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1. Introduction
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Initially reported by Dailey et al. in 1955, the correlation of papillary thyroid carcinoma (PTC)—the most common thyroid cancer (TC) histotype—with Hashimoto’s thyroiditis (HT) [1] has long been pursued, rekindling the ancient link between inflammation and cancer [2]. Bearing in mind the rising incidence of PTC over the last decades [3], establishing causality between PTC and HT—an issue highly contested—could lay the groundwork for a preventive policy. Moreover, harnessing the interrelationship of PTC with HT could refine therapeutics with respect to PTC. The present chapter dissects the correlation of PTC with HT, delving into a strongly insinuated immunological link. A comprehensive review of current literature emphasizes on the bewildering clinical significance of the interrelationship of PTC with HT. The intriguing predictive and prognostic value of serum concentrations of thyroid autoantibodies and thyroid-stimulating hormone (TSH) in the context of PTC coexistent with HT paints a more nuanced and sophisticated picture.
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2. Tailoring the treatment of PTC: where does coexistent HT stand?
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Thyroid cancer (TC) is the most common endocrine malignancy [4], though comprising only 2.1% of global cancer burden [5]. It is estimated that 52,070 new TC cases will occur in 2019 in the United States, while 2170 patients will die of this cancer type [6]. Derived from follicular epithelial cells, PTC constitutes the most common TC subtype in iodine sufficient areas, accounting for 85% of differentiated TC (DTC) [7] and 70–80% of TC [8]. In light of the interface between “TC epidemic” and “epidemic of diagnosis,” a true increase of the incidence of PTC due to environmental, hormonal, and lifestyle risk factors appears to be merged with overdiagnosis of subclinical disease owing to meticulous screening [3, 9, 10, 11].
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The indolent nature of PTC imposes a paradigm shift from ameliorating 10-year survival rates exceeding 90% to eliminating the recurrence incidence that hovers at 15–30% [12]. Individualization of therapeutic approach is deemed to confront the emerging challenges [13]. Seminal studies [4, 14, 15] recently illuminated the “dark matter” of the previously unidentified driver genetic events in 96% of PTC [4], being translated into molecular-based risk-adapted therapeutic strategies [7]. Although surgery is the cornerstone of treatment of PTC, a tailored approach with respect to the extent of thyroidectomy and lymph node dissection, the radioiodine ablation, and the management of radioiodine-refractory recurrent/metastatic disease has been endorsed [7].
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Provided that the clinical relevance of the increasingly reported interrelationship of PTC with HT is clarified, the incorporation thereof in current PTC risk stratification systems may empower a personalized treatment. This perspective is anticipated to build on accomplishing a fine-tuned balance in terms of decision-making concerning PTC, precluding both overestimating an innocent disease and ignoring a metastatic potential.
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3. HT at a glance
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HT, originally designated as “struma lymphomatosa” by Dr. Hakaru Hashimoto in 1912 [16], is the most common autoimmune thyroid disease and the most common cause of hypothyroidism in iodine sufficient areas, showing a worldwide annual incidence varying from 0.3 to 1.5 cases per 1000 individuals [17]. An insightful approach concerning the multifactorial etiology of HT has been proposed by Weetman et al.: aligned in a way reminiscent of the wholes of the Swiss cheese are genetic factors acting as susceptibility loci—major histocompatibility human leukocyte antigen (HLA) genes, immunoregulatory genes, thyroid specific genes-environmental factors—excess iodine intake, viral infections, stress, endocrine disruptors—as well as non-modifiable intrinsic factors—female sex, parity, age. Traversed by a hypothetical arrow, this conceivable line translates in a catastrophic event [18].
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The histopathologically confirmed HT is characterized by diffuse lymphocytic infiltrate, formation of lymphoid follicles with germinal centers within normal thyroid tissue [19], and, potentially, atrophy of parenchymal tissue gradually replaced by fibrous tissue [20]. The identification of the autoantibodies hallmark of HT in 1936 [21] paved the way for Rose and Witebsky to designate HT as the archetype of autoimmune destructive disorders [22]. Whereas the pathogenesis of HT is unclear, crucial is considered the imbalance between T-helper (Th)2 cells—Th CD (cluster of differentiation)4+ cells credited with stimulation of B cells, which in turn produce thyroid autoantibodies- and Th1 cells-cytotoxic Th CD4+ cells directly attacking the thyroid follicular cells. This concept has been refined by the imbalance between Th17 cells and Th cells producing mainly IL-17, involved also in carcinomas- and T regulatory (Treg) cells-Th CD4+ cells deemed to halt the immune response [23]. Especially, an increased TH17/Treg ratio ascribed to both enhancement of TH17 expression and decrease of Treg is involved in the pathogenesis of HT [24]. Incriminated for the depletion of thyrocytes in HT is principally the autocrine/paracrine Fas-/Fas ligand (FasL)-induced extrinsic apoptotic pathway [24, 25].
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4. Rationality in the investigation of the interrelationship of PTC with HT
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Apart from the well-established connection of HT with thyroid lymphoma [26], which is beyond the scope of the present chapter, the association of TC with HT concerns almost exclusively the PTC [27], alluding to a discriminating, though unknown, pathogenetic link.
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Since PTC is conceived as the main culprit for the explosive rise of TC incidence [3], the hypothesis that the increasing incidence of HT hastens the “TC epidemic” is appealing. Considering that the inflammation has been envisaged as the “seventh hallmark of cancer” [28], the autoimmunity-induced inflammatory milieu [29] merits further interrogation as the missing piece in the puzzle of the interrelationship of PTC with HT.
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An alternative explanation that cannot be ruled out is that third extraneous variables actually cause the coexistence of PTC with HT. Indeed, both PTC and HT are precipitated by an interplay among genetic factors and environmental influences most of which are shared by the two entities. Emphasis is placed on risk factors implicated in the pathogenesis of both PTC and HT, such as female predominance, excess iodine intake, and exposure to radiation [30, 31, 32, 33, 34], implying a spurious correlation.
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Nonetheless, a common origin of PTC and HT from cancer stem cells expressing p63 proteins—homologs of p53 proteins postulated to regulate squamous stem cell commitment—has been suggested. In fact, the cancer stem cells constitute pluripotent cells deemed to remain undifferentiated or undergo benign squamoid and glandural maturation or be differentiated to follicular epithelial cells, harboring the potential to elicit both PTC and HT [35, 36].
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The interrelationship of PTC with HT spurs a realm of intense research, principally in four respects. Firstly, the pathogenetic link between HT and PTC remains elusive; however, accumulative evidence suggests that these two entities are immunologically linked [29]. Secondly, some authors argue that this interrelationship is merely epiphenomenon of selection bias inherent in studies encompassing surgical series [37, 38]. Thirdly, equivocal—favorable versus unfavorable—is the impact of HT on the prognosis of concurrent PTC [39, 40, 41, 42, 43, 44, 45, 46, 47, 48]. Finally, the translation of the serum concentrations of thyroid autoantibodies [49, 50, 51, 52, 53, 54, 55, 56] and thyroid-stimulating hormone (TSH) [55, 57, 58, 59, 60, 61, 62, 63] into predictive and prognostic PTC biomarkers incites a perpetual conflict.
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5. Exploring the immunological link between PTC and HT
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Compelling evidence insinuate that the PTC and the HT represent two extremes in the continuum of immune response. In cancer, dominant is an anti-inflammatory response dictated by cancer cells per se, counteracting the antitumor immune surveillance. Quite the contrary, an overactivated inflammatory response owing to breakage of self-tolerance attacks host tissue cells, resulting in tissue damage in the context of autoimmune diseases. Despite the fundamental differences between the tumor microenvironment and the autoimmune milieu, certain parallel aspects of these two landscapes have been recognized [64]. For instance, the macrophages (M) and the neutrophils (N)—cells of myeloid origin—are encountered in both cancer and autoimmunity that act as well-coordinated partners to orchestrate the innate immune attack. Showing plasticity, these cells transition from proinflammatory M1/N1 polarization, devoted to kill pathogens or cancer cells, to anti-inflammatory M2/N2 polarization, dedicated to repair tissue damage and promote angiogenesis. A shift toward M2 macrophage polarization is a core component of tumor microenvironment, observed in autoimmune milieu as well, providing a hint to the interface thereof. Furthermore, supportive of the tumor-promoting M2 macrophage polarization is the local hypoxic milieu inherent in both autoimmune and cancerous diseases [64].
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The elucidation of the continuum of immune response could provide insights into the pathogenetic background of the coexistence of PTC with HT. Given that the macrophage phenotype M2 is considered tumor-promoting contrary to the antitumor effect of M1 phenotype, an appealing hypothesis connecting PTC with HT is derived from the intrathyroidal immune profiling of euthyroid HT conducted very recently by Imam et al. [65]. The immune infiltrate in euthyroid HT proved to contain low count of natural killer (NK) cells, facilitating the differentiation of the macrophage phenotype M0 to the M2 phenotype, which in concert with the observed low count of M1 macrophages may interpret the higher risk of PTC inherent in euthyroid HT [65].
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Interestingly, overexpression of Toll-like receptors (TLR)—cell surface receptors credited with recognition of pathogen-related molecules, crucial for activation of innate and adaptive immunity—is detected immunohistochemically in human thyrocytes surrounded by immune cells in all patients with HT. The high basal TLR3 mRNA levels observed in PTC, reinforcing the shared immunological landscape, are consistent [66, 67].
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Dissecting the interface of HT with PTC is expected to unveil novel targets for immunomodulation. For instance, triggering the innate immunity via the TLR5 agonist flagellin, being already in clinical trials as inducer of NK activation [68], could be interrogated as a modality to reverse the M2 macrophage phenotype in PTC coexistent with HT.
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In pursuit of the immunological link connecting PTC with HT, three hypotheses, rather interrelated, shape a conceptual framework outlined below.
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5.1. Thyroid malignancy develops despite immune response in the context of HT
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Manifold mechanisms have been proposed to underlie the escape of PTC cells from immune response in the context of autoimmunity: (i) the ability of PTC cells to manipulate the expression of immune-regulatory cytokines, editing the immune response; (ii) the enhancement of Treg known to suppress the NK cell effector functions, mainly the cytotoxicity; and (iii) the promotion of expression of specific surface molecules facilitating tumor development and growth, such as the membrane-bound transforming growth factor b (TGFb), histocompatibility antigen, class 1, G (HLA-G), FasL, and B7 homolog 1(B7H1) [28].
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Moreover, the interrelationship of PTC with HT may empower the escape of cancer cells from immune surveillance, consolidating the dogma that “cancer is a wound that never heals since tumor cells hijack the wound healing machinery for their own gain” [69]. In fact, a recently discovered “unexpected player”, the T cell double negative (DN) CD4(−) CD8(−), expressed both in PTC and in thyroid autoimmunity, downregulates the proliferation of activated T effector cells and the cytokine production, fostering an immunosuppressive microenvironment [70]. Favoring immune tolerance, the FOXP3+ Treg cells—crucial players of thyroid autoimmunity [71]—are encountered also in PTC [70]. The dendritic cells (DCs), beyond governing the autoimmune milieu, are also expressed in PTC, being responsible for the expansion of FOXP3+ Treg cells, allowing the tumor immune evasion and, thus, enabling the PTC progression [72].
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5.2. Thyroid malignancy develops owing to thyroid autoimmunity
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The first detection of lymphocytes in neoplastic tissues by Virchow in 1863 [73] paved the way for the endorsement of chronic inflammation as a precipitating factor for certain cancer types. In that respect, thyroid gland could be conceived as an intersection of HT-induced chronic inflammation and cancer; however, a causal relationship is yet to be defined. In light of the cancer-related inflammation (CRI), the concurrence of PTC with HT might reflect either the malignant transformation ascribed to an autoimmunity-induced chronic inflammatory milieu (extrinsic pathway) or the inflammatory response to tumor (intrinsic pathway) [74].
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The perpetually overactive immune response in the context of HT initiates an inflammatory vicious cycle with the potential to gear the journey of normal cells toward malignancy, rendering the interrelationship of PTC with HT the epitome of the extrinsic pathway of CRI [74].
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Central in the extrinsic pathway is the “smoldering inflammation,” an ungoverned inflammatory milieu orchestrated by immune/inflammatory cells, involving macrophages, immature DCs, and mast cells, expressing a myriad of cytokines, chemokines, and growth factors, such as interleukin (IL)-1b, tumor necrosis factor a (TNFa), IL-6, (C-C motif) ligand 2 (CCL2)/monocyte chemoattractant protein 1 (MCP-1), CXC chemokine ligand (CXCL8)/IL-8, vascular endothelial growth factor (VEGF), as well as reactive oxygen species (ROS) and reactive nitrogen species (RNS), spurring tissue damage, neo-angiogenesis, and tissue remodeling [75, 76]. Implicated in this milieu is the hypoxic microenvironment, inherent in both PTC and HT, favoring the progression of tumor, reinforcing, among others, the neo-angiogenesis and the shift of metabolism toward anaerobic glycolysis [64].
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Overexpression of cyclooxygenase-2 (COX-2)—an enzyme involved in initiation [77] and progression of thyroid tumors [78]—and inducible nitric oxide synthases (iNOS), key elements of CRI, has been observed in epithelial cells of lymphocytic thyroiditis, follicular adenoma, and PTC contrary to the absence or the limited expression thereof in normal thyroid epithelium, potentially linking carcinogenesis to autoimmunity [79].
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Intertwined with the extrinsic pathway is the intrinsic pathway: genetic alterations caused by DNA damage induced by the “smoldering inflammation” [80] trigger a proinflammatory transcriptional program [74]. For instance, the oncogene RAS is involved in the induction of chemokine CXCL8 [75], an inflammatory mediator of both cancer [75] and autoimmunity [64]. Moreover, phosphatase and tensin homolog (PTEN) mutation, a key element of the oncogenic phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway, leads to upregulation of hypoxia-inducible factor-1 (HIF1), which, in turn, upregulates the CXC chemokine receptor 4 (CXCR4) [75], well-recognized player of autoimmunity [81]. Accordingly, the observed activation of the PI3K/AKT pathway in HT, PTC, and HT coexistent with PTC contrary to the absence of activation thereof in normal follicles is rational [82].
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Illustrating the common molecular background shared by PTC and HT, the rearranged during transfection (RET)/PTC rearrangements—landmarks of PTC—are detected in 95% of HT [83]. Moreover, the RET/PTC1 rearrangement has been detected more frequently in PTC coexistent with autoimmunity than PTC alone (31% versus 13%, respectively) [84]. The inflammatory milieu fosters the genesis of RET/PTC rearrangements either via secreting ROS and RNS [85]—the main culprit for mutagenic-mediated DNA damage [2]—or sustaining the survival of thyroid cells that harbor RET/PTC rearrangements.
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The oncogenic RET/PTC-RAS-BRAF-mitogen-activated protein kinase (MAPK) cascade [74] may connect the oxyphil cell metaplasia of HT with PTC, considering the enhancement of the expression of RET, nuclear RAS, and extracellular signal-regulated kinases (ERKs)—core components of MAPK cascade—not only in PTC but also in oxyphil cells in the context of HT [86].
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Further, experimental data unravel that the RET/PTC1 exogenously expressed on normal human thyroid cells induces an inflammatory milieu involving crucial chemokines and their receptors, promoting functions vital for tumor progression, such as proliferation and survival of cancer cells [e.g., CXCR4/CXCL1] as well as neo-angiogenesis (e.g., CXL1, 2, 3, 5, 6, and 8) [87].
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Additionally, a constellation of RET/PTC1-induced molecules fosters the genesis and evolution of cancer, including (i) matrix metalloproteinases (MMPs) and dipeptidyl peptidase IV (DPP IV), molecules crucial for tissue remodeling, tumor invasiveness, and neo-angiogenesis [87]; (ii) urokinase-type plasminogen activator (UPA) and urokinase-type plasminogen activator receptor (UPAR), involved in cancer progression and metastasis [87]; (iii) l-selectin [87], an adhesion molecule facilitating metastasis [88]; and (iv) osteopontin (OPN) and CD44, implicated in proliferation and invasion of transformed PCCl 3 cells, rat thyroid follicular cells [89].
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An intriguing RET/PTC3-induced mechanism pivotal for tumor progression is the recruitment of CD11b+Gr1+ myeloid-derived suppressor cells, providing cancer cells with the advantage of evading immune surveillance [90, 91].
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However, skepticism raise the technical limitations of the applied PCR techniques and the lack of reproducibility of the results of studies detecting the RET/PTC rearrangements in HT [92]. Furthermore, the equivocal nature of RET/PTC-induced transcriptional program—tumor-promoting versus antitumor—should be considered [87].
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5.3. The immune attack against PTC triggers thyroid autoimmunity
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The association of PTC with HT seems more intricate than initially conceived in view of a seminal cyclic model governed by the overactive immune response, acting as a driving force for carcinogenesis, while being also a marker of tumor immunity [93]. An assumption that merits further exploration is whether the cross reaction of antitumor immunity with normal thyrocytes may precipitate HT in PTC patients genetically predisposed to thyroid autoimmunity, consolidating the hypothesis of “tumor defense-induced autoimmunity” [29]. With the advent of the era of cancer immunotherapy, new light on the coexistence of HT with PTC is shed by the increasingly reported development of HT as an adverse event of the monoclonal antibodies blocking programmed cell death (PD) protein 1 (PD-1) and PD ligand 1 (PD-L1). This revolutionary anticancer treatment unleashes the antitumor immunity at the expense of abrogating the self-tolerance, exemplifying the “tumor defense-induced” immunity [94]. For instance, a loss of circulatory PD1+ CD4+ and CD8+ T cells, an increase in peripheral CD56+CD16+ NK cells and an increase in activated monocytes have been implicated in pembrolizumab (anti-PD1 monoclonal antibody)-induced thyroiditis [94].
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6. Does the coexistence of HT with PTC really exist?
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An issue of major concern is whether the coexistence of PTC with HT is real or a myth nurtured by methodological pitfalls implicit in studies addressing this issue.
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The great variety of the incidence of the coexistence of PTC with HT ranging from 0.5 to 38% [95] or, alternatively, from 5 to 85% is noticeable [96]. The results of the meta-analyses addressing the coexistence of PTC with HT are highly divergent [40, 48, 96, 97], as depicted in Table 1. The broad array of the mean rate of PTC among patients with HT extending from 1.1 to 40.1% blurs the landscape [97]. Nevertheless, according to a systematic review, the correlation of PTC with HT is statistically significant with a relative risk (RR) of HT among PTC equal to 2.36 and a RR of PTC among HT equal to 1.40 [98].
Frequency of HT in PTC: ≈23% 2.8 times higher occurrence rate of HT in PTC than in benign thyroid diseases (p < 0.001) 2.4 times higher incidence of HT in PTC than in other TC (p < 0.001) Significant association of PTC concurrent with HT with female sex (OR: 2.7; p < 0.001), multifocality (OR: 1.5, p = 0.010), absence of ETE (OR: 1.3, p = 0.002) and LNM (OR: 1.3, p = 0.041), long recurrence-free survival (HR: 0.6, p = 0.001)
2.77 times elevated rate of PTC in patients with HT compared with control population (OR: 2.77, 95% CI, 1.24–6.21) 1.89 times higher rate of HT in patients with PTC compared with other TC types (OR: 1.89, 95% CI, 1.02–3.50) Increased PTC-free survival in patients with coexistent HT (r: 0.08, 95% CI, 0.05–0.12) Increased overall survival in PTC patients with coexistent HT (r: 0.11; 95% CI, 0.07–0.14)
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Table 1.
Meta-analyses addressing the correlation of PTC with HT.
In an attempt to annotate the diverse epidemiological profile of the coexistence of PTC with HT, attention should be paid to the discrepancy among pertinent studies concerning the design, the enrolled populations, and the histopathologic definitions of HT [99]. Moreover, certain caveats hamper hitherto the interpretation of the lymphocytic infiltration and the positivity of thyroid autoantibodies. Firstly, thyroid lymphocytic infiltration confirmed on histology has been significantly associated with PTC even in the absence of thyroid autoantibodies [100]. Secondly, the pattern of Tg recognition by anti-thyroglobulin autoantibodies (TgAbs) differs between autoimmune and non-autoimmune thyroid disorders, being more restricted in autoimmune disorders as compared with nodular goiter and PTC harboring no thyroid lymphocytic infiltration [101]. However, in PTC correlated with histopathologically confirmed HT, the pattern of Tg recognition does not differ from that observed in HT [101]. Thirdly, it should be mentioned that the thyroid autoantibodies may be detected in healthy individuals [102]. Finally, the discordance among available TgAbs assays should be considered [103].
\n
Another hurdle in evaluating the coexistence of PTC with HT is the selection bias inherent in data derived from surgical specimens wherein the prevalence of PTC is a priori higher than that in fine needle aspiration biopsy (FNAB) studies. Jankovic et al. showed that the average prevalence rate of PTC in HT patients differed significantly between FNAB and thyroidectomy studies: 1.20 and 27.56%, respectively. Likewise, the relative risk of PTC in HT patients extended from 0.39 to 1.00 in the FNAB studies, significantly lower than that observed in the thyroidectomy studies (1.15–4.16) [37]. In that respect, Castagna et al. demonstrated absence of association of nodular HT with TC based on cytology. The same authors observed a significantly higher prevalence of DTC in nodular HT compared to nodular Graves’ disease, nodular goiter with either negative or positive thyroid autoantibodies, according to surgical series. This result raised the possibility of selection bias ascribed to the fact that 60.7% of patients with nodular HT underwent surgery due to cytological data suspicious of thyroid malignancy [38]. The FNAB data from 10,508 patients revealing no statistically significant relationship between PTC and HT are consistent [104].
\n
Nevertheless, the fear of the selection bias was abolished by the recent demonstration of a significant association of PTC with HT based on either pathological examination of surgical specimens or FNAB studies [60].
\n
\n
\n
7. Effect of HT on coexistent PTC: host protective or tumor protective?
\n
Irrespectively of whether HT is etiologically linked to PTC or merely judged “guilty by association,” the importance of this coexistence lies on its clinical significance. Since a complex immune network has been considered a core component of PTC microenvironment, it is rational to assume that HT—the epitome of aberrant immune reaction—influences the progression of coexistent PTC [105]. In that respect, the positive association of a favorable outcome of coexistent PTC with HT, tumor-associated macrophage infiltration, and CD8+ lymphocytes highlights the antitumor potential of the immunological landscape intrinsic in HT [106]. The recently reported negative correlation of RORγt—a nuclear transcription protein of Th17—with lymph node metastases in PTC concurrent with HT is consistent. In fact, RORγt is positively associated with the upregulation of caveolin 1, a tumor suppressor gene [107]. Another plausible mechanism underlying the host-protective effect of HT coexistent with PTC could be the lower frequency of BRAF V600E mutation—a genetic alteration associated with aggressive PTC phenotype—in PTC concurrent with HT compared with PTC alone [41, 42].
\n
A rich repertoire of features indicative of auspicious PTC prognosis are significantly associated with coexistent HT, including increased relapse-free and overall survival [39], increased survival rate [96, 108], decreased risk of recurrence [108], lower rate [108] or absence of extrathyroidal extension [96], and lower rate [41] or absence of lymph node metastases [96], observed in PTC coexistent with HT compared with PTC alone. The results of a recent meta-analysis including 71 published studies with 44,034 participants revealing that PTC coexistent with HT significantly correlated with reduced incidence of extrathyroidal extension, lymph node, and distant metastasis and increased recurrence-free survival duration compared with PTC alone are seminal [47]. Noticeably, the coexistence of HT with PTC has been proven an independent indicator of favorable prognosis of PTC [105], irrespectively of the extent of lymph node dissection [46], though inconsistently [108]. On the other hand, the reported absence of host-protective effect of HT on coexistent PTC [42, 43, 44, 45] hampers the endorsement of HT as a prognostic PTC biomarker.
\n
In fact, the inflammatory cell infiltration of tumor microenvironment plays an equivocal role, tumor-promoting versus antitumor, posing a “Dr. Jekyll or Mr. Hyde” enigma [109]. Challenging is the illumination of the precise factors that define the fate of cancer cells in the context of the interface of PTC with HT.
\n
\n
\n
8. Thyroid autoantibodies in the context of HT coexistent with PTC: predictive and/or prognostic PTC biomarkers or not?
\n
Whether HT constitutes the driving force for PTC or vice versa remains elusive; nevertheless, the thyroid autoantibodies, the landmark of HT, and especially the anti-thyroperoxidase autoantibodies (TPOAbs)—a more sensitive marker of HT than the TgAbs—merit interrogation as potential hallmarks of the interrelationship of PTC with HT.
\n
A great body of evidence sustains that the positivity of thyroid autoantibodies translates into predictive and prognostic knowledge. In particular, the positivity of TPOAbs [49, 52, 53], TgAbs [51, 53, 110], as well as TPOAbs coexistent with TgAbs [52], has been shown to harbor a predictive value. Moreover, the positivity of TPOAbs [52, 57] and TgAbs [50, 51, 52, 53, 110] has been designated as an independent predictive factor for thyroid malignancy in nodular goiter. Interestingly, the coexistence of TgAbs and TPOAbs is associated with a PTC risk greater than that connected with isolated positivity of either TgAbs or TPOAbs [52]. A host-protective role of TPOAbs in the context of coexistent PTC has been demonstrated [27, 54, 55], rationalized by the speculation that the TPOAbs exert a cytotoxic effect [110].
\n
However, skepticism imposes a multivariate analysis failing to consolidate the host-protective effect of thyroid autoantibodies in the case of coexistent PTC [55]. Importantly, awareness raises the correlation of the positivity of thyroid autoantibodies with features indicative of ominous PTC prognosis, such as advanced disease stage [52]. As a potential link between positive thyroid autoantibodies and aggressive phenotype of PTC could be suggested the excess iodine intake that unmasks a cryptic epitope on Tg, triggering the development of TgAbs [33, 34], while exerting stimulative effect on the genesis of BRAF V600E mutation as well [111]. However, this hypothesis is debunked by the observation that the BRAF V600E mutation in DTC is inversely correlated with coexistent HT [42]. In the light of the foregoing, the designation of thyroid autoantibodies as predictive and/or prognostic biomarkers of PTC is not yet feasible.
\n
\n
\n
9. Elevated TSH levels in HT coexistent with PTC: the mediator of the effect of HT on PTC?
\n
Considering that TSH constitutes a growth factor for thyrocytes [58], rational is the designation of increased, even within the normal range, serum TSH levels, in the case of PTC concurrent with HT, as a predictor of PTC risk [49, 52, 58] and a harbinger of aggressive tumor behavior [55, 59].
\n
A strong argument in favor of the role of TSH in thyroid tumorigenesis is the detection of activating mutations of TSH receptors (TSH-R) in DTC [112]. Moreover, the cross-talk between the TSH-R/protein kinase A (PKA) signaling transduction and the well-recognized oncogenic pathways involving Wingless/int-1 (Wnt), PI3K, and MAPK has been implicated in initiation and progression of TC [113]. However, many arguments against the pathogenetic role of TSH in TC have been raised [114, 115, 116, 117].
\n
Nevertheless, the demonstration of HT as a risk factor for PTC in univariate analysis while being a host-protective factor in multivariate analysis after controlling TSH levels should be mentioned [61]. Similarly, multivariate analysis showed that increased TSH levels were an independent risk factor of malignancy in most FNAB studies, albeit not consistently related to HT [60]. Consequently, the subclinical or overt hypothyroidism due to autoimmune destruction of thyroid—and not HT per se—could be the real culprit for the increased PTC risk in the context of HT.
\n
Experimental data derived from mouse models suggest the TSH-induced signaling mediated via cyclic adenosine monophosphate (cAMP) as a prerequisite for the BRAF V600E-stimulated PTC genesis, providing a plausible explanation for the implication of elevated TSH levels in PTC [62]. Furthermore, a protein kinase C (PKC)-mediated pathway has been demonstrated in vitro to transduce the TSH-induced signaling, dictating the invasiveness and the growth of human follicular TC cell lines [118].
\n
However, the reported association of subclinical hypothyroidism with a less aggressive PTC phenotype compared with euthyroidism cannot be ignored [119]. Consistent is the higher risk of DTC enclosed in HT requiring low levothyroxine (LT4) replacement doses as compared with HT-induced hypothyroidism requiring higher LT4 replacement doses [27]. A hypothesis mandating further exploration is that the toxic effect of TSH mediated by H2O2—an element essential for thyroid hormone synthesis being simultaneously a mitogenic and mutagenic factor—concerns the residual functioning thyroid tissue, while sparing the completely destructed thyroid [27].
\n
Intriguingly, according to the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, low TSH levels may induce DTC [63], likely forming a less differentiated epithelium susceptible to malignant transformation [27]. Interestingly, two genetic variants predisposing to PTC located on 9q22.23 and 14q13.3 have been also associated with low TSH levels [120]. Consequently, the perplexing role of TSH in PTC fuels a contention regarding the endorsement of TSH levels as predictive and/or prognostic biomarker of PTC.
\n
\n
\n
10. Conclusions
\n
Despite the major strides toward the elucidation of the correlation of PTC with HT, integrating coexistent HT per se, as well as thyroid autoantibodies and TSH levels into PTC risk stratification systems, awaits further consolidation. Translating the coexistence of PTC with HT into the therapeutic approach of PTC is currently uncertain. A burning question is whether the broad clinical spectrum of HT, mirroring the wide array of HT histopathology, defines the trajectory of the coexistence of PTC with HT. The designation of HT as a premalignant lesion or PTC as a precipitating factor for HT is thwarted by the blurred, till now, pathogenetic landscape. Illuminating the temporal precedence, a parameter sine qua non for the embracement of a causal relationship between PTC and TC, is daunting. Nevertheless, harnessing the immunological link between PTC and HT should guide future efforts in clinical research, aiming to widen the horizons of immunotherapy.
\n
In the interim, active surveillance of HT cannot be undermined, since it yields a tangible perspective of a prompt therapeutic intervention in the case of coexistent PTC.
\n
Nonetheless, striking is, to date, the dearth of solid evidence to guide clinical decision-making on surveillance of HT based on the presumptive correlation thereof with PTC; in fact, a patient-oriented standard of care of HT should be applauded. Although thyroid ultrasonography (US) is not required for diagnosing and monitoring the majority of HT, an individualized approach should be endorsed in clinical settings. Bearing in mind the negativity of TPOAbs and/or TgAbs in 10% of HT patients [121] and approximately 20% of patients with subclinical hypothyroidism [122], identifying a hypoechoic or an inhomogeneous US thyroid pattern will provide invaluable information as regards the diagnosis of HT. Even though a thyroid/neck US is not routinely recommended unless a palpable thyroid lesion is detected [7], averting underdiagnosis of a PTC smaller than 1 centimeter (cm) in greatest dimension—the so-called papillary thyroid microcarcinoma—raises awareness. In that respect, US could unravel a nodular variant of HT that merits further evaluation. The management of nodules in the context of HT is governed by the rules applied for any thyroid nodule irrespectively of HT, based on US-guided stratification of risk of malignancy [7]. FNAB is indicated in (i) nodules equal to or larger than 1 cm in greatest dimension presenting sonographic features of high or intermediate suspicion for PTC, (ii) nodules equal to or greater than 1.5 cm in greatest dimension presenting sonographic features of low suspicion for PTC, and (iii) nodules equal to or greater than 2 cm in greatest dimension presenting features of very low suspicion for PTC. Lower size cutoffs are embraced in the presence of clinical risk factors for PTC [7]. Pending the illumination of the clinical significance of the correlation of PTC with HT, clinicians should rely on their discretion and judgment, implementing the principle “primum non nocere.”
\n
\n
Conflict of interest
The authors declare no conflicts of interest.
AKT
protein kinase B
B7H1
B7 Homolog 1
cAMP
cyclic adenosine monophosphate
CCL
chemokine (C-C motif) ligand
CD
cluster of differentiation
cm
centimeter
COX-2
cyclooxygenase-2
CRI
cancer-related inflammation
CXCL
CXC chemokine ligand
CXCR4
CXC chemokine receptor 4
DCs
dendritic cells
DN
double negative
DPP IV
dipeptidyl peptidase IV
DTC
differentiated thyroid cancer
ERKs
extracellular signal-regulated kinases
FasL
Fas ligand
FNAB
fine needle aspiration biopsy
HIF-1
hypoxia-inducible factor-1
HLA
human leukocyte antigen
HLA-G
histocompatibility antigen, class 1, G, known also as human leukocyte antigen G
HT
Hashimoto’s thyroiditis
IL
interleukin
iNOS
inducible nitric oxide synthases
LT4
levothyroxine
M
macrophages
MAPK
mitogen-activated protein kinase
MCP-1
monocyte chemoattractant protein 1
MMPs
matrix metalloproteinases
N
neutrophils
NK
natural killer
OPN
osteopontin
PD
programmed cell death
PD-1
PD protein 1
PD-L1
programmed cell death ligand 1
PI3K
phosphoinositide 3-kinase
PKA
protein kinase A
PKC
protein kinase C
PTC
papillary thyroid carcinoma
PTEN
phosphatase and tensin homolog
RET
rearranged during transfection
RNS
reactive nitrogen species
ROS
reactive oxygen species
TC
thyroid cancer
TgAbs
anti-thyroglobulin autoantibodies
TGFb
transforming growth factor b
Th
T-helper
TLR
Toll-like receptors
TNFa
tumor necrosis factor a
TPOAbs
anti-thyroperoxidase autoantibodies
Treg
T regulatory cells
TSH
thyroid-stimulating hormone
TSH-R
TSH receptor
UPA
urokinase-type plasminogen activator
UPAR
urokinase-type plasminogen activator receptor
US
ultrasonography
VEGF
vascular endothelial growth factor
Wnt
Wingless/int-1
\n',keywords:"papillary thyroid carcinoma, hashimoto’s thyroiditis, anti-thyroglobulin autoantibodies, anti-thyroperoxidase autoantibodies, thyroid-stimulating hormone",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/66252.pdf",chapterXML:"https://mts.intechopen.com/source/xml/66252.xml",downloadPdfUrl:"/chapter/pdf-download/66252",previewPdfUrl:"/chapter/pdf-preview/66252",totalDownloads:1107,totalViews:0,totalCrossrefCites:0,totalDimensionsCites:2,totalAltmetricsMentions:1,impactScore:1,impactScorePercentile:48,impactScoreQuartile:2,hasAltmetrics:1,dateSubmitted:"December 2nd 2018",dateReviewed:"February 12th 2019",datePrePublished:"April 10th 2019",datePublished:"September 4th 2019",dateFinished:"March 20th 2019",readingETA:"0",abstract:"Illustrating the ancient link connecting inflammation with cancer, the correlation of papillary thyroid carcinoma (PTC) with Hashimoto’s thyroiditis (HT) has long been pursued as intersection of autoimmunity-induced chronic inflammation and tumor-induced immunity. The dramatic rise of the incidence of PTC οver the last decades—the main culprit for “thyroid cancer (TC) epidemic”—parallels the increasing incidence of HT, potentially reflecting a pathogenetic link that could be harnessed in diagnostics and therapeutics. Prompted by this perspective, in the present chapter, we dissect the hitherto elusive interrelationship of PTC with HT, focusing on four issues: firstly, an unresolved conundrum is whether PTC emerges due to or notwithstanding immune response or mirrors the “tumor defense-induced autoimmunity.” Secondly, the interrelationship of HT with PTC may be merely epiphenomenon of selection bias inherent in thyroidectomy series. Thirdly, the impact of HT on coexistent PTC is equivocal—host protective versus tumor protective. Fourthly, translating serum concentrations of thyroid autoantibodies and thyroid-stimulating hormone (TSH) into predictive and prognostic PTC biomarkers dichotomizes, till now, the researchers. In the era of precision medicine, illuminating whether HT precipitates PTC or vice versa is awaited with anticipation in order to refine the preventive and therapeutic policy counteracting “TC epidemic.”",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/66252",risUrl:"/chapter/ris/66252",book:{id:"7883",slug:"knowledges-on-thyroid-cancer"},signatures:"Maria V. Deligiorgi and Dimitrios T. Trafalis",authors:[{id:"217004",title:"Prof.",name:"Dimitrios",middleName:null,surname:"Trafalis",fullName:"Dimitrios Trafalis",slug:"dimitrios-trafalis",email:"dtrafal@med.uoa.gr",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null},{id:"288030",title:"Ph.D.",name:"Maria",middleName:null,surname:"Deligiorgi",fullName:"Maria Deligiorgi",slug:"maria-deligiorgi",email:"mdeligiorgi@yahoo.com",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Tailoring the treatment of PTC: where does coexistent HT stand?",level:"1"},{id:"sec_3",title:"3. HT at a glance",level:"1"},{id:"sec_4",title:"4. Rationality in the investigation of the interrelationship of PTC with HT",level:"1"},{id:"sec_5",title:"5. Exploring the immunological link between PTC and HT",level:"1"},{id:"sec_5_2",title:"5.1. Thyroid malignancy develops despite immune response in the context of HT",level:"2"},{id:"sec_6_2",title:"5.2. Thyroid malignancy develops owing to thyroid autoimmunity",level:"2"},{id:"sec_7_2",title:"5.3. The immune attack against PTC triggers thyroid autoimmunity",level:"2"},{id:"sec_9",title:"6. Does the coexistence of HT with PTC really exist?",level:"1"},{id:"sec_10",title:"7. Effect of HT on coexistent PTC: host protective or tumor protective?",level:"1"},{id:"sec_11",title:"8. Thyroid autoantibodies in the context of HT coexistent with PTC: predictive and/or prognostic PTC biomarkers or not?",level:"1"},{id:"sec_12",title:"9. Elevated TSH levels in HT coexistent with PTC: the mediator of the effect of HT on PTC?",level:"1"},{id:"sec_13",title:"10. Conclusions",level:"1"},{id:"sec_17",title:"Conflict of interest",level:"1"},{id:"sec_16",title:"",level:"1"}],chapterReferences:[{id:"B1",body:'Dailey ME, Lindsay S, Skahen R. Relation of thyroid neoplasms to Hashimoto disease of the thyroid gland. AMA Archives of Surgery. 1955;70:291-297. DOI: 10.1001/archsurg.1955.01270080137023\n'},{id:"B2",body:'Coussens LM, Werb Z. Inflammation and cancer. Nature. 2002;420:860-867. DOI: 10.1038/nature01322\n'},{id:"B3",body:'Pellegriti G, Frasca F, Regalbuto C, Squatrito S, Vigneri R. Worldwide increasing incidence of thyroid cancer: Update on epidemiology and risk factors. Journal of Cancer Epidemiology. 2013;2013:965212. 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Associations between Hashimoto thyroiditis and clinical outcomes of papillary thyroid cancer: A meta-analysis of observational studies. Endocrinology and Metabolism (Seoul, Korea). 2018;33:473-484. DOI: 10.3803/EnM.2018.33.4.473\n'},{id:"B49",body:'Cho YA, Kong S-Y, Shin A, Lee J, Lee EK, Lee YJ, et al. Biomarkers of thyroid function and autoimmunity for predicting high-risk groups of thyroid cancer: A nested case–control study. BMC Cancer. 2014;14:873. DOI: 10.1186/1471-2407-14-873\n'},{id:"B50",body:'Zhang X, Zhang X, Chang Z, Wu C, Guo H. Correlation analyses of thyroid-stimulating hormone and thyroid autoantibodies with differentiated thyroid cancer. JBUON. 2018;23:1467-1471\n'},{id:"B51",body:'Kim ES, Lim DJ, Baek KH, Lee JM, Kim MK, Kwon HS, et al. Thyroglobulin antibody is associated with increased cancer risk in thyroid nodules. Thyroid. 2010;20:885-891. DOI: 10.1089/thy.2009.0384\n'},{id:"B52",body:'Wu X, Lun Y, Jiang H, Gang Q , Xin S, Duan Z, et al. Coexistence of thyroglobulin antibodies and thyroid peroxidase antibodies correlates with elevated thyroid-stimulating hormone level and advanced tumor stage of papillary thyroid cancer. Endocrine. 2013;46:554-560. DOI: 10.1007/s12020-013-0121-x\n'},{id:"B53",body:'Qin J, Yu Z, Guan H, Shi L, Liu Y, Zhao N, et al. High thyroglobulin antibody levels increase the risk of differentiated thyroid carcinoma. Disease Markers. 2015;2015:648670. DOI: 10.1155/2015/648670\n'},{id:"B54",body:'Souza SL, da Assumpção LVM, Ward LS. Impact of previous thyroid autoimmune diseases on prognosis of patients with well-differentiated thyroid cancer. Thyroid. 2003;13:491-495. DOI: 10.1089/105072503322021160\n'},{id:"B55",body:'McLeod DS, Cooper DS, Ladenson PW, Ain KB, Brierley JD, Fein HG, et al. The national thyroid cancer treatment cooperative study group. Prognosis of differentiated thyroid cancer in relation to serum thyrotropin and thyroglobulin antibody status at time of diagnosis. 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Multiple associations between a broad spectrum of autoimmune diseases, chronic inflammatory diseases and cancer. Anticancer Research. 2012;32:1119-1136\n'},{id:"B94",body:'Girotra M, Hansen A, Farooki A, Byun DJ, Min L, Creelan BC, et al. The current understanding of the endocrine effects from immune checkpoint inhibitors and recommendations for management. JNCI Cancer Spectrum. 2018;2:pky021. DOI: 10.1093/jncics/pky021\n'},{id:"B95",body:'Zhang Y, Ma XP, Deng FS, Liu ZR, Wei HQ , Wang XH, et al. The effect of chronic lymphocytic thyroiditis on patients with thyroid cancer. World Journal of Surgical Oncology. 2014;12:277. DOI: 10.1186/1477-7819-12-277\n'},{id:"B96",body:'Lee JH, Kim Y, Choi JW, Kim YS. The association between papillary thyroid carcinoma and histologically proven Hashimoto’s thyroiditis: A meta-analysis. European Journal of Endocrinology. 2013;15(168):343-349. DOI: 10.1530/EJE-12-0903\n'},{id:"B97",body:'Lai X, Xia Y, Zhang B, Li J, Jiang Y. A meta-analysis of Hashimoto’s thyroiditis and papillary thyroid carcinoma risk. Oncotarget. 2017;8:62414-62424. DOI: 10.18632/oncotarget.18620\n'},{id:"B98",body:'Resende de Paiva C, Grønhøj C, Feldt-Rasmussen U, von Buchwald C. Association between Hashimoto’s thyroiditis and thyroid cancer in 64,628 patients. Frontiers in Oncology. 2017;7:53. DOI: 10.3389/fonc.2017.00053\n'},{id:"B99",body:'McLeod DSA, Cooper DS. The incidence and prevalence of thyroid autoimmunity. Endocrine Journal. 2012;42:252-265\n'},{id:"B100",body:'Fiore E, Rago T, Scutari M, Ugolini C, Proietti A, Di Coscio G, et al. Papillary thyroid cancer, although strongly associated with lymphocytic infiltration on histology, is only weakly predicted by serum thyroid auto-antibodies in patients with nodular thyroid diseases. Journal of Endocrinological Investigation. 2009;32:344-335. DOI: 10.1007/BF03345725\n'},{id:"B101",body:'Fiore E, Latrofa F, Vitti P. Iodine, thyroid autoimmunity and cancer. 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Hashimoto’s thyroiditis predicts outcome in intrathyroidal papillary thyroid cancer. Endocrine-Related Cancer. 2017;24:485-493. DOI: 10.1530/ERC-17-0085\n'},{id:"B106",body:'Cunha LL, Morari EC, Guihen AC, Razolli D, Gerhard R, Nonogaki S, et al. Infiltration of a mixture of immune cells may be related to good prognosis in patients with differentiated thyroid carcinoma. Clinical Endocrinology. 2012;77:918-925. DOI: 10.1111/j.1365-2265.2012.04482.x\n'},{id:"B107",body:'Zeng R, Lyu Y, Zhang G, et al. Positive effect of RORγt on the prognosis of thyroid papillary carcinoma patients combined with Hashimoto’s thyroiditis. American Journal of Translational Research. 2018;10:3011-3024\n'},{id:"B108",body:'Jeong JS, Kim HK, Lee CR, Park S, Park JH, Kang SW, et al. Coexistence of chronic lymphocytic thyroiditis with papillary thyroid carcinoma: Clinical manifestation and prognostic outcome. Journal of Korean Medical Science. 2012;27:883-889. 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European Journal of Cancer. 1993;29A:1190-1192\n'},{id:"B118",body:'Hoelting T, Tezelman S, Siperstein AE, Duh QY, Clark OH. Thyrotropin stimulates invasion and growth of follicular thyroid cancer cells via PKC- rather than PKA-activation. Biochemical and Biophysical Research Communications. 1993;195:1230-1236. DOI: 10.1006/bbrc.1993.2176\n'},{id:"B119",body:'Ahn D, Sohn JH, Kim JH, Shin CM, Jeon JH, Park JY. Preoperative subclinical hypothyroidism in patients with papillary thyroid carcinoma. American Journal of Otolaryngology. 2013;34:312-319. DOI: 10.1016/j.amjoto.2012.12.013. Epub 2013 Jan 26\n'},{id:"B120",body:'Gudmundsson J, Sulem P, Gudbjartsson DF, Jonasoon JG, Sigurdsson A, Bergthorsson JT, et al. Common variants on 9q22.33 and 14q13.3 predispose to thyroid cancer in European populations. Nature Genetics. 2009;41:460-464. DOI: 10.1038/ng.339\n'},{id:"B121",body:'Mincer DL, Jialal I. Hashimoto thyroiditis. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018\n'},{id:"B122",body:'Pearce SH, Brabant G, Duntas LH, Monzani F, Peeters RP, Razvi S, et al. 2013 ETA guideline: Management of subclinical hypothyroidism. European Thyroid Journal. 2013;2:215-228\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Maria V. Deligiorgi",address:"mdeligiorgi@yahoo.com",affiliation:'
Clinical Pharmacology Unit, Laboratory of Pharmacology, Medical School, National and Kapodistrian University of Athens, Athens, Greece
'},{corresp:null,contributorFullName:"Dimitrios T. Trafalis",address:null,affiliation:'
Clinical Pharmacology Unit, Laboratory of Pharmacology, Medical School, National and Kapodistrian University of Athens, Athens, Greece
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\n
1. Introduction
\n
In the past, Japanese houses were ridiculed as being “rabbit hutches” as they were smaller in scale, lower in quality, and shorter in average service life than those of Western countries, and examples were often given illustrating Japan as having the worst residential environment among major advanced countries. However, after the period of high economic growth since the chaotic postwar period, this environment has already greatly improved. In recent years high-performance housing stock has accumulated, and housing with functions not found in other countries have become common.
\n
Needless to say, when attempting an analysis of a housing market, it is necessary to fully understand the characteristics of the country. Below, we set out the reasons that have led to the false perception of Japanese housing still belonging to the era when they were ridiculed as rabbit hutches.
\n
Although commonalities can be found in many parts of the Japanese housing market in comparison with the European and US housing markets, the following heterogeneity is conceivable as the postwar historical origin is different. It is possible that these are the cause of many misunderstandings.
\n
In Japan, many houses were destroyed due to the large-scale air raids during the Second World War, not only in metropolitan areas but also in regional cities. In particular, a large number of houses were destroyed in the Tokyo metropolitan area,1 and very-low-quality houses were built in a disorganized manner to satisfy the urgent housing demand in the chaotic postwar period. In the so-called high economic growth period that began in the mid-1950s, such houses were rapidly upgraded as large numbers of apartment buildings came up throughout Japan.2 In addition, the drastic change in Japanese lifestyle through the rapid economic growth triggered the renewal of old housing stock by Westernizing the traditional housing style of Japan.
\n
The private sector led construction to realize such a large-scale housing supply because the public sector was saddled with the large financial burden of postwar reconstruction. In particular, the government established a personal loan system to promote housing investment by households, and as a result, the ownership rate in postwar Japan significantly increased in comparison to before the war. Furthermore, as the supply of public housing was limited, a dedicated housing market for single-person renters formed in the rental housing market, which was rarely seen in Europe and the United States.
\n
As a result of these short-term housing renewals, Japanese housing was brought into a state where their style, quality, and housing equipment were greatly different depending on the period of construction. In addition, due to natural disasters such as the Great Hanshin earthquake3 and the Great East Japan earthquake,4 housing earthquake resistance and other legal regulations have been successively strengthened, thereby rapidly increasing the performance requirements of housing.5\n
\n
This history is also closely related to the shortness of service life, which is a characteristic of the previously ridiculed Japanese houses. Several reasons can be envisaged to explain the short service life of Japanese houses, but the two most influential factors are considered to be the urgent task of promoting the renovation of low-quality housing stock that was built to temporarily compensate for the housing shortage after the war and the fact that the stock renewal was promoted by strengthening public regulations due to large-scale earthquakes and other disasters.
\n
In addition, the high urban renewal rate can also be cited as a reason. In the rapid economic growth of postwar Japan, the main industrial structure shifted from primary to secondary industry in a single stroke, and urbanization was promoted throughout the country in the 1970s by developing highway and railway networks across the country, known as “Japanese archipelago remodeling.” In the 1980s, a policy was developed to transform the industrial structure, which was centered on secondary industry to tertiary industry. The transformation of Tokyo into an international financial center was a symbolic policy, and against this background, redevelopment rapidly advanced in major cities. Under such circumstances, the conversion of building use of even physically usable housing into offices, commercial facilities, and so on was promoted through rebuilding, and the advancement of land use was promoted [1].
\n
As a result, it can be said that the average service life of housing seen throughout the stock as a whole has been shortened over a long period.
\n
In addition to these features, it should be noted that the speed of technological innovation in Japanese housing is fast. “Technological innovation” here refers not only to the improvement of productivity on the manufacturing side but also the significant improvement of household welfare levels through the release of new products developed by R&D. In recent years, smart houses utilizing IOT and so on have become symbolic of advancing technology, but functions such as TV intercoms, bathroom dryers, system kitchens, and toilets with washlets, which are not often seen in European and American houses, have become common functions in Japanese houses and have greatly improved household living standards.
\n
However, in a market where products with such new features arrive so quickly, the speed of obsolescence also increases. In these markets, when a new product appears, the old product is ordered to be withdrawn from the market, or its commodity value is greatly depreciated, that is, the service life of products is shortened.
\n
This study aims to measure the economic value of the functions of housing with new quality in the rental housing market in Tokyo, where technological advancement has been the greatest, and to clarify how much economic depreciation is occurring due to obsolescence. In Section 2, we present the model and the framework for empirical analysis together with the data, and in Section 3, we present the estimated results. According to the obtained results, new functions are being added sequentially to Japanese rental housing according to the age of the building, and these functions are non-negligible in the determination of housing rent, even when compared with location (LC) and the building structure (ST). The effect of obsolescence due to the addition of new functions was roughly—5%. In Section 4, we summarize the results by way of a conclusion.
\n
\n
\n
2. Empirical analysis: data and estimation model
\n
\n
2.1 Literature review
\n
A technique known as the hedonic approach is effective to decompose prices of commodities corresponding to different qualities. Since the hedonic approach theoretically depicts the behavior of suppliers and consumers in a market with diverse quality and presents a framework for empirical analysis, it is possible to approximately measure the household limit shadow price for new functions and to identify economic deterioration accompanying obsolescence [2, 3].
\n
Generally, the construction of household selection models in the residential market faces many difficulties compared to regular commodities and service markets. Not only is consumption expenditure high for housing, but consumers are also troubled by its highly nonuniform nature. Even when located in the same place, prices vary depending on the quality of housing, and even if the buildings are of the same quality, prices vary depending on the location. Furthermore, since housing has durability, depreciation has to be taken into consideration.
\n
In such a market, the law of one price assumed by traditional pricing theory cannot be applied. Furthermore, the application of a model that deals with differentiated products as analyzed by Lancaster [4] is not effective both theoretically and in empirical analysis. Accordingly, Rosen [5] theoretically clarified the type of market mechanism that is generated when commodity price data are a bundle of such attributes. Specifically, the relationship between the offer function of the commodity supplier, the bid function of the commodity consumer, and the market price function established by the equilibrium of these is closely examined, and the market price is characterized from the behavior of consumers and producers [6].
\n
However, when attempting to estimate the hedonic function, we face various difficulties. The first is the existence of unobservable variables, the so-called omitted variable bias problem [7]. In general, in the estimation of a hedonic function for the housing market, only the location and building attributes, which are easy to obtain, are taken into consideration. However, it is also easy to envisage that the actual market price of housing will change depending on the environment surrounding the house and the various kinds of performance of the building.
\n
As for variable selection in the estimation of hedonic functions in Tokyo’s rental housing market, Nishi et al. [8] have conducted an exhaustive survey of the previous research. Nishi et al. [8] pointed that the housing amenities used in hedonic analyses are categorized as “location or accessibility,” “housing features,” and “site advantages.” This paper is focused on housing features, because they can be reflected in the rent due to the technological progress in the information systems and supply management.
\n
Accessibility is defined as the “main accessibility related to commuting.” Housing features are defined as “amenities that can be changed by landlords.” Accessibility and housing features are the basic characteristics used as explanatory variables in hedonic models and are widely used in previous studies [2, 6, 9, 10].
\n
Site advantages have also been researched recently using variables calculated using geographical information system or GIS [11, 12]. Shimizu [11] demonstrates that the environment surrounding housing is important in the case where house prices are determined by building use conditions and the characteristics of neighboring residents and suggests that in the case such variables are not taken into consideration and the estimated statistics of the hedonic function lack robustness. Nishi et al. [8] also show that there is a similar problem with estimated statistics when housing equipment is not taken into consideration. Fuerst and Shimizu [13] show that in the new condominium market in Tokyo, the offered value for highly novel functionality such as environmental performance differs greatly when taking the household’s annual income into account.
\n
As can be understood from these facts, attention must be given to the kind of variables that are used in estimating the hedonic function. According to Nelson [14], housing characteristics to be considered in function estimation are classified as follows.
\n
Excluding characteristics related to traffic convenience, Nelson [14] considers it possible to categorize the positional characteristics of housing into housing equipment and location. Of these, “housing equipment” is variable and depends on the owner of the house, and “location” is an element that cannot be changed. Meanwhile, Chau and Chin [15] and Shimizu [11] add neighborhood characteristics.
\n
In addition to location and building structure, this study classifies housing equipment into equipment ancillary to the room (room equipment (RE)) and to the building (building equipment (BE)) and also takes the conditions of the contract into account to estimate their marginal price effect by estimating the hedonic function and to estimate the extent of obsolescence caused by the appearance of products with new performance.
\n
\n
\n
2.2 Data
\n
Since the latter half of the 1990s, the use of the Internet for real estate advertising has expanded rapidly in Japan, and websites dealing with a large amount of rental advert data have been developed. This study uses the data on homes managed by LIFULL Co., Ltd. which is a major real estate portal site.6\n
\n
Multiple real estate companies post concurrent advertisements for the same property on the real estate website, so we eliminated the duplicates from the data by grouping them by the criteria of address, property name, and room number.7 Furthermore, we independently assigned daytime railway travel time from Tokyo station to the nearest station to the property (minutes), which was not included in the data posted on the portal.
\n
Since the aim of this study is to identify the effect due to the addition of new functions over time, we hypothesize that the price structure will change according to the period of construction.8 Data were segmented into the following three stocks:
Old stock: built between 1968 and 1981
Main stock: built between 1982 and 1999
New stock: built between 2000 and 2018
\n\n
Earthquake resistance standards were greatly revised in 1981 according to the Building Standards Act, which stipulates building quality in Japan, and the earthquake resistance of buildings differs greatly according to whether they were built in or before 1981 or in or after 1982; buildings were therefore categorized using 1981 as a basis. There was also a major change in earthquake resistance standards in 2000, so this was also used as the standard for a category. In addition, the data used are for the 23 wards of Tokyo where a large volume of housing stocks was supplied due to a large population inflow.
\n
As a result of this process, 53,550 data points were acquired as data for analysis.9\n
where y is the explanatory variable, p is the housing rent, xi\n is the explanatory variable (housing characteristic), and βi\n and α are the estimation parameters.
\n
In this study, in addition to the commonly used location and building structure, housing equipment was added to the estimation of the hedonic function for the housing market. Specifically, we classified housing equipment into equipment ancillary to the room (room equipment) and equipment ancillary to the building (building equipment) and took the conditions of contract (CC) into account to construct a hedonic function.
In Eq. (1), ln pit\n represents the log rent for i property at time t (October 2018). \n\n\nAge\nit\n\n\n is the years since construction, \n\n\nST\njit\n\n\n is the period of construction dummy (old/main/new), \n\n\nS\nit\n\n\n is the floor area, \n\n\nTS\nit\n\n\n is the number of minutes on foot from the nearest station, \n\n\nDT\nit\n\n\n is the number of minutes by train from Tokyo station, \n\n\nStr\njit\n\n\n is the structure dummy, \n\n\nW\nmit\n\n\n is the ward dummy, \n\n\nTR\nhit\n\n\n is the high-rise condominium and ground floor room position dummy, \n\n\nRE\nkit\n\n\n is the room equipment dummy, \n\n\nBE\nkit\n\n\n is the building equipment dummy, \n\n\nCC\nkit\n\n\n is the contract condition (CC) dummy, \n\n\nβ\n0\n\n\n is a constant term, and \n\n\n\nε\nit\n\n\n is an error term.
\n
\n
\n
\n
3. Verification analysis
\n
\n
3.1 Descriptive statistics for analysis data
\n
Before analysis, we calculated the descriptive statistics of the data to be analyzed (\nTable 1\n). From the descriptive statistics, there are several features as follows, depending on the period of construction:
There is little difference between old and main stocks in average rent, but it is about 20% higher for new stock than the old stock.
There is no significant difference in the average floor area, the number of minutes by foot from the nearest station, and the number of minutes by train from Tokyo station.
Concerning the years since construction, the average of the total is 18.5 years and the standard deviation is 12.7 years, and the average value and standard deviation by construction date are consistent with the classification.
\n\n
\n
\n
\n
\n
\n
\n
\n\n
\n
Variable
\n
Type
\n
Mean
\n
Std. dev.
\n
Min.
\n
Max.
\n
\n\n\n
\n
Monthly rent
\n
All
\n
94,779
\n
34,873
\n
30,000
\n
249,000
\n
\n
\n
(JYE)
\n
Old stock
\n
84,968
\n
30,631
\n
30,000
\n
240,000
\n
\n
\n
\n
Main stock
\n
85,305
\n
32,566
\n
30,000
\n
249,000
\n
\n
\n
\n
New stock
\n
103,040
\n
34,994
\n
45,000
\n
249,000
\n
\n
\n
\n
New/old
\n
121.3%
\n
114.2%
\n
150.0%
\n
103.8%
\n
\n
\n
Floor space
\n
All
\n
31.3
\n
13.4
\n
15.0
\n
100.0
\n
\n
\n
(m2)
\n
Old stock
\n
32.5
\n
12.4
\n
15.0
\n
91.4
\n
\n
\n
\n
Main stock
\n
32.0
\n
15.3
\n
15.0
\n
100.0
\n
\n
\n
\n
New stock
\n
30.6
\n
12.1
\n
15.0
\n
99.5
\n
\n
\n
\n
New/old
\n
94.3%
\n
97.7%
\n
100.0%
\n
108.9%
\n
\n
\n
Monthly rent/m3\n
\n
All
\n
3192
\n
806
\n
988
\n
8134
\n
\n
\n
(JYE)
\n
Old stock
\n
2717
\n
668
\n
1076
\n
6528
\n
\n
\n
\n
Main stock
\n
2864
\n
701
\n
988
\n
7535
\n
\n
\n
\n
New stock
\n
3501
\n
766
\n
1165
\n
8134
\n
\n
\n
\n
New/old
\n
128.9%
\n
114.8%
\n
108.3%
\n
124.6%
\n
\n
\n
Age of unit
\n
All
\n
18.5
\n
12.7
\n
0.0
\n
50.0
\n
\n
\n
(year)
\n
Old stock
\n
42.3
\n
3.8
\n
37.0
\n
50.0
\n
\n
\n
\n
Main stock
\n
27.4
\n
4.4
\n
19.0
\n
36.0
\n
\n
\n
\n
New stock
\n
8.3
\n
5.5
\n
0.0
\n
18.0
\n
\n
\n
\n
New/old
\n
19.7%
\n
144.0%
\n
0.0%
\n
36.0%
\n
\n
\n
Time to the nearest station
\n
All
\n
7.7
\n
4.6
\n
0.6
\n
41.0
\n
\n
\n
(minutes)
\n
Old stock
\n
7.4
\n
4.4
\n
1.0
\n
41.0
\n
\n
\n
\n
Main stock
\n
8.1
\n
4.8
\n
1.0
\n
40.0
\n
\n
\n
\n
New stock
\n
7.4
\n
4.4
\n
0.6
\n
38.0
\n
\n
\n
\n
New/old
\n
99.4%
\n
98.8%
\n
62.5%
\n
92.7%
\n
\n
\n
Time to Tokyo station
\n
All
\n
27.2
\n
8.6
\n
1.0
\n
48.0
\n
\n
\n
(minutes)
\n
Old stock
\n
26.5
\n
8.3
\n
4.0
\n
48.0
\n
\n
\n
\n
Main stock
\n
28.8
\n
8.1
\n
4.0
\n
48.0
\n
\n
\n
\n
New stock
\n
26.2
\n
8.8
\n
1.0
\n
48.0
\n
\n
\n
\n
New/old
\n
99.1%
\n
105.4%
\n
25.0%
\n
100.0%
\n
\n
\n
Number of observations (all) = 53,550
\n
\n\n
Table 1.
Descriptive statistics.
\n
Based on these features, there is found to be little difference between the physical space distribution due to the period of construction and only the building quality changes.
\n
\n
\n
3.2 Distribution of analysis data by ward
\n
Next, we examined the distribution of old/main/new stock for each of the 23 wards (\nTable 2\n). The ratio of new stock ratio exceeds 70% in Chiyoda, Chuo, and Minato wards, which make up the center of Tokyo. As previously mentioned, the probability of large-scale redevelopment and so on being carried out increases for more urban areas, which may have caused this result due to active stock renewal.10\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n\n
\n
\n
Number of observations
\n
Ratio
\n
\n
\n
Item
\n
Total
\n
Old stock
\n
Main stock
\n
New stock
\n
Total
\n
Old stock
\n
Main stock
\n
New stock
\n
New-old
\n
\n\n\n
\n
\nRoom equipment\n
\n
\n
\n
Air conditioning
\n
49.088
\n
4029
\n
17.883
\n
27.176
\n
91.7%
\n
82.8%
\n
89.5%
\n
94.7%
\n
11.9%
\n
\n
\n
Hot water supply
\n
44.841
\n
3879
\n
16.961
\n
24.001
\n
83.7%
\n
79.7%
\n
84.9%
\n
83.6%
\n
3.9%
\n
\n
\n
Indoor WM area
\n
43.954
\n
2663
\n
14.696
\n
26.595
\n
82.1%
\n
54.7%
\n
73.5%
\n
92.7%
\n
38.0%
\n
\n
\n
Separate bath and toilet
\n
43.943
\n
3447
\n
12.851
\n
27.645
\n
82.1%
\n
70.8%
\n
64.3%
\n
96.3%
\n
25.5%
\n
\n
\n
Flooring
\n
43.269
\n
3364
\n
14.915
\n
24.990
\n
80.8%
\n
69.1%
\n
74.6%
\n
87.1%
\n
18.0%
\n
\n
\n
Balcony
\n
40.851
\n
3204
\n
15.276
\n
22.371
\n
76.3%
\n
65.8%
\n
76.4%
\n
77.9%
\n
12.1%
\n
\n
\n
System kitchen
\n
27.758
\n
1093
\n
5666
\n
20.999
\n
51.8%
\n
22.5%
\n
28.4%
\n
73.2%
\n
50.7%
\n
\n
\n
Separate washroom
\n
26.292
\n
1412
\n
6221
\n
18.659
\n
49.1%
\n
29.0%
\n
31.1%
\n
65.0%
\n
36.0%
\n
\n
\n
1 gas stove
\n
25.300
\n
1416
\n
6396
\n
17.488
\n
47.2%
\n
29.1%
\n
32.0%
\n
60.9%
\n
31.8%
\n
\n
\n
Washlet
\n
23.221
\n
1089
\n
3265
\n
18.867
\n
43.4%
\n
22.4%
\n
16.3%
\n
65.7%
\n
43.4%
\n
\n
\n
Bathroom dryer
\n
20.322
\n
186
\n
1077
\n
19.059
\n
37.9%
\n
3.8%
\n
5.4%
\n
66.4%
\n
62.6%
\n
\n
\n
2 gas stoves
\n
18.632
\n
1081
\n
3304
\n
14.247
\n
34.8%
\n
22.2%
\n
16.5%
\n
49.6%
\n
27.4%
\n
\n
\n
Reheating bath
\n
15.127
\n
1268
\n
3459
\n
10.400
\n
28.2%
\n
26.0%
\n
17.3%
\n
36.2%
\n
10.2%
\n
\n
\n
Washroom with shower
\n
12.678
\n
364
\n
1764
\n
10.550
\n
23.7%
\n
7.5%
\n
8.8%
\n
36.8%
\n
29.3%
\n
\n
\n
Own house rental
\n
7187
\n
497
\n
1588
\n
5102
\n
13.4%
\n
10.2%
\n
7.9%
\n
17.8%
\n
7.6%
\n
\n
\n
IH stovetop
\n
6623
\n
215
\n
2653
\n
3755
\n
12.4%
\n
4.4%
\n
13.3%
\n
13.1%
\n
8.7%
\n
\n
\n
Walk-in closet
\n
3694
\n
88
\n
235
\n
3371
\n
6.9%
\n
1.8%
\n
1.2%
\n
11.7%
\n
9.9%
\n
\n
\n
Counter kitchen
\n
3409
\n
70
\n
516
\n
2823
\n
6.4%
\n
1.4%
\n
2.6%
\n
9.8%
\n
8.4%
\n
\n
\n
With loft
\n
2110
\n
19
\n
754
\n
1337
\n
3.9%
\n
0.4%
\n
3.8%
\n
4.7%
\n
4.3%
\n
\n
\n
Underfloor heating
\n
1147
\n
8
\n
87
\n
1052
\n
2.1%
\n
0.2%
\n
0.4%
\n
3.7%
\n
3.5%
\n
\n
\n
\nBuilding equipment\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
Bicycle parking lot
\n
33.795
\n
2096
\n
11.385
\n
20.314
\n
63.1%
\n
43.1%
\n
57.0%
\n
70.8%
\n
27.7%
\n
\n
\n
Fiber optic Internet
\n
27.307
\n
2085
\n
10.056
\n
15.166
\n
51.0%
\n
42.8%
\n
50.3%
\n
52.8%
\n
10.0%
\n
\n
\n
TV intercom
\n
26.689
\n
953
\n
4232
\n
21.504
\n
49.8%
\n
19.6%
\n
21.2%
\n
74.9%
\n
55.4%
\n
\n
\n
Automatic entrance door
\n
26.042
\n
337
\n
5062
\n
20.643
\n
48.6%
\n
6.9%
\n
25.3%
\n
71.9%
\n
65.0%
\n
\n
\n
Cable TV
\n
23.211
\n
1316
\n
8314
\n
13.581
\n
43.3%
\n
27.0%
\n
41.6%
\n
47.3%
\n
20.3%
\n
\n
\n
BS antenna
\n
20.013
\n
472
\n
4430
\n
15.111
\n
37.4%
\n
9.7%
\n
22.2%
\n
52.7%
\n
43.0%
\n
\n
\n
Elevator
\n
19.587
\n
1189
\n
5387
\n
13.011
\n
36.6%
\n
24.4%
\n
27.0%
\n
45.3%
\n
20.9%
\n
\n
\n
Tiling wall
\n
15.751
\n
561
\n
5265
\n
9925
\n
29.4%
\n
11.5%
\n
26.3%
\n
34.6%
\n
23.1%
\n
\n
\n
Delivery locker
\n
15.163
\n
119
\n
1550
\n
13.494
\n
28.3%
\n
2.4%
\n
7.8%
\n
47.0%
\n
44.6%
\n
\n
\n
Security camera
\n
12.694
\n
302
\n
1849
\n
10.543
\n
23.7%
\n
6.2%
\n
9.3%
\n
36.7%
\n
30.5%
\n
\n
\n
CS antenna
\n
11.888
\n
304
\n
1837
\n
9747
\n
22.2%
\n
6.2%
\n
9.2%
\n
34.0%
\n
27.7%
\n
\n
\n
Garbage 24H available
\n
6670
\n
130
\n
728
\n
5812
\n
12.5%
\n
2.7%
\n
3.6%
\n
20.3%
\n
17.6%
\n
\n
\n
Bike parking lot
\n
6335
\n
354
\n
1875
\n
4106
\n
11.8%
\n
7.3%
\n
9.4%
\n
14.3%
\n
7.0%
\n
\n
\n
Design by artist
\n
4068
\n
29
\n
286
\n
3753
\n
7.6%
\n
0.6%
\n
1.4%
\n
13.1%
\n
12.5%
\n
\n
\n
Seismic structure
\n
3827
\n
37
\n
702
\n
3088
\n
7.1%
\n
0.8%
\n
3.5%
\n
10.8%
\n
10.0%
\n
\n
\n
\nContract conditions\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
with NO guarantor
\n
20.257
\n
1214
\n
6274
\n
12.769
\n
37.8%
\n
24.9%
\n
31.4%
\n
44.5%
\n
19.6%
\n
\n
\n
No pets
\n
8417
\n
733
\n
3540
\n
4144
\n
15.7%
\n
15.1%
\n
17.7%
\n
14.4%
\n
-0.6%
\n
\n
\n
NO musical instrument
\n
6704
\n
605
\n
2702
\n
3397
\n
12.5%
\n
12.4%
\n
13.5%
\n
11.8%
\n
-0.6%
\n
\n
\n
NO office use
\n
5253
\n
297
\n
1731
\n
3225
\n
9.8%
\n
6.1%
\n
8.7%
\n
11.2%
\n
5.1%
\n
\n
\n
FREE Internet
\n
4682
\n
100
\n
616
\n
3966
\n
8.7%
\n
2.1%
\n
3.1%
\n
13.8%
\n
11.8%
\n
\n
\n
Pet consultation
\n
3906
\n
210
\n
801
\n
2895
\n
7.3%
\n
4.3%
\n
4.0%
\n
10.1%
\n
5.8%
\n
\n
\n
Pets allowed
\n
2189
\n
150
\n
437
\n
1602
\n
4.1%
\n
3.1%
\n
2.2%
\n
5.6%
\n
2.5%
\n
\n
\n
Contract with limited term
\n
1673
\n
311
\n
511
\n
851
\n
3.1%
\n
6.4%
\n
2.6%
\n
3.0%
\n
-3.4%
\n
\n
\n
Office use allowed
\n
1319
\n
362
\n
508
\n
449
\n
2.5%
\n
7.4%
\n
2.5%
\n
1.6%
\n
-5.9%
\n
\n
\n
\nBuilding structure\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
Wooden
\n
10.851
\n
1285
\n
4273
\n
5293
\n
20.3%
\n
26.4%
\n
21.4%
\n
18.4%
\n
-8.0%
\n
\n
\n
Steel frame
\n
13.796
\n
891
\n
6044
\n
6861
\n
25.8%
\n
18.3%
\n
30.2%
\n
23.9%
\n
5.6%
\n
\n
\n
RC
\n
23.654
\n
2074
\n
7635
\n
13.945
\n
44.2%
\n
42.6%
\n
38.2%
\n
48.6%
\n
6.0%
\n
\n
\n
SRC
\n
3644
\n
599
\n
1626
\n
1419
\n
6.8%
\n
12.3%
\n
8.1%
\n
4.9%
\n
-7.4%
\n
\n
\n
Others
\n
1605
\n
19
\n
404
\n
1182
\n
3.0%
\n
0.4%
\n
2.0%
\n
4.1%
\n
3.7%
\n
\n
\n
\nOthers\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
High-rise block (16F over)
\n
387
\n
3
\n
54
\n
330
\n
0.7%
\n
0.1%
\n
0.3%
\n
1.1%
\n
1.1%
\n
\n
\n
Room on the first floor
\n
13.265
\n
894
\n
5217
\n
7154
\n
24.8%
\n
18.4%
\n
26.1%
\n
24.9%
\n
6.6%
\n
\n\n
Table 2.
Distribution of equipment in old stock, main stock, and new stock.
\n
Outside the three wards of the city center, the ratio of new stock is over 70% in Taito and Sumida wards and over 60% in Koto and Shinagawa wards, but this may be due to the supply of large-scale high-rise condominiums due to the relaxation of regulations in the 1990s. The ratio of new stock in other wards is around 50% (\nTable 3\n).
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n\n
\n
Ward
\n
Old stock
\n
Main stock
\n
New stock
\n
Total
\n
Old stock
\n
Main stock
\n
New stock
\n
\n\n\n
\n
Chiyoda
\n
39
\n
65
\n
342
\n
446
\n
8.7%
\n
14.6%
\n
76.7%
\n
\n
\n
Chuo
\n
57
\n
117
\n
740
\n
914
\n
6.2%
\n
12.8%
\n
81.0%
\n
\n
\n
Minato
\n
137
\n
182
\n
927
\n
1246
\n
11.0%
\n
14.6%
\n
74.4%
\n
\n
\n
Shinjuku
\n
284
\n
574
\n
1264
\n
2122
\n
13.4%
\n
27.0%
\n
59.6%
\n
\n
\n
Bunkyo
\n
144
\n
379
\n
706
\n
1229
\n
11.7%
\n
30.8%
\n
57.4%
\n
\n
\n
Taito
\n
86
\n
210
\n
796
\n
1092
\n
7.9%
\n
19.2%
\n
72.9%
\n
\n
\n
Sumida
\n
103
\n
348
\n
1077
\n
1528
\n
6.7%
\n
22.8%
\n
70.5%
\n
\n
\n
Kouto
\n
134
\n
454
\n
1056
\n
1644
\n
8.2%
\n
27.6%
\n
64.2%
\n
\n
\n
Shinagawa
\n
190
\n
650
\n
1463
\n
2303
\n
8.3%
\n
28.2%
\n
63.5%
\n
\n
\n
Meguro
\n
134
\n
537
\n
789
\n
1460
\n
9.2%
\n
36.8%
\n
54.0%
\n
\n
\n
Ota
\n
458
\n
2022
\n
3054
\n
5534
\n
8.3%
\n
36.5%
\n
55.2%
\n
\n
\n
Setagaya
\n
494
\n
2605
\n
2450
\n
5549
\n
8.9%
\n
46.9%
\n
44.2%
\n
\n
\n
Shibuya
\n
188
\n
425
\n
908
\n
1521
\n
12.4%
\n
27.9%
\n
59.7%
\n
\n
\n
Nakano
\n
292
\n
996
\n
1367
\n
2655
\n
11.0%
\n
37.5%
\n
51.5%
\n
\n
\n
Suginami
\n
421
\n
1915
\n
1778
\n
4114
\n
10.2%
\n
46.5%
\n
43.2%
\n
\n
\n
Toshima
\n
189
\n
687
\n
1019
\n
1895
\n
10.0%
\n
36.3%
\n
53.8%
\n
\n
\n
Kita
\n
300
\n
797
\n
1061
\n
2158
\n
13.9%
\n
36.9%
\n
49.2%
\n
\n
\n
Arakawa
\n
100
\n
339
\n
582
\n
1021
\n
9.8%
\n
33.2%
\n
57.0%
\n
\n
\n
Itabashi
\n
291
\n
1254
\n
1441
\n
2986
\n
9.7%
\n
42.0%
\n
48.3%
\n
\n
\n
Nerima
\n
243
\n
1639
\n
1796
\n
3678
\n
6.6%
\n
44.6%
\n
48.8%
\n
\n
\n
Adachi
\n
182
\n
1020
\n
1518
\n
2720
\n
6.7%
\n
37.5%
\n
55.8%
\n
\n
\n
Katsushika
\n
177
\n
926
\n
1074
\n
2177
\n
8.1%
\n
42.5%
\n
49.3%
\n
\n
\n
Edogawa
\n
225
\n
1841
\n
1492
\n
3558
\n
6.3%
\n
51.7%
\n
41.9%
\n
\n
\n
Total
\n
4868
\n
19,982
\n
28,700
\n
53,550
\n
9.1%
\n
37.3%
\n
53.6%
\n
\n\n
Table 3.
Spatial distribution of rental housing.
\n
\n
\n
3.3 Ancillary equipment rate by period of construction
\n
\n\nTable 4\n shows the ancillary equipment rate by period of construction. Equipment was classified into that ancillary to the room, ancillary to the building, and conditions of contract.11\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n\n
\n
Dependent variable
\n
ln (monthly rent) JPY
\n
\n
\n
\n
\n
\n
\n
\n\n\n
\n
Estimation method
\n
\n
OLS
\n
\n
\n
Number of observations
\n
\n
53,520
\n
4867
\n
19,975
\n
28,678
\n
\n
\n
\n
Adj R-squared
\n
\n
0.894
\n
0.853
\n
0.897
\n
0.892
\n
\n
\n
\n
\nIndependent variables\n
\n
\nMark\n
\n
\nAll\n
\n
\nOld stock\n
\n
\nMain stock\n
\n
\nNew stock\n
\n
New-old
\n
\n
\n
\nCoef.\n
\n
\nP>t\n
\n
\nCoef.\n
\n
\nP>t\n
\n
\nCoef.\n
\n
\nP>t\n
\n
\nCoef.\n
\n
\nP>t\n
\n
Coef.
\n
\n
\n
Age of unit (year)
\n
\n
−0.53%
\n
0.00
\n
−0.13%
\n
0.01
\n
−0.43%
\n
0.00
\n
−0.63%
\n
0.00
\n
−0.50%
\n
\n
\n
Old stock dummy
\n
\n
1.53%
\n
0.00
\n
(Omitted)
\n
(Omitted)
\n
(Omitted)
\n
−
\n
\n
\n
Main stock dummy
\n
−0.54%
\n
0.01
\n
(Omitted)
\n
(Omitted)
\n
(Omitted)
\n
−
\n
\n
\n
New stock dummy
\n
Baseline
\n
(Omitted)
\n
(Omitted)
\n
(Omitted)
\n
−
\n
\n
\n
Floor space (m2)
\n
\n
1.69%
\n
0.00
\n
1.60%
\n
0.00
\n
1.61%
\n
0.00
\n
1.73%
\n
0.00
\n
0.13%
\n
\n
\n
Time to Tokyo station (minutes)
\n
−0.70%
\n
0.00
\n
−0.67%
\n
0.00
\n
−0.77%
\n
0.00
\n
−0.64%
\n
0.00
\n
0.03%
\n
\n
\n
Time to the nearest station (minutes)
\n
−0.62%
\n
0.00
\n
−0.53%
\n
0.00
\n
−0.61%
\n
0.00
\n
−0.64%
\n
0.00
\n
−0.11%
\n
\n
\n
Building
\n
Wooden
\n
\n
Baseline
\n
Baseline
\n
Baseline
\n
Baseline
\n
−
\n
\n
\n
Structure
\n
Steel frame
\n
4.28%
\n
0.00
\n
7.22%
\n
0.00
\n
3.67%
\n
0.00
\n
3.51%
\n
0.00
\n
−3.71%
\n
\n
\n
\n
RC
\n
\n
9.26%
\n
0.00
\n
13.04%
\n
0.00
\n
8.41%
\n
0.00
\n
8.17%
\n
0.00
\n
−4.87%
\n
\n
\n
\n
SRC
\n
\n
10.75%
\n
0.00
\n
13.10%
\n
0.00
\n
9.72%
\n
0.00
\n
8.99%
\n
0.00
\n
−4.11%
\n
\n
\n
\n
Others
\n
\n
4.01%
\n
0.00
\n
6.83%
\n
0.11
\n
4.20%
\n
0.00
\n
3.25%
\n
0.00
\n
−3.58%
\n
\n
\n
Wards
\n
Chiyoda
\n
\n
−1.44%
\n
0.01
\n
8.72%
\n
0.00
\n
3.21%
\n
0.03
\n
−3.03%
\n
0.00
\n
−11.75%
\n
\n
\n
\n
Chuo
\n
\n
−3.77%
\n
0.00
\n
0.14%
\n
0.94
\n
−2.84%
\n
0.01
\n
−4.29%
\n
0.00
\n
−4.43%
\n
\n
\n
\n
Minato
\n
\n
12.01%
\n
0.00
\n
17.08%
\n
0.00
\n
11.20%
\n
0.00
\n
10.75%
\n
0.00
\n
−6.34%
\n
\n
\n
\n
Shinjuku
\n
\n
0.54%
\n
0.07
\n
3.46%
\n
0.00
\n
0.15%
\n
0.77
\n
−0.54%
\n
0.14
\n
−4.00%
\n
\n
\n
\n
Bunkyo
\n
\n
−5.38%
\n
0.00
\n
−4.39%
\n
0.00
\n
−5.82%
\n
0.00
\n
−5.52%
\n
0.00
\n
−1.13%
\n
\n
\n
\n
Taito
\n
\n
−14.43%
\n
0.00
\n
−12.95%
\n
0.00
\n
−14.68%
\n
0.00
\n
−14.73%
\n
0.00
\n
−1.78%
\n
\n
\n
\n
Sumida
\n
\n
−15.60%
\n
0.00
\n
−15.02%
\n
0.00
\n
−14.04%
\n
0.00
\n
−16.21%
\n
0.00
\n
−1.19%
\n
\n
\n
\n
Koto
\n
\n
−13.38%
\n
0.00
\n
−12.53%
\n
0.00
\n
−12.56%
\n
0.00
\n
−13.80%
\n
0.00
\n
−1.27%
\n
\n
\n
\n
Shinagawa
\n
\n
−6.09%
\n
0.00
\n
−2.83%
\n
0.02
\n
−6.83%
\n
0.00
\n
−6.62%
\n
0.00
\n
−3.79%
\n
\n
\n
\n
Meguro
\n
\n
8.18%
\n
0.00
\n
10.71%
\n
0.00
\n
6.95%
\n
0.00
\n
7.76%
\n
0.00
\n
−2.95%
\n
\n
\n
\n
Ota
\n
\n
−11.59%
\n
0.00
\n
−9.71%
\n
0.00
\n
−10.11%
\n
0.00
\n
−13.14%
\n
0.00
\n
−3.42%
\n
\n
\n
\n
Setagaya
\n
\n
Baseline
\n
Baseline
\n
Baseline
\n
Baseline
\n
−
\n
\n
\n
\n
Shibuya
\n
\n
10.74%
\n
0.00
\n
12.23%
\n
0.00
\n
7.93%
\n
0.00
\n
11.20%
\n
0.00
\n
−1.03%
\n
\n
\n
\n
Nakano
\n
\n
−4.79%
\n
0.00
\n
−3.33%
\n
0.00
\n
−3.76%
\n
0.00
\n
−6.01%
\n
0.00
\n
−2.68%
\n
\n
\n
\n
Suginami
\n
\n
−5.20%
\n
0.00
\n
−4.42%
\n
0.00
\n
−4.99%
\n
0.00
\n
−5.64%
\n
0.00
\n
−1.22%
\n
\n
\n
\n
Toshima
\n
\n
−7.34%
\n
0.00
\n
−4.23%
\n
0.00
\n
−6.35%
\n
0.00
\n
−9.01%
\n
0.00
\n
−4.79%
\n
\n
\n
\n
Kita
\n
\n
−16.82%
\n
0.00
\n
−14.43%
\n
0.00
\n
−16.10%
\n
0.00
\n
−17.69%
\n
0.00
\n
−3.25%
\n
\n
\n
\n
Arakawa
\n
\n
−19.82%
\n
0.00
\n
−17.14%
\n
0.00
\n
−18.83%
\n
0.00
\n
−20.71%
\n
0.00
\n
−3.57%
\n
\n
\n
\n
Itabashi
\n
\n
−15.50%
\n
0.00
\n
−15.73%
\n
0.00
\n
−15.13%
\n
0.00
\n
−15.86%
\n
0.00
\n
−0.12%
\n
\n
\n
\n
Nerima
\n
\n
−12.61%
\n
0.00
\n
−10.86%
\n
0.00
\n
−12.29%
\n
0.00
\n
−12.95%
\n
0.00
\n
−2.09%
\n
\n
\n
\n
Adachi
\n
\n
−27.31%
\n
0.00
\n
−24.71%
\n
0.00
\n
−27.17%
\n
0.00
\n
−27.90%
\n
0.00
\n
−3.19%
\n
\n
\n
\n
Katsushika
\n
\n
−26.27%
\n
0.00
\n
−24.68%
\n
0.00
\n
−26.83%
\n
0.00
\n
−25.97%
\n
0.00
\n
−1.29%
\n
\n
\n
\n
Edogawa
\n
\n
−21.84%
\n
0.00
\n
−19.56%
\n
0.00
\n
−21.90%
\n
0.00
\n
−21.92%
\n
0.00
\n
−2.35%
\n
\n
\n
Difference between max. and min.
\n
39.32%
\n
\n
41.79%
\n
\n
38.37%
\n
\n
39.10%
\n
\n
−2.69%
\n
\n\n
Table 4.
Results of hedonic equations: main estimated results.
\n
Housing equipment items are arranged in descending order of ancillary rate in all samples, and a comparison is made between old, main, and new stocks.
\n
In terms of room equipment, the five items (i) air conditioning, (ii) hot water supply, (iii) indoor washing machine area, (iv) separate bath and toilet, and (v) flooring have a high ancillary rate of over 80%. The equipments for which there is a large difference in ancillary rate between old and new stocks (ancillary rate increased) are bathroom dryer (+62.6%), system kitchen (+50.7%), toilet with washlet (+43.4%), indoor washing machine area (+38.0%), and separate washroom (+36.0%).
\n
In terms of building equipment, the ancillary rate is over 50% for the bicycle parking lot and fiber optic Internet. The equipment for which there is a large difference in ancillary rate between old and new stocks (ancillary rate increased) is automatic entrance door (+65.0%), TV intercom (+55.4%), delivery locker (+44.6%), BS antenna (+43.0%), and security camera (+30.5%). In the conditions of contract, there are no items of note except for guarantor unnecessary, which is high at 37.8%, and only guarantor unnecessary (+19.6%) has a large difference in ancillary rate between old and new stocks (ancillary rate increased), but free Internet is also +11.8%.12\n
\n
Overall, the rise in security equipment is significant in building equipment, and the rise in the equipment that improves the living convenience is significant in room equipment. In addition, the ratio of building structures also shows changes, such as wooden buildings decreasing by 8.0% and SRC by 7.4%, while steel frames increase by 5.6% and RC by 6.0%.13\n
\n
\n
\n
3.4 Estimated results
\n
\n\nTable 5\n shows the estimated results of the model. In addition, \nFigure 1\n illustrates the dummy partial regression coefficients for the equipment.
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n
\n\n
\n
Independent variables
\n
All
\n
Old stock
\n
Main stock
\n
New stock
\n
New-old
\n
\n
\n
Coef.
\n
P>t
\n
Coef.
\n
P>t
\n
Coef.
\n
P>t
\n
Coef.
\n
P>t
\n
Coef.
\n
\n\n\n
\n
High-rise block (16F over)
\n
8.74%
\n
0.00
\n
14.12%
\n
0.08
\n
4.35%
\n
0.01
\n
9.22%
\n
0.00
\n
−4.89%
\n
\n
\n
Room on the first floor
\n
−2.76%
\n
0.00
\n
−0.55%
\n
0.28
\n
−2.94%
\n
0.00
\n
−3.00%
\n
0.00
\n
−2.44%
\n
\n
\n
RE
\n
Air conditioning
\n
\n
0.82%
\n
0.00
\n
1.87%
\n
0.00
\n
0.18%
\n
0.48
\n
0.02%
\n
0.96
\n
−1.86%
\n
\n
\n
\n
Hot water supply
\n
\n
−1.77%
\n
0.00
\n
0.58%
\n
0.24
\n
−1.03%
\n
0.00
\n
−2.42%
\n
0.00
\n
−3.01%
\n
\n
\n
\n
Indoor WM area
\n
\n
1.27%
\n
0.00
\n
2.73%
\n
0.00
\n
1.73%
\n
0.00
\n
−0.77%
\n
0.00
\n
−3.50%
\n
\n
\n
\n
Flooring
\n
\nA\n
\n
0.16%
\n
0.22
\n
3.35%
\n
0.00
\n
0.50%
\n
0.01
\n
−1.81%
\n
0.00
\n
−5.17%
\n
\n
\n
\n
Separate bath and toilet
\n
\nA\n
\n
5.07%
\n
0.00
\n
5.58%
\n
0.00
\n
6.46%
\n
0.00
\n
1.55%
\n
0.00
\n
−4.03%
\n
\n
\n
\n
balcony
\n
\nA\n
\n
0.84%
\n
0.00
\n
3.28%
\n
0.00
\n
1.82%
\n
0.00
\n
0.01%
\n
0.95
\n
−3.27%
\n
\n
\n
\n
System kitchen
\n
\n
1.85%
\n
0.00
\n
4.62%
\n
0.00
\n
2.40%
\n
0.00
\n
0.79%
\n
0.00
\n
−3.83%
\n
\n
\n
\n
Separate washroom
\n
\n
2.11%
\n
0.00
\n
2.18%
\n
0.00
\n
2.35%
\n
0.00
\n
2.16%
\n
0.00
\n
−0.03%
\n
\n
\n
\n
1 gas stove
\n
\n
−0.52%
\n
0.00
\n
−1.09%
\n
0.04
\n
0.13%
\n
0.52
\n
−1.13%
\n
0.00
\n
−0.05%
\n
\n
\n
\n
Washlet
\n
\nA\n
\n
2.20%
\n
0.00
\n
3.17%
\n
0.00
\n
2.75%
\n
0.00
\n
1.16%
\n
0.00
\n
−2.01%
\n
\n
\n
\n
Bathroom dryer
\n
\nA\n
\n
1.35%
\n
0.00
\n
4.90%
\n
0.00
\n
3.07%
\n
0.00
\n
1.29%
\n
0.00
\n
−3.61%
\n
\n
\n
\n
2 gas stoves
\n
\n
−0.34%
\n
0.01
\n
−0.03%
\n
0.95
\n
1.17%
\n
0.00
\n
−0.09%
\n
0.55
\n
−0.05%
\n
\n
\n
\n
Reheating bath
\n
\nC\n
\n
2.22%
\n
0.00
\n
0.26%
\n
0.56
\n
0.06%
\n
0.82
\n
3.45%
\n
0.00
\n
3.18%
\n
\n
\n
\n
Washroom with shower
\n
\n
−1.16%
\n
0.00
\n
0.64%
\n
0.41
\n
−0.18%
\n
0.55
\n
−1.33%
\n
0.00
\n
−1.97%
\n
\n
\n
\n
Own house rental
\n
\nD\n
\n
−2.92%
\n
0.00
\n
−0.54%
\n
0.45
\n
−1.87%
\n
0.00
\n
−3.42%
\n
0.00
\n
−2.88%
\n
\n
\n
\n
IH stovetop
\n
\nD\n
\n
−1.03%
\n
0.00
\n
−0.65%
\n
0.49
\n
−1.68%
\n
0.00
\n
−1.62%
\n
0.00
\n
−0.97%
\n
\n
\n
\n
Walk-in closet
\n
\nB\n
\n
1.22%
\n
0.00
\n
4.33%
\n
0.00
\n
0.77%
\n
0.29
\n
0.88%
\n
0.00
\n
−3.45%
\n
\n
\n
\n
Counter kitchen
\n
\n
1.10%
\n
0.00
\n
2.83%
\n
0.08
\n
0.03%
\n
0.95
\n
0.72%
\n
0.00
\n
−2.11%
\n
\n
\n
\n
With loft
\n
\n
4.72%
\n
0.00
\n
5.59%
\n
0.07
\n
4.08%
\n
0.00
\n
4.19%
\n
0.00
\n
−1.40%
\n
\n
\n
\n
Underfloor heating
\n
\nC\n
\n
5.19%
\n
0.00
\n
−1.55%
\n
0.73
\n
−1.09%
\n
0.36
\n
4.97%
\n
0.00
\n
6.52%
\n
\n
\n
BE
\n
Bicycle parking lot
\n
\n
−0.94%
\n
0.00
\n
−0.71%
\n
0.09
\n
−0.70%
\n
0.00
\n
−0.96%
\n
0.00
\n
−0.25%
\n
\n
\n
\n
Fiber optic Internet
\n
\n
−1.04%
\n
0.00
\n
−1.83%
\n
0.00
\n
−0.93%
\n
0.00
\n
−0.91%
\n
0.00
\n
0.92%
\n
\n
\n
\n
TV intercom
\n
\nA\n
\n
1.08%
\n
0.00
\n
3.99%
\n
0.00
\n
1.71%
\n
0.00
\n
−0.15%
\n
0.34
\n
−4.14%
\n
\n
\n
\n
Automatic entrance door
\n
\nA\n
\n
1.74%
\n
0.00
\n
4.47%
\n
0.00
\n
2.72%
\n
0.00
\n
1.63%
\n
0.00
\n
−2.84%
\n
\n
\n
\n
Cable TV
\n
\n
−0.63%
\n
0.00
\n
−1.61%
\n
0.00
\n
−0.26%
\n
0.13
\n
−0.51%
\n
0.00
\n
1.10%
\n
\n
\n
\n
BS antenna
\n
\n
−1.25%
\n
0.00
\n
−2.58%
\n
0.01
\n
−0.05%
\n
0.83
\n
−1.45%
\n
0.00
\n
1.13%
\n
\n
\n
\n
Elevator
\n
\n
2.52%
\n
0.00
\n
2.89%
\n
0.00
\n
2.10%
\n
0.00
\n
2.63%
\n
0.00
\n
−0.26%
\n
\n
\n
\n
Tiling wall
\n
\n
−1.44%
\n
0.00
\n
−1.91%
\n
0.00
\n
−1.21%
\n
0.00
\n
−0.97%
\n
0.00
\n
0.93%
\n
\n
\n
\n
Delivery locker
\n
\nA\n
\n
2.03%
\n
0.00
\n
4.55%
\n
0.00
\n
1.42%
\n
0.00
\n
2.68%
\n
0.00
\n
−1.87%
\n
\n
\n
\n
Security camera
\n
\nC\n
\n
1.33%
\n
0.00
\n
0.62%
\n
0.45
\n
1.06%
\n
0.00
\n
1.61%
\n
0.00
\n
0.99%
\n
\n
\n
\n
CS antenna
\n
\n
0.60%
\n
0.00
\n
1.76%
\n
0.15
\n
−0.69%
\n
0.04
\n
1.25%
\n
0.00
\n
−0.51%
\n
\n
\n
\n
Garbage 24H available
\n
\nC\n
\n
−0.13%
\n
0.49
\n
−1.58%
\n
0.18
\n
−0.84%
\n
0.06
\n
0.98%
\n
0.00
\n
2.56%
\n
\n
\n
\n
Bike parking lot
\n
\nC\n
\n
0.75%
\n
0.00
\n
−0.38%
\n
0.61
\n
0.29%
\n
0.28
\n
0.94%
\n
0.00
\n
1.32%
\n
\n
\n
\n
Design by artist
\n
\n
0.45%
\n
0.02
\n
0.62%
\n
0.80
\n
1.78%
\n
0.01
\n
0.52%
\n
0.01
\n
−0.09%
\n
\n
\n
\n
Seismic structure
\n
\n
−2.25%
\n
0.00
\n
−4.11%
\n
0.05
\n
−1.95%
\n
0.00
\n
−1.82%
\n
0.00
\n
2.29%
\n
\n
\n
CC
\n
with NO guarantor
\n
\nD\n
\n
−0.82%
\n
0.00
\n
−1.47%
\n
0.00
\n
−1.07%
\n
0.00
\n
−0.23%
\n
0.08
\n
1.24%
\n
\n
\n
\n
No pets
\n
\n
0.06%
\n
0.77
\n
−1.46%
\n
0.12
\n
0.37%
\n
0.25
\n
0.47%
\n
0.07
\n
1.93%
\n
\n
\n
\n
Pet consultation
\n
\n
3.24%
\n
0.00
\n
2.85%
\n
0.00
\n
4.13%
\n
0.00
\n
3.10%
\n
0.00
\n
0.25%
\n
\n
\n
\n
Pets allowed
\n
\n
2.57%
\n
0.00
\n
2.17%
\n
0.05
\n
3.40%
\n
0.00
\n
2.35%
\n
0.00
\n
0.18%
\n
\n
\n
\n
No musical instrument
\n
\n
−0.32%
\n
0.15
\n
1.61%
\n
0.11
\n
0.22%
\n
0.54
\n
−0.83%
\n
0.00
\n
−2.44%
\n
\n
\n
\n
No office use
\n
\n
0.81%
\n
0.00
\n
−1.18%
\n
0.18
\n
0.01%
\n
0.97
\n
1.13%
\n
0.00
\n
2.31%
\n
\n
\n
\n
Office use allowed
\n
\nC\n
\n
5.04%
\n
0.00
\n
2.34%
\n
0.00
\n
4.01%
\n
0.00
\n
6.11%
\n
0.00
\n
3.77%
\n
\n
\n
\n
Free Internet
\n
\nB\n
\n
0.82%
\n
0.00
\n
3.01%
\n
0.02
\n
0.58%
\n
0.19
\n
0.68%
\n
0.00
\n
−2.33%
\n
\n
\n
\n
Contract with limited term
\n
\nB\n
\n
−0.82%
\n
0.00
\n
−2.80%
\n
0.00
\n
−0.86%
\n
0.08
\n
−0.30%
\n
0.39
\n
2.50%
\n
\n
\n
_cons
\n
\n
\n
0.00%
\n
0.00
\n
0.00%
\n
0.00
\n
0.00%
\n
0.00
\n
0.00%
\n
0.00
\n
–
\n
\n\n
Table 5.
Estimated results of room equipment (RE), building equipment (BE), and contract conditions (CC).
\n
Figure 1.
Marginal price effect on RE, BE, and CC.
\n
Looking at the estimated results, as floor area increases, rent goes up, and as the number of minutes on foot from the station increases or the railway travel time from Tokyo station increases, the rent goes down. When taking a wooden structure as the baseline of the building structure, the rent will increase in the order of steel frame, RC, and SRC. The rent varies greatly depending on the ward in which the property is located; a high-rise condominium is a positive driver, and a 1F apartment positions a negative driver for rent. These results are consistent with previous studies and the intuition of market participants.
\n
The effect of the number of years since construction differs depending on the period of construction, and as a whole, there is a −0.53% reduction in rent per year after construction. However, looking at the old/main/new period of construction dummy, the speed of reduction is high for new stock and low for old stock. This shows that the effect of years since construction is nonlinear, indicating that the decline in rent will be considerably smaller after a certain number of years. Such nonlinearity is also consistent with a series of previous studies.
\n
The influence of the ancillary equipment situation on the rent changes according to the period of construction (\nFigure 1\n). The change can be classified into the following four patterns.14\n
Pattern A: Items considered to have lost value because of commonness
In Pattern A, it is assumed that the equipment premium that was once a differentiating factor for price was lost because of the advancing commonness of equipment. This corresponds to room equipment (RE) such as flooring, separate bath and toilet, balcony, toilet with washlet, and bathroom dryer and building equipment (BE) such as TV intercom, automatic entrance door, delivery locker, and so on. In all cases, the ancillary rate has increased, so the superiority of the ancillary equipment falls, the influence on rent differs between old and new stocks, and such influence is generally small in new stock. Flooring and TV intercoms have a negative impact on new stock. This indicates that flooring and TV intercoms are no longer special equipment and do not offer price advantages.
Pattern B: Items considered to have lost value because they satisfied limited needs
In Pattern B, it is assumed that the price premium of the equipment was lost because the needs the equipment satisfied were limited in the first place and have been satisfied. The walk-in closet corresponds to this in room equipment (RE), nothing corresponds to this in building equipment (BE), and free Internet and contract with limited term correspond to this in contract conditions (CC). Contract with limited term has a negative impact on rent in new stock.
Pattern C: Items for which demand is considered to be increasing but the ancillary rate is low, and value is increasing
Pattern C is such that although consumer demand is increasing over time, a price premium exists because of the low ancillary rate in the housing stock. Equipment such as a reheating bath and underfloor heating corresponds to this in room equipment (RE), and security cameras, garbage disposal available 24-hours a day, and bike parking correspond to this in building equipment (BE). Items such as use as an office correspond to this in contract conditions (CC). In particular, the reheating bath and use as an office have a significant influence of +3.45 and +3.77%, respectively.
Pattern D: Items considered to be due to other individual factors
Items for which a price premium exists due to other factors correspond to owner-owned condominium for lease in room equipment (RE) and guarantor unnecessary in contract conditions (CC). Regarding condominium for lease, the effect of the increase in supply is considered to be caused by the change in the social situation, where the tendency for relatives to avoid guaranteeing rent obligations has strengthened.
\n\n
\n
\n
3.5 Influence of ancillary equipment situation on equipment depreciation rate
\n
\n\nFigure 2\n shows the depreciation rate of all rents (All) and for the case where the ancillary equipment situation is poor (Poor). The equipment being poor indicates there is no (i) washlet, (ii) bathroom dryer, (iii) reheating bath, (iv) TV intercom, (iv) automatic entrance door, (iv) delivery locker, or (vii) security camera. These types of equipment have become more common in recent years and can be installed in existing buildings.
\n
Figure 2.
Depreciation in rental housing.
\n
There were 13,033 properties with poor equipment; a regression analysis similar to the previous one was carried out with the logarithm of the rent as a target variable, and the regression coefficient of the years since construction was obtained. That is, as of October 2018, data points without the aforementioned equipment exist regardless of whether they are new, main, or old stock. This means that low-quality rental housing that does not have equipment that has become popular in recent years is still supplied. By extracting such data and comparing the depreciation of rental housing with new functions that benefited from technological progress and the depreciation of low-quality rental housing with no new functions, it is possible to extract the depreciation that accompanies obsolescence.
\n
In \nFigure 2\n, the depreciation rate for each period is calculated with the rent at the time of construction as 100 to demonstrate the theoretical effect of the increasing number of years since construction on rent. When comparing the depreciation rate of all rents with that of rents of properties with a poor ancillary equipment situation, the depreciation rate increases in all cases (new, main, and old stocks). Roughly 60 years after construction, the difference was found to be 5.5%.
\n
In addition to the measurement of the magnitude of the age effect accompanying obsolescence, this result means that rent depreciation can be mitigated if appropriate ancillary equipment investment is made with respect to the demands for housing equipment that have increased with economic growth and changes in lifestyle. We believe that this will provide pointers for high-level policy with respect to Japan’s rental housing market, where the aging of stock will advance in the future.
\n
\n
\n
\n
4. Conclusion and future tasks
\n
Changes in prices over time are broken down into changes due to supply-demand relationships and those caused by quality changes. In particular, this means that in markets with rapid technological progress, the price rise accompanying quality change increases as new products are introduced successively, but at the same time, in markets where such new products are introduced, the speed of obsolescence is fast.
\n
Compared with Western countries, new products are easy to create in the Japanese housing market. The background to this is there are many housing providers and a comparatively large number of companies that do business throughout Japan and overseas. Such companies possess, for example, think tanks to develop new products, and are developing integrated business from large-scale procurement of raw materials to design, construction, sales, and management.
\n
In this study, we focused on the period in which the housing was supplied and clarified the types of functions and equipment supplied to the market in each period and the extent of the marginal price effect in 2018. In addition, we measured the magnitude of obsolescence that accompanies the addition of a new function.
\n
The conclusion can be summarized as follows.
Rent is strongly influenced by the floor area, years since construction, building structure, number of minutes on foot from the nearest station, railway travel time from Tokyo station, location, and so on. This confirms conclusions provided by previous studies.
The ancillary conditions of housing equipment vary greatly depending on the construction year. This suggests that the Japanese rental housing market is strongly influenced by regulations such as the Building Standards Act and the improvement of living standards by economic growth.
Some ancillary conditions have a large influence on rent, but if the ancillary rate increases, the influence becomes smaller due to commonness, and housing equipment responding to new needs have a positive influence on rent.
Even if the number of years since construction is large, depreciation of the rent can be reduced if additional investment in appropriate housing equipment is carried out.
\n\n
These evaluations are for the present time, and they are expected to change in the future as housing equipment ancillary rates change and social conditions, lifestyles, and resident demands evolve. The conclusion of this study shows the possibility of increasing profitability by responding to resident demands and raising rent through adding ancillary equipment, even in countries in Europe and in the United States, where housing building restrictions are strict.
\n
However, several tasks remain. First, it is possible to add new functionality even to housing classified as old stock through large-scale renovation investment. In this sense, this study has not been able to measure the effect of investment in renovation. Moreover, in order to generalize the study result, it is necessary to identify appropriate housing equipment according to changes in lifestyle and social conditions, in addition to the influence of housing equipment on rent. Even if the scope is restricted to Japan, it is also necessary to consider points such as the type of differences that arise depending on the scale of the city and the standard of living and climate in different regions, as well as whether the necessary housing equipment differs according to the age, gender, family composition, income, and so on of the residents.
\n
We would like to clarify these questions as future research tasks.
\n
\n
Acknowledgments
\n
The second author gratefully acknowledges the financial support of the Nomura Foundation.
\n
\n',keywords:"quality change, housing equipment, hedonic approach, depreciation, obsolescence, cohort effectJEL classification: R31—housing supply and markets; R32—other spatial production and pricing analysis",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/67038.pdf",chapterXML:"https://mts.intechopen.com/source/xml/67038.xml",downloadPdfUrl:"/chapter/pdf-download/67038",previewPdfUrl:"/chapter/pdf-preview/67038",totalDownloads:823,totalViews:0,totalCrossrefCites:1,dateSubmitted:"October 25th 2018",dateReviewed:"April 2nd 2019",datePrePublished:"May 10th 2019",datePublished:"May 13th 2020",dateFinished:"May 10th 2019",readingETA:"0",abstract:"The Tokyo housing market is considered to be one of the fastest evolving markets in the world. In recent years, functions such as TV intercoms, bathroom dryers, system kitchens, and toilets with washlets, which are not often seen in European and US houses, have spread and become common in Japanese houses. Under such circumstances, the importance of various equipment ancillary to housing, together with the location and quality of the building, is increasingly a factor for determining the value of housing in Tokyo. This is because when a new product appears, the old product is ordered to be withdrawn from the market, or its commodity value is greatly depreciated. This study measured the economic value of improving the quality of housing with new equipment in the Tokyo rental housing market and clarified the extent of economic depreciation that is occurring due to obsolescence. According to the obtained results, new functions are being added sequentially to the Japanese rental housing according to the age of the building, and these functions are non-negligible in the determination of housing rent, even when compared with location and building structure. The effect of obsolescence due to the addition of new functions was roughly—5%.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/67038",risUrl:"/chapter/ris/67038",signatures:"Takeshi So and Chihiro Shimizu",book:{id:"8924",type:"book",title:"Modern Perspectives in Business Applications",subtitle:null,fullTitle:"Modern Perspectives in Business Applications",slug:"modern-perspectives-in-business-applications",publishedDate:"May 13th 2020",bookSignature:"Syed Abdul Rehman Khan and Selay Ilgaz Sümer",coverURL:"https://cdn.intechopen.com/books/images_new/8924.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-78984-973-8",printIsbn:"978-1-78984-972-1",pdfIsbn:"978-1-78985-225-7",isAvailableForWebshopOrdering:!0,editors:[{id:"254664",title:"Prof.",name:"Syed Abdul Rehman",middleName:null,surname:"Khan",slug:"syed-abdul-rehman-khan",fullName:"Syed Abdul Rehman Khan"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:null,sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Empirical analysis: data and estimation model",level:"1"},{id:"sec_2_2",title:"2.1 Literature review",level:"2"},{id:"sec_3_2",title:"2.2 Data",level:"2"},{id:"sec_4_2",title:"2.3 Estimation model",level:"2"},{id:"sec_6",title:"3. Verification analysis",level:"1"},{id:"sec_6_2",title:"3.1 Descriptive statistics for analysis data",level:"2"},{id:"sec_7_2",title:"3.2 Distribution of analysis data by ward",level:"2"},{id:"sec_8_2",title:"3.3 Ancillary equipment rate by period of construction",level:"2"},{id:"sec_9_2",title:"3.4 Estimated results",level:"2"},{id:"sec_10_2",title:"3.5 Influence of ancillary equipment situation on equipment depreciation rate",level:"2"},{id:"sec_12",title:"4. Conclusion and future tasks",level:"1"},{id:"sec_13",title:"Acknowledgments",level:"1"}],chapterReferences:[{id:"B1",body:'\nShimizu C, Karato K, Asami Y. Estimation of redevelopment probability using panel data-asset bubble burst and office market in Tokyo. Journal of Property Investment and Finance. 2010;28(4):285-300\n'},{id:"B2",body:'\nSirmans GS, David A, Emily N. The composition of hedonic pricing models. Journal of Real Estate Literature. 2005;13(1):1-44\n'},{id:"B3",body:'\nYoo S, Im J, Wagner JE. Variable selection for hedonic model using machine learning approaches: A case study in Onondaga County, NY. Landscape and Urban Planning. 2012;107(3):293-306\n'},{id:"B4",body:'\nLancaster K. A new approach to consumer theory. Journal of Political Economy. 1966;74(2):132-157\n'},{id:"B5",body:'\nRosen S. Hedonic prices and implicit markets: Product differentiation in pure competition. Journal of Political Economy. 1974;82(1):34-55\n'},{id:"B6",body:'\nShimizu C, Karato K. Property price index theory and estimation: A survey. CSIS Discussion Paper Series. The University of Tokyo; 2018. Available from: http://www.csis.u-tokyo.ac.jp/wp-content/uploads/2018/11/156.pdf\n\n'},{id:"B7",body:'\nEkeland I, Heckman J, Nesheim L. Identification and estimation of hedonic models. Journal of Political Economy. 2004;112(S1):S60-S109\n'},{id:"B8",body:'\nNishi H, Asami Y, Shimizu C. Housing features and rent: Estimating the microstructures of rental housing. International Journal of Housing Market and Analysis. 2018. forthcoming. DOI: 10.1108/IJHMA-09-2018-0067\n'},{id:"B9",body:'\nBillings SB. Hedonic amenity valuation and housing renovations. Real Estate Economics. 2015;43(3):652-682\n'},{id:"B10",body:'\nMcMillen DP, Thorsnes P. Housing renovations and the quantile repeat sales price index. Real Estate Economics. 2006;34(4):567-584\n'},{id:"B11",body:'\nShimizu C. Estimation of hedonic single-family house price function considering neighborhood effect variables. Sustainability (Switzerland). 2014;6(5):2946-2960\n'},{id:"B12",body:'\nGao X, Asami Y. The external effects of local attributes on living environment in detached residential blocks in Tokyo. Urban Studies. 2001;38(3):487-505\n'},{id:"B13",body:'\nFuerst F, Shimizu C. The rise of eco-labels in the Japanese housing market. Journal of Japanese and International Economy. 2016;39:108-122\n'},{id:"B14",body:'\nNelson RH. Housing facilities, site advantages and rent. Journal of Regional Science. 1972;12(2):249-259\n'},{id:"B15",body:'\nChau KW, Chin TL. A critical review of literature on the hedonic price model. International Journal for Housing Science and Its Applications. 2003;2(27):145-165\n'},{id:"B16",body:'\nShimizu C, Nishimura K, Watanabe T. Housing prices in Tokyo: A comparison of hedonic and repeat sales measures. Journal of Economics and Statistics. 2010b;230:792-813\n'},{id:"B17",body:'\nShimizu C, Takatsuji H, Ono H, Nishimura KG. Structural and temporal changes in the housing market and hedonic housing price indices. International Journal of Housing Markets and Analysis. 2010c;3(4):351-368\n'},{id:"B18",body:'\nKarato K, Movshuk O, Shimizu C. Semiparametric estimation of time, age and cohort effects in an hedonic model of house prices. Asian Economic Journal. 2015;29(4):325-345\n'},{id:"B19",body:'\nShimizu C, Nishimura KG, Karato K. Nonlinearity of housing price structure—Secondhand condominium market in Tokyo Metropolitan Area. International Journal of Housing Markets and Analysis. 2014;7(3):459-488\n'},{id:"B20",body:'\nDiewert WE, Shimizu C. Residential property price indexes for Tokyo. Macroeconomic Dynamics. 2015;19(8):1659-1714\n'},{id:"B21",body:'\nDiewert WE, Shimizu C. Hedonic regression models for Tokyo condominium sales. Regional Science and Urban Economics. 2016;60:300-315\n'},{id:"B22",body:'\nDiewert WE, Shimizu C. Alternative approaches to commercial property price indexes for Tokyo. Review of Income and Wealth. 2017;63(3):492-519\n'},{id:"B23",body:'\nDiewert WE, Shimizu C. Alternative land price indexes for commercial properties in Tokyo. In: Discussion Paper 17–07. Vancouver School of Economics: University of British Columbia; 2017\n'}],footnotes:[{id:"fn1",explanation:"The Bombing of Tokyo was a series of firebombing air raids in Second World War. This was conducted on the night of 9–10 March 1945, 16 square miles (41 km2) of central Tokyo were destroyed, leaving an estimated 100,000 civilians dead and over 1 million homeless."},{id:"fn2",explanation:"Although the improvement of low-quality stock developed during the postwar reconstruction period has been carried out in many areas, some areas remain in which stock has not improved, referred to as “high density wooden structure areas.” Since these areas are vulnerable to earthquake disasters and so on, improvement is urgently required."},{id:"fn3",explanation:"The Great Hanshin earthquake, or Kobe earthquake, occurred on January 17, 1995 in the southern part of Hyōgo Prefecture, Japan, when combined with Osaka, known as Hanshin. Up to 6434 people lost their lives."},{id:"fn4",explanation:"The Great East Japan Earthquake occurred on March 11, 2011. The report from the Japanese National Police Agency report in 2018 confirms 15,896 deaths, 6157 injured, and 2537 people missing across twenty prefectures."},{id:"fn5",explanation:"In response to major disasters, the Japanese Building Standards Law was revised. The first major revision of the Building Standards Law was in 1991, and the revision strengthened the earthquake resistance standards. After that, following the two great earthquakes, the standards strengthened."},{id:"fn6",explanation:"It should be noted that the data used are only for adverts appearing as of October 2018, and do not represent the situation of the entire housing stock."},{id:"fn7",explanation:"Analytical data were prepared using the following conditions. (a) The average and standard deviation of the rent was calculated, and data of a value that is the average plus twice the standard deviation (249,000 yen) were deleted. At the same time, data on rents of 30,000 yen or less that market participants recognize as the lower limit of market rent were deleted (this level is a value larger than the average minus twice the standard deviation). (b) Data on floor area less than 15 m2 (rental housing of floor area less than this is generally considered unsuitable for habitation) or over 100 m2 (generally housing of over 100 m2 is for the very wealthy) were deleted. (c) Data on housing exceeding 50 years of age (built before 1967), which were exceedingly few, were deleted."},{id:"fn8",explanation:"When the market structure changes, it is necessary to construct a model to absorb the change [16, 17]. In addition, Karato et al. [18] propose an estimation method to discriminate between aging, period of construction, and time effects. In this research, we avoided these problems by using cross-sectional data and simply classified it into three period categories according to age."},{id:"fn9",explanation:"The number of old stock data for 1968–1981 was relatively small at 4868, the number of properties built between 1992 and 1999 was 19,982, and the number of properties built between 2000 and 2018 was 28,700."},{id:"fn10",explanation:"This result is consistent with the results of Shimizu et al. [1]."},{id:"fn11",explanation:"Although it seems that the housing equipment ancillary to the room and building fluctuates somewhat due to renewal and so on, the equipment seems to be influenced by the construction date. Attention must be given to the fact that contract conditions may be changed regardless of the construction date because physical investment is unnecessary."},{id:"fn12",explanation:"Traditionally, when renting out a house in the Japanese rental housing market, it is necessary to have a guarantor to hedge the risk of nonpayment of rent. Since the guarantor is liable in the case of unpaid rent, relatives often become the guarantor, but as the size of families decreases, it is becoming difficult to find a guarantor. Under such circumstances, rent-guarantee companies have appeared, and systems that eliminate the need for a guarantor by paying a set insurance premium have been introduced."},{id:"fn13",explanation:"In addition, although the ratio of high-rise condominiums is rising, it is at about 1%, and even the number of 1F room positions is increasing."},{id:"fn14",explanation:"Shimizu et al. [19] and Diewert and Shimizu [20, 21, 22] estimate a depreciation structure for the detached house and apartment market and the office market in Tokyo. The estimated results in this study show roughly the same form. As Diewert and Shimizu [23] covers the office market, durability is longer than for rental housing. Therefore, it has been reported that this will become a positive driver for rent at a stage exceeding 40 years after construction. The same tendency is observed in research targeting commercial real estate markets in Europe, the United States, and so on. The reason for this could be the influence of large costs for large-scale repairs and survivorship bias caused by higher-quality buildings having longer service life and only such buildings remaining. In this study, such bias is not observed, as it is limited to a certain period of time."}],contributors:[{corresp:null,contributorFullName:"Takeshi So",address:null,affiliation:'
Institute of Future Design in Housing Market, Daito Trust Construction Co. Ltd., Japan
Center for Spatial Information Science, The University of Tokyo, Japan
Center for Spatial Information Science, The University of Tokyo, Japan
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Increased numbers of both clinical and research articles associated with the accelerated orthodontic treatment have been published in peer-reviewed journals in the last couple of years. Biochemical approaches such as administration of drugs, vitamins, and proteins and/or physical approaches such as surgery, vibration, and photobiomodulation have been widely reported and demonstrated the predicted outcome; however, the results are controversial. Very few reports addressed on genetic background of patients or utilization of molecular biological approach on the accelerated orthodontic treatment. 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Le Fort I osteotomy in maxilla and sagittal split ramus osteotomies (SSRO) in mandible are commonly used techniques to solve the deformity problems of the facial skeleton; therefore, the scope of this chapter is going to be including my personal experience and some technical details with Le Fort I and SSRO.",book:{id:"7139",slug:"current-approaches-in-orthodontics",title:"Current Approaches in Orthodontics",fullTitle:"Current Approaches in Orthodontics"},signatures:"Mustafa Sancar Atac",authors:[{id:"256903",title:"Dr.",name:"Mustafa Sancar",middleName:null,surname:"Atac",slug:"mustafa-sancar-atac",fullName:"Mustafa Sancar Atac"}]},{id:"48165",title:"3D Scanning, Imaging, and Printing in Orthodontics",slug:"3d-scanning-imaging-and-printing-in-orthodontics",totalDownloads:6462,totalCrossrefCites:22,totalDimensionsCites:39,abstract:null,book:{id:"4574",slug:"issues-in-contemporary-orthodontics",title:"Issues in Contemporary Orthodontics",fullTitle:"Issues in Contemporary Orthodontics"},signatures:"Emilia Taneva, Budi Kusnoto and Carla A. 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The quantitative aspect of pain was assessed using the Visual Analogue Scale, while the qualitative aspect of pain was evaluated using the Moroccan Short Form of McGILL Pain questionnaire. In all three groups experienced pain after activation tended to decrease in the following week. This pain was greater in patients with conventional braces and less in patients with aligners. Using the M-SF-MPQ to describe the qualitative aspect of the pain revealed that the “cramping مزير,” “aching تيألم ” aspect was most accentuated in the 3 groups. Medication intake was correlated with the intensity of pain experienced in all 3 systems. As for the impact of pain on daily activities, patients in groups of conventional and self-ligating braces showed more pain than those in the aligners group. Overall, aligners were less painful than conventional and self-ligating appliances. Patients did not suffer from an alteration in their quality of life due to orthodontic treatment.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Farid Bourzgui, Rania Fastani, Salwa Khairat, Samir Diouny, Mohamed El Had, Zineb Serhier and Mohamed Bennani Othmani"},{id:"80223",title:"Bridging the Gap: Nasoalveolar Moulding in Early Cleft Palate Rehabilitation",slug:"bridging-the-gap-nasoalveolar-moulding-in-early-cleft-palate-rehabilitation",totalDownloads:56,totalDimensionsCites:0,doi:"10.5772/intechopen.101986",abstract:"Orofacial clefts (OFC) are among the commonest birth defect in developed and developing countries alike. In underdeveloped and developing countries, babies born with oral clefts are generally anaemic with low birth weight and may be unfit for surgery. The surgical reconstruction is also challenging and the aesthetic outcome cannot be guaranteed by the surgeon. Presurgical nasoalveolar moulding (PNAM) has been suggested to bridge the gap between the clefted segments before surgical repair. It is a simple yet effective technique that needs to be initiated at the right time and age to achieve ideal functional and aesthetic outcomes. This chapter highlights the effectiveness of the nasoalveolar moulding technique and details the manner in which the appliance is fabricated and activated.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Amanda Nadia Ferreira"},{id:"80186",title:"Effects of Various Dentofacial Orthopedic and Orthognathic Treatment Modalities on Pharyngeal Airway",slug:"effects-of-various-dentofacial-orthopedic-and-orthognathic-treatment-modalities-on-pharyngeal-airway",totalDownloads:73,totalDimensionsCites:0,doi:"10.5772/intechopen.101719",abstract:"The function of respiration is highly relevant to orthodontic diagnosis and treatment planning. Significant relationships between pharyngeal, craniofacial as well as dentofacial structures have been reported in several studies. Many authors have emphasized that mouth breathing is concomitantly associated with constricted airway causing obstructive sleep apnoea. Associated symptoms can be cured with correction of either skeletal or dental problems or both. Therefore it would be very intriguing to understand and interpret the airway during diagnosis and treatment planning for a clear view of changes in the airway dimensions during the course of orthodontic treatment using various treatment modalities. Therefore a complete understanding of the concept of airway should be considered as an important one. This chapter gives us an insight to the intricate detailing on how the various orthodontic and dentofacial orthopedic treatment signifies the changes in the dimensions of pharyngeal airway.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Tejashri Pradhan and Aarti Sethia"},{id:"78834",title:"Current Methods for Acceleration of Orthodontic Tooth Movement",slug:"current-methods-for-acceleration-of-orthodontic-tooth-movement",totalDownloads:108,totalDimensionsCites:0,doi:"10.5772/intechopen.100221",abstract:"The awareness of the society and, accordingly, the number of patients who need orthodontic treatment has increased gradually. Nowadays, the importance of the concept of time has focused the attention of researchers on the completion of orthodontic treatments in a shorter time. Heavy forces applied to shorten the treatment period in orthodontic treatments cause many undesirable conditions, such as root resorption, crushing of periodontal fibers, and formation of hyalinization tissue. Therefore, researchers are working on methods that will accelerate orthodontic tooth movement and shorten the treatment time. In this section, applications that accelerate orthodontic tooth movement will be discussed.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Mehmet Akin and Leyla Cime Akbaydogan"},{id:"79100",title:"Orthodontics and the Periodontium: A Symbiotic Relationship",slug:"orthodontics-and-the-periodontium-a-symbiotic-relationship",totalDownloads:66,totalDimensionsCites:0,doi:"10.5772/intechopen.100801",abstract:"The force applied by the orthodontist to facilitate the orderly movement of teeth to their new position may have deleterious effects on the most important structure involved in the procedure—the periodontium. This chapter endeavors to provide an overview of the biological processes that play a role in achieving the patient’s as well as the orthodontist’s objective.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Betsy Sara Thomas and Mohan Alexander"},{id:"79680",title:"Digital Workflow for Homemade Aligner",slug:"digital-workflow-for-homemade-aligner",totalDownloads:180,totalDimensionsCites:0,doi:"10.5772/intechopen.100347",abstract:"Advanced digital technology is rapidly changing the world, as well as transforming the dental profession. The adoption of digital technologies in dental offices allied with efficient processes and accurate high-strength materials are replacing conventional aligners workflows to improve overall patients’ experiences and outcomes. Various digital devices such as 3D printers, intraoral and face scanners, cone-beam computed tomography (CBCT), software for computer 3D ortho setup, and 3D printing provide new potential alternatives to replace the traditional outsourced workflow for aligners. With this new technology, the entire process for bringing clear aligner production in-office can significantly reduce laboratory bills and increase patient case acceptance to provide high-quality and customized aligner therapy.",book:{id:"10780",title:"Current Trends in Orthodontics",coverURL:"https://cdn.intechopen.com/books/images_new/10780.jpg"},signatures:"Dalal Elmoutawakkil and Nabil Hacib"}],onlineFirstChaptersTotal:17},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:9,numberOfPublishedChapters:87,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:98,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:27,numberOfPublishedChapters:287,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:139,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:0,numberOfUpcomingTopics:2,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!1},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:10,numberOfPublishedChapters:103,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:12,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:0,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!1},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:10,numberOfOpenTopics:4,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. 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