Nutrition and the Hard Tissues

CHAPTER 9 Nutrition and the Hard Tissues




OBJECTIVES


By the end of this chapter you should be able to:



• understand the dynamic nature of skeletal metabolism


• define osteomalacia, rickets and osteoporosis


• discuss the role of vitamin D and calcium nutrition in skeletal health


• appreciate the role of other nutrients in skeletal health


• give definitions for dental caries, erosion, abrasion and periodontal disease


• describe the indices used for the measurement of dental caries


• describe the epidemiology and trends of dental caries in Western and other countries


• outline the structure of the tooth


• explain the mechanisms of the decay process


• summarize evidence for the role of dietary sugars and fluoride in the causation and prevention of decay


• compare the relative cariogenicity of various sugars and other carbohydrates


• summarize the interaction of protective effects of fluoride and destructive effects of sugars



9.1 INTRODUCTION


This chapter concerns the physiology and nutritional factors affecting the hard tissues of the body. The first section deals with bones and their two main nutrition related disorders, osteoporosis, and osteomalacia or rickets, and the second section with teeth and their main diet related disorder, dental caries.



9.2 BONE STRUCTURE AND CHANGES



Bone composition


Bone has several functions. It provides: mechanical support and protection for internal organs; a function in acid–base balance; defence against some toxins such as lead, which can be adsorbed to bone; and production of blood cells (haematopoiesis).


The human adult skeleton weighs approximately 3–4 kg, and is about 10% water, 60% inorganic material (minerals), and 30% organic matrix which consists largely (95%) of a single protein, type I collagen. The minerals consist chiefly of calcium, phosphate and carbonate in a crystalline form called hydroxyapatite. Deficiency or excess of these components in bone may contribute to loss of bone strength and to fractures.


There are two main types of bone cells, osteoclasts and osteoblasts, which have opposite functions. Osteoclasts are responsible for bone resorption and osteoblasts for bone formation.



Types of bone


The skeleton is composed of two types of bone, cortical or compact bone, which forms the outer shell of bones and accounts for about 80% of skeletal mass, and trabecular or spongy or cancellous bone, which forms the interior scaffolding of bone and accounts for as much as 70% of bone surface area and metabolic activity. The spaces between the trabeculae contain red marrow which is responsible for the formation of blood cells (haematopoiesis).



Bone changes


Bone is a metabolically active tissue. Although the total amount of bone tissue in an adult is relatively static, about 5–10% of existing bone is replaced through ‘remodelling’ each year. Bone growth, and change in bone shape in children occurs by a mechanism called ‘modelling’ through differences between bone formation and resorption.


The ‘calciotropic hormones’ regulate the process of bone formation and resorption. These include parathyroid hormone (PTH) which stimulates bone resorption, but can also stimulate bone formation; vitamin D and its metabolites which influence mineral supply; sex steroids (oestradiol and testosterone) which decrease bone remodelling; glucocorticoids, of which the predominant effect is to inhibit bone formation; and growth hormone, insulin-like growth factors and thyroid hormones which increase bone remodelling.


The fetal skeleton is initially composed mainly of unmineralized cartilage, and mineralization occurs mainly during the last 10 weeks of pregnancy at a rate of more than 100 mg calcium/day. This continues after birth as the size and shape of bones changes during growth. Skeletal mass increases from about 100 g in the neonate to about 3000 g in an adult (peak bone mass) at about age 35. Over 90% of peak bone mass is achieved by age 18, and so children and adolescents are a particularly important target for interventions to increase bone mass for later life. Bone mineral content declines in the elderly, and is particularly rapid in women after the menopause, caused in large part by a reduced ovarian production of oestradiol. Peak bone mass is the most important predictor of bone mineral content in later life.


Genetic and lifestyle factors influence bone mineral accrual during growth, including exercise, calcium intake, general nutritional status, smoking and use of medications such as corticosteroids and some contraceptives.


Pregnancy and lactation increase calcium requirements, which are met by increased efficiency of calcium absorption from the diet and by maternal bone mineral loss. Calcium requirements of the fetus are relatively small (approximately 30 g) in comparison with lactation (up to 1 g of calcium per day for milk production) which is largely obtained through skeletal mineral loss. This does not appear to have any long lasting effect on bone mineral content or on later fracture risk.


A wide variety of genetic and acquired diseases such as collagen disorders, cancer and infections can influence the skeleton. The two most common diseases affecting the skeleton are (a) osteoporosis, and (b) osteomalacia or rickets due to vitamin D deficiency, in both of which nutrient supply plays a role. Disorders which influence intake or gastrointestinal absorption of nutrients (such as anorexia nervosa, coeliac disease and inflammatory bowel disease) may also cause skeletal disease due to deficient nutrient supply, drug therapy, immobility, endocrine disturbances and the response to inflammation.



9.3 SKELETAL FRACTURE


Skeletal fractures occur as a result of excessive stress or poor bone health, mainly reduced mineral content. Fractures are most common in children and in the very elderly. In children these involve mainly long bones, are more common in males, and are only weakly associated with bone mineral content, while in the elderly they classically occur in bones which have a high proportion of trabecular bone (the wrist, hip and spine), are more common in women, and are strongly associated with low bone mineral content (osteoporosis). The healthcare costs and morbidity associated with these fractures are substantial.


Obese individuals have a lower fracture risk than lean individuals as fat provides ‘padding’ during falls and they have higher bone mineral density due to increased production of oestrogens in fatty tissue, and to mechanical strains induced by excess body weight. Anorexia nervosa results in marked loss of bone mineral content and an increased risk of fracture during later life.



9.4 OSTEOPOROSIS, OSTEOMALACIA AND RICKETS



Osteoporosis


Osteoporosis is characterized by low bone mass and ‘microarchitectural’ deterioration of bone, resulting in an increased risk of fracture. The World Health Organization (WHO) defines osteoporosis as a bone mineral density value less than 2.5 standard deviations below that expected for young adults, and osteopenia when bone mineral density is between 1 and 2.5 standard deviations below the young adult mean. However many osteoporotic fractures occur in individuals who do not fulfil these criteria for a diagnosis of osteoporosis.


At least 30% of postmenopausal women in Western countries are defined as having osteoporosis according to WHO criteria. However, differences in the length and width of bones as well as non-skeletal factors, such as frequent falling, poor muscle strength, low body mass and poor vision, also influence fracture risk. Many of these risk factors may be influenced by nutritional status.


Treatment aims to increase bone mineral density, reduce bone remodelling, and decrease the risk of falls. Measures include avoidance of smoking, increasing dietary intake of calcium, ensuring adequate vitamin D status, and exercise and a variety of drugs such as bisphosphonates, oestrogens, selective oestrogen receptor modulators and intermittent parathyroid hormone.



Osteomalacia


Osteomalacia results from defective mineralization of bone matrix (osteoid). The commonest cause is vitamin D deficiency. Other causes include disorders of phosphate metabolism, genetic defects, and excessive intake of nutrients such as fluoride.



Rickets


Rickets is osteomalacia that occurs when bones are still growing. Rickets has been an important cause of childhood illness and deformity for many centuries. Following the industrial revolution, the combination of urbanization, pollution and poor diet resulted in increased prevalence of the disease in England. Rickets continues to be an important disease in the developing world, and is still seen in developed countries, particularly in non-Caucasians.


Children with rickets classically present with knock-knees or bowed legs, muscle weakness, and short stature. In breast-fed infants, rickets can develop within the first few months of birth, particularly when the mothers of these infants have vitamin D deficiency. These infants may have craniotabes (soft areas of the skull causing a ‘ping-pong’ ball sensation on pressure), thickening of the wrists and ankles, and enlargement of the costochondral junctions (rachitic rosary). Fractures and other deformities can occur. Children with rickets also have poor muscle development and tone. The skeleton is poorly mineralized, and the growth plates are widened (cupped) and irregular on x-ray. As in adult osteomalacia, there is an excess of unmineralized osteoid. Infants with rickets may develop respiratory infections, and are more likely to have tuberculosis. Many of the clinical features of rickets resolve within a short period after administration of adequate amounts of vitamin D but pelvic deformities can lead to later difficulties during labour.


In the early part of the 20th century it was discovered that rickets could be cured by a fat-soluble nutrient or sunshine exposure. An unfortified infant diet contains a very small amount of vitamin D, although there are small amounts in milk and egg yolk. Causes of osteomalacia and rickets include high dietary intakes of phytate; increased skin pigmentation or traditional dress; calcium deficiency; genetic or acquired disorders of phosphate metabolism or vitamin D metabolism; and deficiency of the enzyme alkaline phosphatase (Box 9.1).



Box 9.1 Factors contributing to vitamin D insufficiency




1. Deficiency of sunlight-derived vitamin D


• Failure to go out-of-doors

• Limited UV-B exposure in wintertime

• Countries with limited UV-B exposure

• Decreased skin exposure due to traditional dress

• Use of sunscreen creams

• Ageing

• Darker skin colour

2. Gastrointestinal disease


• Pancreatic disease (fat malabsorption)

• Coeliac disease

• Other malabsorption syndromes

3. Anticonvulsant drug therapy


4. Defective renal production of 1,25(OH)2D


• Renal insufficiency

• Genetic vitamin D pseudodeficiency rickets


9.5 THE ROLE OF CALCIUM AND VITAMIN D IN BONE (SEE CHAPTER 5)


The risk of poor bone mineralization is greater in modern society than for our distant ancestors. The genetic constitution of modern humans has changed little over the past 10,000 years, but the environment has altered markedly. Cultivated plant foods such as cereal grains have far less calcium than do other vegetable food sources and dietary calcium intake was probably twice as great in pre-agricultural humans. Modern humans get less exercise and far less sunshine exposure than did our evolutionary ancestors. There is very little vitamin D in the unsupplemented diet of most modern humans.


Increasing calcium intake through supplements or dairy foods results in a reduction in bone resorption within two hours, and a decrease in serum PTH after several weeks of intervention. Several studies have shown that calcium supplementation alone or with vitamin D reduces the risk of osteoporotic fracture in elderly men and women living in institutions or at home. Calcium supplementation appears to have less influence on bone loss in the years immediately after the menopause, possibly due to the overriding importance of oestrogen deficiency during this time.


Children and adolescents are a particularly important target for interventions to increase bone mass. Randomized controlled trials of calcium or dairy supplementation in children for periods up to 3 years found a greater bone mass accrual in the order of 1–7%, possibly due to a reduction in the rate of bone remodelling.


Calcium supplementation and adequate protein intake has important therapeutic value in osteoporosis and combined supplements of calcium and vitamin D are often recommended to patients with osteoporosis. Most calcium supplementation studies which have shown a skeletal effect have used intakes of at least 1000 mg per day. Maintenance of body weight is critical, since moderate weight loss and low body weight are associated with loss of bone mass and risk of fracture. However, excessive calcium intake can result in hypercalcaemia, renal insufficiency or renal stones, and impaired absorption of other nutrients such as iron, phosphorus and zinc.



9.6 PROTEIN, ACID–BASE BALANCE AND BONE

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Jun 13, 2016 | Posted by in ENDOCRINOLOGY | Comments Off on Nutrition and the Hard Tissues

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