless treated, periodontosis results in severe gingivitis and loss of teeth by age 5 years. No significant correlation has been demonstrated between the level of periodontal infection and the severity of skin affections, which supports the concept that these major components of this syndrome are unrelated to each other. Patients exhibit increased susceptibility to cutaneous and systemic infections. Scaly, psoriasiform lesions are often observed over the knees, elbows, and interphalangeal joints. Finally, patients may have malodorous hyperhidrosis.
Histological findings include hyperkeratosis with irregular parakeratosis and moderate perivascular infiltration. Electron microscopic features include lipid-like vacuoles in corneocytes and granulocytes, a reduction in tonofilaments, and irregular keratohyalin granules. Molecular biology findings include mutations in the gene for cathepsin C, mapping to 11q14-q21, which are responsible for this syndrome. Cathepsin C is a lysosomal protease known to activate enzymes that are vital to the body\'s defenses. The susceptibility factor may involve defective immune function or pleiotropic effect of the single mutant Cathepsin C gene [13].
Treatment includes oral retinoids for the PPK. Elective extraction of involved teeth may prevent excess bone resorption. Appropriate antibiotic therapy may be required for periodontitis and recurrent cutaneous and systemic infections. Treatment with acitretin starting at an early age shows promise in allowing patients to have normal adult dentition. Early treatment and compliance with the prevention program are the major determinants for preserving permanent teeth in young patients. By extracting all primary teeth and eradicating periodontal pathogens, the patient\'s adult teeth can erupt into a safe environment. Treatment may be more beneficial if it is started during the eruption and maintained during the development of the permanent teeth. Recommended therapy includes aggressive local measures to control plaque including rigorous oral hygiene, chlorhexidine mouth rinses, frequent professional prophylaxis, and periodic appropriate antibiotic therapy needed for long-term maintenance.
Naxos disease is a rare autosomal recessive inherited association of right ventricular dysplasia/dilated cardiomyopathy with woolly hair and PPK [14]. The disease has an adverse prognosis, especially in young patients. In a long-term study of an unselected population of patients with Naxos disease it was shown that risk factors for sudden death include history of syncope, the appearance of symptoms, severely progressive disease of the right ventricle before the age of 35 years, and the involvement of the left ventricle [15]. Symptoms of right heart failure appear during the end stages of the disease. One-third of patients become symptomatic before the 30th year of life. In some cases, a few clinical findings of early heart disease can be detected during childhood.
Clinically, a diffuse, nontransgredient keratoderma with an erythematous border appears during the first year of life. Woolly (dense, rough, and bristly) scalp hair is present at birth. Cardiac disease, manifested by arrhythmias, heart failure, or sudden death, becomes evident during and after late puberty. Other cutaneous manifestations include acanthosis nigricans, xerosis, follicular hyperkeratosis over the zygoma, and hyperhidrosis. In addition to the woolly hair at birth, PPK develops during the first year of life and cardiomyopathy is clinically manifested by adolescence with 100% penetrance. Patients present with syncope, sustained ventricular tachycardia or sudden death.
Histological findings include hyperkeratosis, hypergranulosis, and acanthosis. Molecular biology findings include a mutation in the plakoglobin gene, mapping to 17q21, which is responsible for Naxos disease. Plakoglobin is an important component of cell-to-cell and cell-to-matrix adhesion complexes of many tissues, including the skin and cardiac junctions. It also plays a role in signaling in the formation of desmosomal junctions. Mutations in the plakoglobin gene may lead to detachment of the cardiac myocytes, resulting in myocyte death. Plakoglobin mutations may also lead to desmosomal junction fragility in hair shafts, explaining the clinical phenotype of woolly hair.
The primary goal of treatment is the prevention of sudden cardiac death. Implantation of an automatic cardioverter defibrillator is indicated in patients who develop symptoms and/or structural progression, particularly before the age of 35 years. Antiarrhythmic drugs are indicated for preventing recurrence of episodes of sustained ventricular tachycardia. In an attempt to control Naxos disease, systematic genetic screening of the populations at risk has been initiated and is starting to identify the heterozygous carriers of the plakoglobin gene mutation.
The focal type is subclassified into focal PPK, focal palmoplantar and gingival keratosis, focal keratoderma with oral leukokeratosis, pachyonychia congenita type 1 (Jadassohn–Lawandowsky type) and type 2 (Jackson–Lawler type), and focal PPK associated with esophageal carcinoma. Focal palmoplantar and gingival keratosis is characterized clinically by focal PPK with leukoplakic appearance on the labial surface of the attached gingival lesion, and histologically by focal epidermolytic PPK [16].
Striate PPK (Brunauer-Fohs-Siemens syndrome) presents with linear hyperkeratosis on the palms and fingers and focal plaques on the plantar aspects of the feet. Onset occurs in infancy or the first few years of life. Striate PPK, woolly hair, and left ventricular dilated cardiomyopathy has been described in both autosomal dominant and autosomal recessive forms, but only the recessive forms have a clear association with dilated cardiomyopathy.
Histopathological features include hyperkeratosis, hypergranulosis, and acanthosis with no epidermolysis. Electron microscopic examination shows diminished desmosomes, clumped keratin filaments, and enlarged keratohyalin granules. The syndrome has been linked to mutations in desmoglein 1, desmoplakin, and keratin 1. Treatment may include keratolytics, oral retinoids, and surgical debridement. Striate PPK is known to be caused by heterozygous mutations in either the desmoglein 1 (type I striate PPK), desmoplakin (type II striate PPK) or keratin 1 (type III striate PPK) gene [17-20].
Buschke-Fischer syndrome is an autosomal dominant disorder characterized by multiple punctate keratoses over the entire palmoplantar surfaces [21]. Punctate PPK presents as asymptomatic, tiny, hyperkeratotic punctate papules on the palmoplantar surface. Many tiny "raindrop" keratoses involve the palmoplantar surface; skin lesions may involve the whole palmoplantar surface, or may be more restricted in their distribution. The prevalence is 1.17 cases per 100,000 population. The age of onset ranges between 12 and 30 years.
This condition is usually manifested bilaterally as asymptomatic, tiny, hyperkeratotic punctate papules/plaque on the palmoplantar surface. The exact etiology of this disorder is not known, but a dual influence of genetic and environmental factors may trigger the disease. Nail abnormalities in the form of longitudinal ridging, onychorrhexis, onychoschizia, trachyonychia, and notching can be seen. Clinically, asymptomatic, tiny, hyperkeratotic papules are present on the palmoplantar surface. Lesions are uncommon in childhood and usually manifest after age 20 years. This condition is not associated with hyperhidrosis. Patients commonly report pruritus. Most individuals lack associated features; however, spastic paralysis, ankylosing spondylitis, and facial sebaceous hyperplasia have been reported. An association with gastrointestinal and pulmonary malignancy is possible.
Histological findings include substantial compact hyperkeratosis over a distinct area of epidermis, hypergranulosis, the presence of a cornoid lamella, and the absence of epidermal dyskeratosis or hydropic change, which help differentiate this condition from porokeratosis. Two punctate PPK loci have been found to map to 15q22-15q24 and to 8q24.13-8q24.21 [22, 23]. Treatment includes keratolytics, topical salicylic acid, mechanical debridement, excision, and topical and systemic retinoids.
Hereditary PPK constitutes a heterogeneous group of disorders characterized by thickening of the palms and the soles of individuals who are affected. The diagnosis and classification are difficult due to inter-individual and intra-individual variations and differences in nomenclature. Dermatologists must be alert during the evaluation of these findings to ensure proper diagnosis, and must perform complete dermatological examination including nails, hair, and mucosa. In addition, future studies should include either a whole genome mapping plan or focus directly on candidate genes, such as SLURP1 gene for differential diagnosis between Mal de Meleda and Nagashima-type PPK. More reports and concise clinical observations with genetic approach may reveal the pathomechanism underlying PPK.
Nanotechnologies aim to ease and to satisfy the needs of regenerative medicine1 by providing multifunctional, theranostic, and stimuli-responsive biomaterials [1, 2]. In particular, stimuli-responsive biomaterials such as magneto-responsive biomaterials are devices capable of reacting to an external magnetic field spatiotemporally in a specific way [3]. This powerful class of biomaterials is a promising candidate as active and therapeutic scaffolds for advanced drug delivery and tissue regeneration applications [3, 4].
\nMultifunctional magnetic-responsive materials can be manufactured by modifying or functionalizing traditional materials employed in tissue engineering or by incorporating magnetic nanoparticles (MNPs) in the biocompatible matrix [4, 5]. Table 1 reports examples of several magnetic biomaterials synthesized in the literature [6]. An approach to create a magnetic biomaterial is the impregnation of a polymer or ceramic (e.g., \n
Type of scaffold | \nSynthesis technique | \nM\n | \nType of MNPs | \nr\n | \n
---|---|---|---|---|
HA/collagen | \nImpregnation | \n0.35–15 | \nFe\n | \n200 | \n
HA/collagen | \nImpregnation | \n0.50 | \n\n\n | \n10–50 | \n
HA/PLA | \nElectrospinning | \n0.05 | \n\n\n | \n5 | \n
\n\n | \nImpregnation | \n0.6–1.2 | \nFe\n | \n250 | \n
Chitosan/PVA membrane | \nElectrospinning | \n0.7–3.2 | \nFe\n | \nn.s. | \n
Calcium silicate/chitosan | \nMixture | \n6–10 | \nSrFe\n | \n500 | \n
PMMA | \nMixture | \nn.s. | \nFe\n | \n10 | \n
Silicate | \nMixture | \nn.s. | \n\n\n | \nn.s. | \n
Fe-doped HA | \nChemical substitution | \n4 | \nHA-Fe\n | \n10–14 | \n
Fe-hardystonite | \nChemical doping | \n0.1–1.2 | \nFe\n | \n20–60 | \n
Bredigite | \nMilling | \n7–25 | \nCa\n | \n120 | \n
HA | \nImpregnation | \n12–20 | \nFe\n | \n200 | \n
HA | \nImpregnation | \n1–2.5 | \n\n\n | \n8 | \n
HA | \nImpregnation | \nn.s. | \n\n\n | \n5 | \n
Chitosan | \nIn situ precipitation | \n4 | \n\n\n | \nn.s | \n
\n\n | \n3D Bioplotting | \n0.2–0.3 | \nFe\n | \n25–30 | \n
PLGA | \nElectrospinning | \n2–10 | \nFe\n | \n8.47 | \n
Magnetic scaffolds divided by composition, production, and MNPs embedded. Redrafted from [5].
In alternative, a stable, repeatable, and controllable manufacturing technique of magnetic-responsive biomaterial is the chemical doping of or substitution with F\n
Given these methods, the magnetic biomaterial can be processed to develop a tissue-guiding structure or a tissue scaffold, i.e., a device intended to be implanted in an injured site for supporting and withstanding the cell adhesion, proliferation, and differentiation, in order to restore tissue continuity and functioning [10]. Magnetic scaffolds (MagS) have been proposed for the following three main applications, as presented in Figure 1 [1, 2, 3, 4, 5, 6, 7, 8, 9]:
To provide a controlled mechanical stimulation of tissues and boost the healing response
To develop a smart and reliable magnetic drug delivery system (MDD)
To generate therapeutic heat and perform local hyperthermia (HT) against cancer cells
Magnetic scaffolds are obtained by the combination of biomaterials and MNPs. They are multifunctional and theranostic nanocomposites. The potential biomedical applications of MagS are shown.
The mechanical stimulation of injured tissues using magneto-responsive scaffolds found application in bone tissue engineering, where static magnetic field (SMF) or low-frequency magnetic field is used to elicit osteoprogenitor cells [1, 2, 3, 4].
\nThe rationale of employing magnetic scaffolds as part of a MDD system is the need to have an “attraction platform” to target and control the attraction of magnetic liposomes or MNPs bio-conjugated with growth factors (GFs) [6, 11]. Indeed, recently several magnetic carriers of biomolecules capable of acting on cell function were developed. However, using an external SMF their delivery to deep tissue and to the site of damage is complicated, and the MNPs tend to distribute where the magnetic force is maximum, i.e., at the body surface, where the field is applied [12]. Having a MagS implanted in the injured tissue allows to attract the MNPs and the GFs while controlling their spatial distribution [13].
\nFinally, if the external magnetic stimulus is a radio-frequency (RF) magnetic field, the population of MNPs embedded in the biomaterial dissipates a huge amount of heat. The deposited power can be exploited as therapeutic heat, enabling to use the magnetic scaffold as a thermo-seed able to perform HT treatment against cancer cells [14].
\nTo date, magnetic scaffolds have been synthesized and characterized in terms of chemical and physical properties while proving experimentally their powerful and promising potential in regenerative medicine and oncology [1, 2, 3, 4]. However, to translate the use of these nanostructured biomaterials in the clinical practice, several limitations have to be overcome, and further investigations are required to predict their behavior [4]. The potential use of magnetic scaffolds as tissue substitutes needs the combined work of material scientists, biomedical engineers, and biologists. In particular, since in the literature there is a clear lack of mathematical and numerical models, which relate the physical properties of these nanocomposite biomaterials with the magnetic drug delivery or the hyperthermia, in this chapter, two mathematical models for their use as hyperthermia agent and as a tool for magnetic drug delivery are provided.
\nSection 2 briefly reviews the use of MagS as magneto-responsive biomaterials for the stimulation of tissues, in particular bone tissues. In Section 3 the nonlinear chemico-physical properties of magnetic scaffolds are presented, described, and used to introduce a recent in silico model for the planning of bone tumor hyperthermia [14]. Finally, in Section 4 the use of MagS as tool for active magnetic drug delivery is discussed. Furthermore, a mathematical model able of providing insights into the parameters of influence of the phenomenon is presented and analyzed [13]. The complete description of magnetic scaffolds favors the assessment of their effectiveness and their potential clinical impact.
\nMagnetic scaffolds have been tested both in vitro and in vivo, using animal models, demonstrating that they can transduce an external magnetic signal in mechanical stimulation to the cells attached to the biomaterial surface (Figure 1) [1, 2, 3, 4]. MagS have been investigated for bone, cartilage, cardiovascular and neuronal regeneration, and repair [2]. The most studied tissue is bone. The injury of skeletal tissue by traumas and diseases, such as osteoporosis, or by a tumor resection calls for the need of a bone substitute or scaffold to guide cell adhesion, proliferation, and differentiation [15]. Moreover, the bone tissue requires a continuous mechanical stimulation. Therefore, the magneto-responsive biomaterials in Table 1 can deliver a direct mechanical stimulation if exposed to SMF, to low-frequency magnetic field (strengths from to 18 \n
To understand the magnetization dynamic and the power losses of magnetic scaffolds, it is necessary to introduce the physical and mathematic descriptions of the response to a RF magnetic field of the MNPs embedded in it. If a population of magnetic nanoparticles in a solution is exposed to a harmonic RF magnetic field, they start to dissipate power due to the hysteresis loss but also to the magnetic dipole and to the Brownian relaxations [16]:
\nwhere \n
The term \n
where \n
where M\n
The term \n
The time required to the magnetic dipole moment to align with the direction of the external magnetic field is called the Néel relaxation time, \n
The pre-exponential factor \n
where K\n
In a FF, the nanoparticles are allowed to rotate and move according to Brownian motion in the viscous medium where they are dispersed. When subject to a time-varying magnetic field, the particles rotate to orient with the direction of the external energy source, thus contributing to the relaxation process. The Brownian relaxation time can be evaluated as [16]:
\nbeing \n
With Eqs. (1) to (9), it is possible to describe the frequency response and the power dissipation of a population of MNPs dispersed in a solution. This set of equations constitutes the theoretical basis for the understanding of magnetic scaffold behavior. However, since MagS are solid nanocomposites, the behavior of their magnetic phase is rather diverse than a FF. In the following, the experimental findings related to material characterizations and a new mathematical framework to account for their response are provided.
\nHyperthermia (HT) is a thermotherapy which aims at increasing the temperature of a target tissue between 41 and 46 C for about 60 min. For biological tissues, especially neoplasms and cancers, these temperatures are sufficient to damage the DNA of cells, altering its replication and also the repair pathways while determining cytotoxicity and activating the response of the host immune system [18, 19]. The rather chaotic vascular architecture of tumors is the reason of the thermo-sensibility of these pathologic tissues. The aforementioned biological effects can lead to the death of cancer cells, but, in the clinical practice, HT is exploited as a coadjuvant therapy combined with chemotherapy or/and radiotherapy rather than as a standalone therapy [19]. The hyperthermia can be induced using different types of energies, such as ultrasounds or electromagnetic (EM) field [14]. Currently different therapeutic modalities are available for HT induced by EM field. In particular, it is thoroughly investigated the local and in situ treatments using nanoparticles or magnetic scaffolds by exposing the target are with an external magnetic field.
\nSeveral magnetic scaffolds from Table 1 demonstrated to be capable of noticeable temperature increases when exposed to magnetic field working at the frequencies from 100 kHz to 1 MHz and with amplitude ranging from 8 to 25 kAm\n
These composite nanomaterials are identified as optimal candidates for local bone tumor hyperthermia [1, 2, 3, 4, 5, 6, 7, 8, 9, 13, 14]. However, their therapeutic potential must be investigated in a critique way. The understanding and the modeling of the heat dissipation of the MNPs embedded in the biomaterial are essential to allow an effective treatment planning.
\nThe physical explanation of the relevant and significant temperature increases measured for MagS is not trivial. Moving from the theory explained in Section 3.1, the resonant Debye model cannot be applied to a system in which highly concentrated MNPs are fixed and embedded in a solid matrix and lattice or constrained in a highly viscous medium [13]. Indeed, the long-range interactions between the magnetic nanoparticles become relevant [20]. The following index \n
where the cubic power of the particle diameter, \n
Therefore, in MagS the only relaxation time is the Néel one.
\nThe influence of long-range interactions between particles, the modified distribution of anisotropy energy, and the different Néel relaxation dynamic are the factors that contribute to enhance the power dissipation of magnetic scaffolds, and all of them can help to explain the hyperthermia behavior of MagS, such as for the magnetic hydroxyapatite and the Fe-doped PCL scaffolds [7]. Relying on the magnetic susceptibility spectra of MNPs in agarose gel measured by Hergt et al. [21], a Cole-Cole model for magnetic scaffolds [13]:
\nEquation (12) can fit the susceptibility data, with a 1.5% relative error, as shown in Figure 2, whereas the Debye model cannot (Eq. (2)). In Eq. (12) \n
Results of the fitting of the magnetic susceptibility spectra of MNPs embedded in agarose: a) real part (in-phase) and b) imaginary (out-of-phase) components are presented [21]. The Debye and Cole-Cole models are used and compared Taken from [13].
With Eqs. (1)–(8), but using Eq. (12) instead of Eq. (2), it is possible to evaluate and estimate the power losses of magnetic scaffolds. At this point it should be noted that the magnetic susceptibility \n
Temperature variation of the pre-exponential term \n\n\nτ\n0\n\n\n and the Neel relaxation time \n\n\nτ\nN\n\n\n. The influence on the equilibrium and the complex magnetic susceptibility \n\n\nχ\n0\n\n\n and \n\nχ\n\nf\n\n\n is represented. The curves are obtained for a magnetic scaffold filled with the 0.2% of magnetite nanoparticles (r\n\n\n\n\nmnp\n\n\n=10 nm, M\n\n\n\n\ns\n\n\n(0) = 2 emu\n\n⋅\n\ng\n\n\n\n\n\n−\n1\n\n\n\n, T\n\n\n\n\nb\n\n\n=150 K).
Given the potential of magnetic scaffolds to be used as local heat source for setting the hyperthermia treatment of cancers, the most studied biological and clinical target of the nanosystems under investigation are bone cancers. Indeed, in clinical practice, currently available techniques such as chemotherapy, radiotherapy, and osteotomies presented a 15% probability of tumor recurrence, and therefore the hyperthermia treatment was proposed as adjuvant therapy [24]. Furthermore, since the surgical intervention causes a bone damage which calls for a graft or bone substitutes, magnetic scaffolds as theranostic, multifunctional, and magnetic-responsive biomaterials can be employed and can express their clinical potential [14].
\nBone tumors are neoplasms mostly affecting subjects with age between 10 and 25 years old, causing impairment and pain, thus ruining the quality of life [23]. Malignant bone cancers such as osteosarcoma (OST) and fibrosarcomas (FIB) are known to affect long bone extremities [23]. OST and FIB are two different forms of bone cancer. The OST is big, aggressive and highly vascularized, whereas FIB is a poorly vascularized neoplasm. The survival rate for patients affected by OST and FIB may vary from 28–40% [14, 23, 24]. To overcome these clinical issues, oncologist investigated the use of immunotherapy or smart nanocarriers of drugs, but local hyperthermia stands out as a very promising therapy [14]. The rationale is to implant a MagS after the bone tumor resection or reduction and then perform a local and in situ hyperthermia treatment by applying an external RF magnetic field. The residual cancer cells would be killed or increase their sensibility to drugs or radiations. Finally, the scaffolds would serve as supporting architecture for healthy cells, favoring tissue repair [14].
\nWith the knowledge of the mechanism of power dissipation of MNPs embedded in a scaffold, recently a numerical scenario, with layered geometry, was proposed to investigate using finite element methods (FEM) the effectiveness of magnetic scaffolds in treating the residual bone cells of OST and FIB tumors [14].
\nAs shown in Figure 4, imagining a surgical intervention of a bone cancer in distal femur, a spherical magnetic scaffold, with radius r\n
Simplified layered geometry for modeling the hyperthermia treatment of bone tumors using magnetic scaffolds. The MagS with radius r\n\n\n\n\ns\n\n\n = 5 mm is surrounded by a surgical fracture gap (r\n\n\n\n\nf\n\n\n = 0.1 mm), the area where residual cancer cells are present (r\n\n\n\n\nt\n\n\n = 0.1 mm–0.5 mm), and the healthy bone tissue (r\n\n\n\n\nb\n\n\n = 5 mm). Taken from [14].
With respect to the geometry in Figure 4, the HT treatment using MagS is carried out applying an external RF magnetic field with strength H\n
where \n
The EM problem is solved employing the RF module of the commercial FEM software COMSOL Multiphysics (COMSOL Inc., Burlington, MA). The MagS studied are the intrinsic magnetic hydroxyapatite and the PCL loaded with magnetite [7], as in [14]. The dielectric properties of scaffold and tissues at T\n
Material or tissue | \nRe[\n | \n\n\n | \n
---|---|---|
Magnetic hydroxyapatite | \n12.5 | \n2.1\n | \n
\n\n | \n2.20 | \n10\n | \n
Fracture gap–inflamed | \n3580 | \n0.545 | \n
Fracture gap–ischemic | \n1321 | \n0.196 | \n
Bone tumors: OST and FIB | \n8000 | \n0.280 | \n
Bone | \n192 | \n0.0214 | \n
Electromagnetic properties of scaffolds and tissues [14].
The power deposited by the MagS and conducted to the tissues in the system of Figure 4 modifies the temperature (\n
where \n
Eq. (14) was implemented in COMSOL using the Bio-Heat transfer module. The initial temperature T\n
Material or tissue | \nk, Wm\n | \nC\n | \nQ \n | \n\n\n | \n
---|---|---|---|---|
Magnetic hydroxyapatite | \n1.33 | \n700 | \n— | \n— | \n
\n\n | \n0.488 | \n3359.2 | \n— | \n— | \n
Fracture gap–inflamed | \n0.558 | \n2450 | \n5262.5 | \n\n\n | \n
Fracture gap–ischemic | \n0.558 | \n2450 | \n5262.5 | \n\n\n | \n
Bone tumors: OST and FIB | \n0.32 | \n1313 | \n57,240 | \n2.42\n | \n
Bone | \n0.32 | \n1313 | \n286.2 | \n0.262\n | \n
Heat transfer properties of scaffolds and tissues [14].
The solution of Eq. (14) is a new temperature field. As previously discussed, the different system temperature determines a change in the magnetic and heat dissipation properties of the scaffolds. Also the dielectric and thermal properties of tissues vary with temperature [14]. To account for the influence of these variations on the outcome of HT treatment, the solution of Eq. (14) should be used to evaluate the EM power solving Eq. (13) for the next time step; then the next temperature distribution can be calculated considering the changed physical properties. This solution scheme is justified by the rather different dynamic of the EM and thermal fields [14].
\nIn the temperature range 37\n
The dielectric properties are assumed to increase linearly with c = 3% C\n
In this condition the strength, frequency, and envelope of the external RF magnetic field required to treat both osteosarcoma and fibrosarcoma cells were investigated.
\nThe temperature pattern resulting from the exposure to the homogeneous RF field is uniform and radial, as shown in Figure 5a. This is a consequence of the homogeneous distribution of the MNPs in the biomaterials [7, 14]. After 60 min of treatment, it can be noticed that the temperature in the healthy bone can reach 47\n
(a) 2D temperature distribution after 60 min of treatment using a RF magnetic field of 30 mT and working at 293 kHz. A OST with r\n\n\n\n\nt\n\n\n=0.5 mm is considered. (b) Average temperature in the region with residual FIB cells. (c) Average temperature in the region with residual OST cells. (MHA = magnetic hydroxyapatite).
Magnetic scaffolds were conceived as a multifunctional platform for tissue engineering applications (see Figure 1) [1, 2, 3, 4, 5]. As presented in the Introduction, they are a platform for magnetically targeted drug delivery of growth factors to control and enhance tissue healing, such as in the case of bone tissue [1, 11]. The bio-nanotechnology research developed magnetic carriers of biomolecules such as VEGF or TGF-\n
Considering the geometry of Figure 4, the analysis domain is limited to the scaffold and the fracture gap, neglecting the bone tumor and assuming that only healthy bone is present, in a way similar to [13]. The MagS and the gap have a radius of 5 mm. An external uniform and static magnetic flux density field of strength B\n
where all symbols have the previous definition. As presented in Table 1, the magnetization response of the scaffolds varies from a minimum of 0.4 emu\n
Due to the presence of the magnetic material, the magnetic field flux lines concentrate in the prosthetic implant, implying that the norm of the gradient of magnetic density field between the MagS and the diamagnetic tissues is relevant [6]. In the literature, it is reported that if the magnetic density field gradients are higher than 1.3 Tm\n
where M\n
where r\n
After having solved Eq. (17) and calculated Eqs. (18) and (19), the spatiotemporal distribution of the concentration of MNPs (C\n
D\n
The magnetic field distribution (Eq. (17)) is derived by solving numerically the magnetostatic problem for the geometry depicted in Figure 4 using the Magnetic Fields No Currents package from the AC/DC module of COMSOL Multiphysics. Then \n
Now, we assume that the MDD system is constituted by an active GF with concentration C\n
Given C\n
Similar to Eq. (20), Eq. (22) is subject to Dirichlet and Neumann boundary conditions, i.e., the diffusive flux of cell population should be null at the scaffold surface, and the cell concentration at host bone is set to a constant value of C\n
With this set of equations, it is possible to model the role of magnetic scaffolds as part of a MDD system studying the influence on the cellular migration and the scaffold colonization, providing valuable insight into the use of MagS as a tool in tissue engineering.
\nThe magnetic scaffolds exposed to the static magnetic flux density field B\n
(a) Normalized magnetic field distribution (\n\n\nH\n¯\n\n/\n\nH\n0\n\n\n). (b) Normalized MNP concentration profile after 48 h (\n\n\nC\nmnp\n\n/\n\nC\n\nm\n,\n0\n\n\n\n). (c) MSC density after 24 h (\n\n\nC\nc\n\n/\n\nC\n\nc\n,\n0\n\n\n\n).
This chapter presented an innovative family of nanocomposite magnetic biomaterials and their biomedical applications. Mixing magnetic nanoparticles with traditional biomaterials, e.g., polymer or ceramics, or chemically doping them allows the manufacturing of a magnetic-responsive biomaterial with multifunctional properties. The so-called magnetic scaffolds have been studied for their ability to transduce an external magnetic signal into mechanical and biological outcome, thus proving to be a powerful platform for cell and tissue stimulation [1, 2, 3, 4]. Exploiting the ability of the MNPs embedded in the biomaterial to dissipate power when exposed to a radio-frequency magnetic field makes MagS a valid candidate to perform local hyperthermia treatment on residual cancer cells. In this chapter the physical properties and the magnetic susceptibility of these novel composite nanosystems are investigated. Then an in silico model to study the feasibility of employing MagS in the treatment of bone cancers, such as osteosarcomas and fibrosarcomas, is presented [14]. The results indicate that further research on the nanomaterial is required to develop an effective and tailored magnetic scaffold. Finally, the potential of MagS to serve as an in vivo attraction site to enhance the magnetic drug delivery of growth factors is faced. To predict the final concentration pattern, a mathematical model which relates the nonlinear magnetic problem and the mass transport issue is presented. Furthermore, the link between these two aspects and the biological influence on cellular migration is challenged [13]. The results indicate that MagS are able to attract MNPs and exert an indirect action on MSCs in a way dependent on the geometrical and material properties.
\nThe authors would like to sincerely thank Prof. G. Mazzarella for the helpful discussions and suggestions to this work.
\nThe authors declare no conflict of interest.
\nbone morphogenetic protein-2
\ndynamic light scattering
\nextracellular matrix
\nfibrosarcoma
\nfinite element method
\nferrofluid
\ngrowth factor
\nmagnetic scaffold
\nmagnetic drug delivery
\nmagnetic field
\nmagnetic hydroxyapatite
\nmesenchymal stem cell
\nmagnetic nanoparticle
\nosteosarcoma
\npoly-caprolactone
\nradio frequency
\nstatic magnetic field
\ntricalcium phosphate
\ntransmission electron microscope
\nvascular endothelial growth factor
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