Anda di halaman 1dari 6
<a href=pediatric dental journal 28 (2018) 1 e 6 Available online at w w w . s c i e n c e d i r e c t . c o m Pediatric Dental Journal journal homepage: w w w . e l s e v i e r . c o m / l o c a t e / p d j Review Impact of a high-fat diet on bone health during growth Yuko Fujita Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, Kitakyushu, Japan article info abstract Article history: Background: An inappropriate eating habit is a relatively easily modified risk factor for Received 16 October 2017 Accepted 1 November 2017 Available online 2 December 2017 obesity and osteoporosis in adults. The consumption of high-fat foods is known to induce obesity. Although numerous studies have documented a relationship between high-fat diet (HFD)-induced obesity and osteoporosis, no consensus has been reached. In addition, few Keywords: data on the relationships between mandibular properties and an HFD in the growth period are available. High-fat diet Objective: This review aims to summarize current findings related to these issues, focusing Obesity on the influence of an HFD on mandibular health, including mechanisms of periodontal Jaw bone disease development. Leptin Main results: Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD-induced obesity reflect a state of noninvasive and noninfective inflammation. Authors ' conclusions: These results are related to the potential association between meta- bolic stress and systemic inflammatory changes occurring in bone and other tissues. © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. Contents 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 2. High-fat diet e induced obesity and bone mass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 3. Relationships among a high-fat diet, leptin, and bone mineral density 2 4. diet and inflammation High-fat in bone tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 5. diet e induced obesity and High-fat periodontal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Conclusion 6. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 * Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, 2-6-1 Manaduru, Kokurakita-ku, 803-8580 Kitakyushu, Japan. E-mail address: y-fujita@kyu-dent.ac.jp . https://doi.org/10.1016/j.pdj.2017.11.003 0917-2394/ © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. " id="pdf-obj-0-7" src="pdf-obj-0-7.jpg">

Available online at www.sciencedirect.com

Pediatric Dental Journal

journal homepage: www.elsevier.com/locate/pdj

<a href=pediatric dental journal 28 (2018) 1 e 6 Available online at w w w . s c i e n c e d i r e c t . c o m Pediatric Dental Journal journal homepage: w w w . e l s e v i e r . c o m / l o c a t e / p d j Review Impact of a high-fat diet on bone health during growth Yuko Fujita Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, Kitakyushu, Japan article info abstract Article history: Background: An inappropriate eating habit is a relatively easily modified risk factor for Received 16 October 2017 Accepted 1 November 2017 Available online 2 December 2017 obesity and osteoporosis in adults. The consumption of high-fat foods is known to induce obesity. Although numerous studies have documented a relationship between high-fat diet (HFD)-induced obesity and osteoporosis, no consensus has been reached. In addition, few Keywords: data on the relationships between mandibular properties and an HFD in the growth period are available. High-fat diet Objective: This review aims to summarize current findings related to these issues, focusing Obesity on the influence of an HFD on mandibular health, including mechanisms of periodontal Jaw bone disease development. Leptin Main results: Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD-induced obesity reflect a state of noninvasive and noninfective inflammation. Authors ' conclusions: These results are related to the potential association between meta- bolic stress and systemic inflammatory changes occurring in bone and other tissues. © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. Contents 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 2. High-fat diet e induced obesity and bone mass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 3. Relationships among a high-fat diet, leptin, and bone mineral density 2 4. diet and inflammation High-fat in bone tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 5. diet e induced obesity and High-fat periodontal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Conclusion 6. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 * Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, 2-6-1 Manaduru, Kokurakita-ku, 803-8580 Kitakyushu, Japan. E-mail address: y-fujita@kyu-dent.ac.jp . https://doi.org/10.1016/j.pdj.2017.11.003 0917-2394/ © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. " id="pdf-obj-0-64" src="pdf-obj-0-64.jpg">
<a href=pediatric dental journal 28 (2018) 1 e 6 Available online at w w w . s c i e n c e d i r e c t . c o m Pediatric Dental Journal journal homepage: w w w . e l s e v i e r . c o m / l o c a t e / p d j Review Impact of a high-fat diet on bone health during growth Yuko Fujita Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, Kitakyushu, Japan article info abstract Article history: Background: An inappropriate eating habit is a relatively easily modified risk factor for Received 16 October 2017 Accepted 1 November 2017 Available online 2 December 2017 obesity and osteoporosis in adults. The consumption of high-fat foods is known to induce obesity. Although numerous studies have documented a relationship between high-fat diet (HFD)-induced obesity and osteoporosis, no consensus has been reached. In addition, few Keywords: data on the relationships between mandibular properties and an HFD in the growth period are available. High-fat diet Objective: This review aims to summarize current findings related to these issues, focusing Obesity on the influence of an HFD on mandibular health, including mechanisms of periodontal Jaw bone disease development. Leptin Main results: Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD-induced obesity reflect a state of noninvasive and noninfective inflammation. Authors ' conclusions: These results are related to the potential association between meta- bolic stress and systemic inflammatory changes occurring in bone and other tissues. © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. Contents 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 2. High-fat diet e induced obesity and bone mass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 3. Relationships among a high-fat diet, leptin, and bone mineral density 2 4. diet and inflammation High-fat in bone tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 5. diet e induced obesity and High-fat periodontal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Conclusion 6. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 * Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, 2-6-1 Manaduru, Kokurakita-ku, 803-8580 Kitakyushu, Japan. E-mail address: y-fujita@kyu-dent.ac.jp . https://doi.org/10.1016/j.pdj.2017.11.003 0917-2394/ © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. " id="pdf-obj-0-66" src="pdf-obj-0-66.jpg">

Review

Impact of a high-fat diet on bone health during growth

Yuko Fujita *

<a href=pediatric dental journal 28 (2018) 1 e 6 Available online at w w w . s c i e n c e d i r e c t . c o m Pediatric Dental Journal journal homepage: w w w . e l s e v i e r . c o m / l o c a t e / p d j Review Impact of a high-fat diet on bone health during growth Yuko Fujita Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, Kitakyushu, Japan article info abstract Article history: Background: An inappropriate eating habit is a relatively easily modified risk factor for Received 16 October 2017 Accepted 1 November 2017 Available online 2 December 2017 obesity and osteoporosis in adults. The consumption of high-fat foods is known to induce obesity. Although numerous studies have documented a relationship between high-fat diet (HFD)-induced obesity and osteoporosis, no consensus has been reached. In addition, few Keywords: data on the relationships between mandibular properties and an HFD in the growth period are available. High-fat diet Objective: This review aims to summarize current findings related to these issues, focusing Obesity on the influence of an HFD on mandibular health, including mechanisms of periodontal Jaw bone disease development. Leptin Main results: Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD-induced obesity reflect a state of noninvasive and noninfective inflammation. Authors ' conclusions: These results are related to the potential association between meta- bolic stress and systemic inflammatory changes occurring in bone and other tissues. © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. Contents 1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 2. High-fat diet e induced obesity and bone mass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 3. Relationships among a high-fat diet, leptin, and bone mineral density 2 4. diet and inflammation High-fat in bone tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 5. diet e induced obesity and High-fat periodontal disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Conclusion 6. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Conflict of interest . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4 * Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, 2-6-1 Manaduru, Kokurakita-ku, 803-8580 Kitakyushu, Japan. E-mail address: y-fujita@kyu-dent.ac.jp . https://doi.org/10.1016/j.pdj.2017.11.003 0917-2394/ © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved. " id="pdf-obj-0-75" src="pdf-obj-0-75.jpg">

Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, Kitakyushu, Japan

article info

abstract

Article history:

Background: An inappropriate eating habit is a relatively easily modified risk factor for

Received 16 October 2017 Accepted 1 November 2017 Available online 2 December 2017

obesity and osteoporosis in adults. The consumption of high-fat foods is known to induce obesity. Although numerous studies have documented a relationship between high-fat diet (HFD)-induced obesity and osteoporosis, no consensus has been reached. In addition, few

Keywords:

data on the relationships between mandibular properties and an HFD in the growth period are available.

High-fat diet

Objective: This review aims to summarize current findings related to these issues, focusing

Obesity

on the influence of an HFD on mandibular health, including mechanisms of periodontal

Jaw bone

disease development.

Leptin

Main results: Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD-induced obesity reflect a state of noninvasive and noninfective inflammation. Authors' conclusions: These results are related to the potential association between meta- bolic stress and systemic inflammatory changes occurring in bone and other tissues. © 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved.

Contents

  • 1. Introduction

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  • 2. High-fat dieteinduced obesity and bone mass

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  • 3. Relationships among a high-fat

 

diet, leptin, and bone mineral density

 

2

  • 4. diet and inflammation

High-fat

in

bone tissue

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  • 5. dieteinduced obesity and

High-fat

periodontal

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Conclusion

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Conflict of interest

 

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Acknowledgements

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References

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* Division of Developmental Stomatognathic Function Science, Department of Health Promotion, Kyushu Dental University, 2-6-1 Manaduru, Kokurakita-ku, 803-8580 Kitakyushu, Japan. E-mail address: y-fujita@kyu-dent.ac.jp.

0917-2394/© 2017 Japanese Society of Pediatric Dentistry. Published by Elsevier Ltd. All rights reserved.

  • 1. Introduction

The prevalence of overweight and obesity is increasing worldwide [1]. In 2015, 107.7 million children and 603.7 million adults were obese. Since 1980, the prevalence of obesity has doubled in more than 70 countries and has increased continuously in most other countries. Although the preva- lence of obesity is lower among children than among adults, the rate of increase in childhood obesity has been greater than the rate of increase in adult obesity in many countries [2]. In recent decades, the eating habits of children and adolescents have undergone many changes due to lifestyle diversification in many countries. [3,4]. In Japan, the National Health and Nutrition Survey showed that mean fat intake increased from 25.8 g/day in 1961 to 57.0 g/day in 2015 [5]. Overweight children are at greater risk of developing type 2 diabetes, hypertension, and hyperlipidemia, which in turn increase the risk of car- diovascular disease later in life.[6] The development of obesity and osteoporosis in adults can be traced to dietary intake and physical activity during childhood and adolescence. Inappropriate nutritional intake is a relatively easily modified risk factor for obesity and oste- oporosis. The relationship between the consumption of high- fat foods and obesity is well established [7], but whether it affects bone architecture in childhood and adolescence re- mains controversial. In this review, I summarize the effects of high-fat diet (HFD)-induced obesity on bone health, including the health of alveolar and periodontal bone, and examine the relationship between leptin and bone mass using current findings from human and animal studies. The mechanisms of bone loss due to HFD-induced obesity are also discussed.

  • 2. High-fat dieteinduced obesity and bone

mass

Although a relationship between obesity and osteoporosis has been proposed in the clinical literature [8e10], no consensus has been reached. Several researchers have observed an increased fracture incidence in obese adolescents and chil- dren compared with age-matched controls [8,9]. Additionally, bone fragility may occur in obese children and adolescents because of malnutrition [10]. In animal studies, a positive correlation between obesity and long-bone density was found in 4-week-old male mice fed an HFD for 19 weeks [11], whereas obesity was correlated negatively with long-bone mass in 6-week-old male mice fed an HFD for 14 weeks and 7-week-old male mice fed an HFD for 24 weeks [12,13]. Bartelt et al. showed that HFD-induced obesity did not significantly affect long-bone mass in 4- week-old male mice treated for 16 weeks [14]. They sug- gested that conflicting results from previous studies regarding the relationship between HFD-induced obesity and bone mass were attributable to differences in the fatty acid profiles of the diets. Several studies have shown associations between the fatty acid compositions of diets and bone health. Weiss et al. reported that a higher ratio of linoleic acid (n-6) to a-linolenic acid (n-3) was associated with detrimental effects on bone

health in humans [15], and Watkins et al. showed that a lower ratio of dietary n-6/n-3 was associated with the promotion of bone formation in rats [16]. Bartelt et al. proposed that more precise data could be obtained by considering the fatty acid ratio of dietary components when choosing standard diets and HFDs [14]. However, regardless of the changes in bone mass, many studies have shown significant increases in the size and number of adipocytes in the long-bone marrow of mice with HFD-induced obesity [13,14,17e19]. These findings suggest that HFD-induced obesity causes significant bone loss in mice, due mainly to resorptive changes in the trabecular architecture caused by the increase in, and enlargement of, adipocytes in bone marrow. However, the factors mediating such environmental changes in bone marrow, and the ways in which those mediators and bone-marrow adiposity affect bone metabolism, remain unclear. In microecomputed tomography analyses, 7-week-old male mice fed an HFD for 4 weeks showed significantly reduced trabecular bone volume, cortical bone thickness, and cortical bone cross-sectional area in the mandible compared with control mice fed a standard diet. In addition, significant de- creases in cortical bone density in HFD-fed mice relative to age- matched controls were observed after 12 weeks of HFD treat- ment. Although cortical bone formation in the mandible was slower in HFD-fed mice than in control mice, bone formation on the periosteal surface increased with age in both groups for 12 weeks [20]. These data support the difference in responses of trabecular and cortical bone to diet-induced obesity; bone loss at these two sites is regulated differentially in mice.

  • 3. Relationships among a high-fat diet,

leptin, and bone mineral density

A clinical investigation of the relationship between obesity and osteoporosis suggested that adipose tissue influences bone mineral density through the production of hormones and adipokines, such as leptin [10]. Generally, leptin is known to be an important circulating signal that inhibits food intake and enhances energy expenditure through its actions in the brain [21]. Therefore, several researchers have suggested that an HFD plays a key role in the development of leptin resistance in animals with HFD-induced obesity [22,23]. In confirmation of this proposed role, Choi et al. showed that energy expenditure was lower in mice fed an HFD than in those few a low-fat diet, despite the similarity in intake between the two groups [24]. The relationship between leptin and bone is complex, with diverging effects depending on whether central or peripheral mechanisms are in operation [25,26]. Centrally, leptin has been shown to inhibit bone formation through a hypotha- lamic relay, and this effect is suppressed by b blockers [27,28]. Peripherally, leptin has a positive effect on bone in rats [29]; an in vitro study also showed that leptin promotes increased production of the potent antiresorptive factor osteoprotegerin by osteoblasts [30]. Studies involving children have documented a direct rela- tionship between the serum leptin concentration and bone mass, but conflicting findings have been reported [31e33]; in one study, the serum leptin concentration was not related to bone mineral density in boys or girls [34].

Seven-week-old male mice fed an HFD for 12 weeks showed a significant increase in the serum leptin level compared with age-matched controls, and the serum leptin level was correlated negatively with trabecular bone mineral density in the tibia [19]; these findings were consistent with those of Patsch et al. [13]. In contrast, Iwaniec et al. demon- strated that leptin was not required for increased femoral cortical bone mass associated with increased body mass in leptin-deficient ob/ob and diet-induced obese mouse models [35]. These data support the correlation between trabecular, but not cortical, bone mass and the serum leptin level in mice with diet-induced obesity.

  • 4. High-fat diet and inflammation in bone

tissue

Several in vitro and in vivo studies have shown that hyper- nutrition leads to endoplasmic reticulum stress induced by free fatty acidemediated reactive oxygen species (ROS), and thus also to inflammation, in adipose tissue [36e38]. Another study showed that oxidative stress causes alveolar bone resorption in a mouse model of metabolic syndrome [39]. Oxidative stress is characterized by an increased ROS level, which disrupts the intracellular reductioneoxidation balance [40]. Recent animal studies have also shown that an HFD contributes to obesity in association with a state of chronic inflammation [41,42], and elevates the production of pro-inflammatory cytokines, including tumor necrosis factor-a, interleukin (IL)-1b, and IL-6, which are released from adipocytes and macrophages via activation of the c-Jun N-terminal kinase and nuclear factor-kB pathways [37,43,44]. These data suggest that an increase in the

ROS level induces inflammatory changes in adipocytes in bone marrow. In addition, Dib et al. showed that leptin acts as a pro- inflammatory adipocytokine in peripheral tissues of mice [45]. These cytokines have been shown to increase osteoclast dif- ferentiation via the RANKL/RANK/OPG pathway [46]. Halade et al. showed that significantly elevated levels of pro- inflammatory cytokines, due to the accumulation of adipo- cytes in bone marrow, result in an increase in bone resorption in mice fed an HFD [47]. Kyung et al. showed that osteoclast differentiation and bone resorption are stimulated in bone marrowederived macrophages from obese mice [48]. Other studies have suggested that obesity increases bone-marrow adipogenesis, while inhibiting osteoblastogenesis, because ad- ipocytes and osteoblasts are derived from a common multi- potent mesenchymal stem cell [49,50]. Moreover, oxidative stress has been shown to inhibit osteoblastogenesis in vitro [51,52]. Thus, these data suggest that the deterioration of bone structure in HFD-fed mice is due to an abnormal ROS level in adipocytes, which increases inflammation in bone marrow and other tissues, increases bone resorption, and decreases bone formation. These findings are summarized in Fig. 1.

  • 5. High-fat dieteinduced obesity and

periodontal disease

In a recent report, researchers suggested that systemic osteo- porosis is linked to periodontal bone loss, based on significant up-regulation of inflammatory cytokines in the bone and bone- marrow cells of rats with osteoporosis [53]. Several animal studies have also linked obesity to type 2 diabetes, and hyper- caloric diet inducedeobesity to morbidity from periodontal

<a href=pediatric dental journal 28 (2018) 1 e 6 3 Seven-week-old male mice fed an HFD for 12 weeks showed a significant increase in the serum leptin level compared with age-matched controls, and the serum leptin level was correlated negatively with trabecular bone mineral density in the tibia [19] ; these findings were consistent with those of Patsch et al. [13] . In contrast, Iwaniec et al. demon- strated that leptin was not required for increased femoral cortical bone mass associated with increased body mass in leptin-deficient ob/ob and diet-induced obese mouse models [35] . These data support the correlation between trabecular, but not cortical, bone mass and the serum leptin level in mice with diet-induced obesity. 4. High-fat diet and inflammation in bone tissue Several in vitro and in vivo studies have shown that hyper- nutrition leads to endoplasmic reticulum stress induced by free fatty acid e mediated reactive oxygen species (ROS), and thus also to inflammation, in adipose tissue [36 e 38] . Another study showed that oxidative stress causes alveolar bone resorption in a mouse model of metabolic syndrome [39] . Oxidative stress is characterized by an increased ROS level, which disrupts the intracellular reduction e oxidation balance [40] . Recent animal studies have also shown that an HFD contributes to obesity in association with a state of chronic inflammation [41,42] , and elevates the production of pro-inflammatory cytokines, including tumor necrosis factor- a , interleukin (IL)-1 b , and IL-6, which are released from adipocytes and macrophages via activation of the c-Jun N-terminal kinase and nuclear factor- k B pathways [37,43,44] . These data suggest that an increase in the ROS level induces inflammatory changes in adipocytes in bone marrow. In addition, Dib et al. showed that leptin acts as a pro- inflammatory adipocytokine in peripheral tissues of mice [45] . These cytokines have been shown to increase osteoclast dif- ferentiation via the RANKL/RANK/OPG pathway [46] . Halade et al. showed that significantly elevated levels of pro- inflammatory cytokines, due to the accumulation of adipo- cytes in bone marrow, result in an increase in bone resorption in mice fed an HFD [47] . Kyung et al. showed that osteoclast differentiation and bone resorption are stimulated in bone marrow e derived macrophages from obese mice [48] . Other studies have suggested that obesity increases bone-marrow adipogenesis, while inhibiting osteoblastogenesis, because ad- ipocytes and osteoblasts are derived from a common multi- potent mesenchymal stem cell [49,50] . Moreover, oxidative stress has been shown to inhibit osteoblastogenesis in vitro [51,52] . Thus, these data suggest that the deterioration of bone structure in HFD-fed mice is due to an abnormal ROS level in adipocytes, which increases inflammation in bone marrow and other tissues, increases bone resorption, and decreases bone formation. These findings are summarized in Fig. 1 . 5. High-fat diet e induced obesity and periodontal disease In a recent report, researchers suggested that systemic osteo- porosis is linked to periodontal bone loss, based on significant up-regulation of inflammatory cytokines in the bone and bone- marrow cells of rats with osteoporosis [53] . Several animal studies have also linked obesity to type 2 diabetes, and hyper- caloric diet induced e obesity to morbidity from periodontal Fig. 1 e Proposed relationship among high-fat diet (HFD)-induced obesity, inflammation, and bone metabolism. " id="pdf-obj-2-80" src="pdf-obj-2-80.jpg">

Fig. 1 e Proposed relationship among high-fat diet (HFD)-induced obesity, inflammation, and bone metabolism.

4 <a href=pediatric dental journal 28 (2018) 1 e 6 Fig. 2 e Inflammation and resorption of periodontal bone. disease [54,55] . However, HFD-induced alveolar bone loss has been taken to reflect a state of noninvasive and noninfective inflammation in mice, such as that characteristic of autoim- mune disorders [20] . Recently, Suganami et al. proposed the concept of “ homeostatic inflammation ” in the pathogenesis of noninfectious inflammatory diseases [56] . This state would account for HFD-induced alveolar bone loss in mice, in which systemic inflammatory changes in bone and other tissues may have developed in association with metabolic stress [20] . In a previous study, rats fed a high-cholesterol diet showed a modest increase in the distance between the cementoena- mel junction and the alveolar bone crest [57] . Additionally, mice fed an HFD for 8 weeks showed significant disruption of the periodontal ligament fibers, which had lost their orienta- tions with respect to the bone surface, and inhibition of the constriction of the periodontal ligament space accompanied by pronounced vasodilatation and inflammatory cell infiltra- tion [20] . These data suggest that increased vascular perme- ability due to inflammatory changes in the blood vessels of the periodontium promotes monocyte adhesion to endothelial cells and migration. In addition, osteoclasts differentiated from those monocytes may have attached to the alveolar bone surface, resulting in increased alveolar bone resorption, in HFD-fed mice ( Fig. 2 ). Together, these findings demonstrate that spontaneous deterioration of periodontal bone is a consequence of HFD- induced obesity during growth. 6. Conclusion Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD- induced obesity reflect a state of noninvasive and noninfec- tive inflammation. These results are related to the potential association between metabolic stress and systemic inflam- matory changes occurring in bone and other tissues. Another possible explanation involves the direct or indirect effects of increased serum leptin levels on trabecular bone in mice fed an HFD. Conflict of interest I declare no conflict of interest. Acknowledgements I appreciate the help of Prof. Kenshi Maki in the editing of the manuscript. This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science and Tech- nology, Japan (25713064 and 17K11967). references [1] Roberto CA, Swinburn B, Hawkes C, Huang TT, Costa SA, Ashe M, et al. Patchy progress on obesity prevention: emerging examples, entrenched barriers, and new thinking. Lancet 2015;385:2400 e 9 . [2] Afshin A, Forouzanfar MH, Reitsma MB, Sur P, Estep K, Lee A, et al. Health effects of overweight and obesity in 195 countries over 25 years. N Engl J Med 2017;377:13 e 27 . [3] Bauer KW, Larson NI, Nelson MC, Story M, Neumark- Sztainer D. Fast food intake among adolescents: secular and longitudinal trends from 1999 to 2004. Prev Med 2009;48:284 e 7 . [4] Yanagisawa Y, Tamura A, Akasaka M, Teramoto Y. Physical properties of food and eating functions. 1: an objective method for the measurement of the physical properties of " id="pdf-obj-3-10" src="pdf-obj-3-10.jpg">

Fig. 2 e Inflammation and resorption of periodontal bone.

disease [54,55]. However, HFD-induced alveolar bone loss has been taken to reflect a state of noninvasive and noninfective inflammation in mice, such as that characteristic of autoim- mune disorders [20]. Recently, Suganami et al. proposed the concept of homeostatic inflammationin the pathogenesis of noninfectious inflammatory diseases [56]. This state would account for HFD-induced alveolar bone loss in mice, in which systemic inflammatory changes in bone and other tissues may have developed in association with metabolic stress [20]. In a previous study, rats fed a high-cholesterol diet showed a modest increase in the distance between the cementoena- mel junction and the alveolar bone crest [57]. Additionally, mice fed an HFD for 8 weeks showed significant disruption of the periodontal ligament fibers, which had lost their orienta- tions with respect to the bone surface, and inhibition of the constriction of the periodontal ligament space accompanied by pronounced vasodilatation and inflammatory cell infiltra- tion [20]. These data suggest that increased vascular perme- ability due to inflammatory changes in the blood vessels of the periodontium promotes monocyte adhesion to endothelial cells and migration. In addition, osteoclasts differentiated from those monocytes may have attached to the alveolar bone surface, resulting in increased alveolar bone resorption, in HFD-fed mice (Fig. 2). Together, these findings demonstrate that spontaneous deterioration of periodontal bone is a consequence of HFD- induced obesity during growth.

6.

Conclusion

Recent data suggest that HFD-induced obesity has a negative impact on the mandible in mice. The loss of trabecular bone and reduction of cortical bone growth in mice with HFD- induced obesity reflect a state of noninvasive and noninfec- tive inflammation. These results are related to the potential

association between metabolic stress and systemic inflam- matory changes occurring in bone and other tissues. Another possible explanation involves the direct or indirect effects of increased serum leptin levels on trabecular bone in mice fed an HFD.

Conflict of interest

  • I declare no conflict of interest.

Acknowledgements

  • I appreciate the help of Prof. Kenshi Maki in the editing of the manuscript. This work was supported by Grants-in-Aid from the Ministry of Education, Culture, Sports, Science and Tech- nology, Japan (25713064 and 17K11967).

references

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