Nutritional Influences on Osteoporosis and Alveolar Bone Density.
© Juliette Reeves 2005
Abstract
Osteoporosis is one of Europe’s most common but least recognised diseases. One in three women and at least one in 12 men will develop osteoporosis during their lifetime. An estimated 3 million people in the UK suffer from osteoporosis costing the NHS and government over £1.5 billion each year. Osteoporosis is responsible for 200,000 fractures per year and 40 deaths a day. The question of whether osteoporosis and alveolar bone loss have a causal relationship remains the subject of much research . Bone modelling and skeletal consolidation result from a sequence of nutritional and hormonal interactions. Because nutrition is a modifiable pathogenic factor in osteoporosis, which also appears to have important oral health implications, it is a topic that deserves some attention. This article looks at the role of calcium and nutritional co-factors such as vitamin D, magnesium, acid base homeostasis,and the effects of caffeine, cola and alcohol on bone density.
Keywords: Osteoporosis, bone density, alveolar bone, calcium, nutrition.
Introduction
Osteoporosis is one of Europe’s most common but least recognised diseases. One in three women and at least one in 12 men will develop osteoporosis during their lifetime.(1) An estimated 3 million people in the UK suffer from osteoporosis (2) costing the NHS and government over £1.5 billion each year (3). Osteoporosis is responsible for 200,000 fractures per year and 40 deaths a day. The question of whether osteoporosis and alveolar bone loss have a causal relationship remains the subject of much research. Recent studies, however, indicate that low bone mineral density (BMD) and female hormone deficiency can influence alveolar bone loss.A piece of research published in the Archives of Internal Medicine (4) as suggested that the positive effects of hormone/oestrogen replacement therapy on post cranial bone density are accompanied by similar positive effects on alveolar bone mass. This study concurs with an earlier report from Payne (5) who was able to show a positive effect of 17ß oestrodiol (E2) on alveolar bone density. Overall, interproximal changes revealedE2 sufficient women exhibiting a net gain of alveolar bone density and E2-deficient women a net loss.
Osteoporosis and Alveolar Bone Loss
In a report in the Journal of Periodontology, Tezal et al (6) reported their findings that skeletal BMD is related to interproximal alveolar bone loss and, to a lesser extent, to clinical attachment loss, implicating post-menopausal osteopenia as a risk indicator for periodontal disease in postmenopausal women. Krall et al (7) report that increased systemic bone loss may be a risk factor for tooth loss by contributing to the resorption of alveolar bone. Elders et al (8) reported no such relationship between periodontitis and systemic bone mass. They compared oral clinical findings to bone mineral content of the lumbar spine and the thickness of the middle three fingers of both hands. When no correlation was found, they suggested the relationship between periodontitis and systemic bone mass was not significant.
What was not examined in this study was whether, in more severe manifestations of periodontitis, a relationship to osteoporosis does exist, and whether general skeletal bone mass has an effect on the severity and progression of pre-existing periodontitis. Perhaps if the subjects had been patients with severe periodontitis and had been studied over a larger age range, a different relationship may have been established between osteoporosis and periodontal disease. In the light of continuing research studies suggesting that it is likely that osteoporosis does not initiate periodontal disease but may produce changes in alveolar bone that contribute to the progress of the disease once it has been established by bacterial plaque and the host response to the biofilm. What is clear, however, is that many of the cytokine activities implicated in systemic osteoporosis closely mirror the pathobiology of periodontitis with alveolar bone loss and the nutritional recommendations for the former could be beneficial for the latter.
Nutritional Influences on Bone Density
Bone modelling and skeletal consolidation result from a sequence of nutritional and hormonal interactions. Because nutrition is a modifiable pathogenic factor in osteoporosis, which also appears to have important oral health implications, it is a topic that deserves some attention. Given the dynamic physiology of alveolar bone, involving osteoblast both and osteoclast activity, and being supported by compact and cancellous bone, it is not unreasonable to extrapolate risk factors in systemic bone density, to alveolar bone in man. Nutrition is an important factor in systemic bone health and may also have implications for the rate at which alveolar bone is lost.
Calcium Metabolism and Bone
The effect of calcium supplementation on systemic bone density is well documented. Calcium deficiency has been identified as a major risk factor in osteoporosis. Michaelsson et al (9) showed a linear relationship between calcium intake and systemic bone density. A number of more recent studies have suggested that alveolar bone mass is sensitive to poor calcium intake. Nishada et al (10)suggests that low dietary calcium is associated with the severity of periodontal disease. It has also been suggested that alveolar bone has a high turnover rate and may be, therefore, affected first and, consequently, more severely in the long term (12).
Co-factors Adequate calcium intake, however, is only part of the picture. In order for the mineral to be incorporated into bone, it needs to be well absorbed and relies on a number of cofactors,including magnesium. For calcium to be absorbed from the diet it also needs hydrochloric acid and vitamin D. Early studies suggest older people tend to lack sufficient HCL, either from a lifetime of nutrient deficiencies or regular use of antacid preparations. (13)
Vitamin D
Vitamin D is acknowledged as an integral part of calcium utilisation in bone formation.Both collagen synthesis and the accumulation of mineralized bone are dependent on adequate levels of vitamin D and calcium. It is of concern, therefore, to read that the prevalence of vitamin D deficiency in healthy postmenopausal women is surprisingly high, according to a study published in the Journal of Bone and Mineral Research (14). In women with osteoporosis, vitamin D levels were approximately 25% lower than in those with normal or marginally low bone density.
A new piece of research has suggested that even when serum levels of vitamin D are within the recommended reference range, calcium absorptive performance can still be significantly reduced (15). Thus, individuals with serum 25-hydroxyvitamin D levels at the low end of the current reference ranges may not be getting the full benefit from their calcium intake. The number of studies on the effects of vitamin D intake on oral outcomes is limited, but most suggest that higher intake levels are associated with a reduced prevalence of clinical attachment loss and lower risk of tooth loss (16,17).
The elderly are thought of as being particularly at risk of vitamin D deficiency if they are infirm or institutionalized (18). Increasingly more attention, however, is being given to other groups, in particular healthy post-menopausal women (14) , adolescent females(19) and veiled ethnic women living in a European climate (20). Most of our vitamin D requirements are primarily met from dehydrocholesterol via exposure to sunlight, rather than diet alone. It is also found in some foods, including oily fish, liver and fortified milk. In many countries, fortified milk is probably the main dietary source of vitamin D. Risk factors for developing vitamin D deficiency include lack of sunlight exposure, avoidance of vitamin D-containing foods (e.g. milk, liver and fish) and diseases that cause malabsorption.
Magnesium
Magnesium acts as an important co-factor in the enzyme-regulated process of Ca+ absorption into bone. Studies have shown that the addition of magnesium supplementation combined with calcium improves BMD (21). Two recent studies have demonstrated how magnesium deficiency impairs bone growth by decreasing osteoblast numbers, increasing osteoclast numbers and stimulating cytokine activity (22,23). Calcium, magnesium, zinc and vitamin C have been shown to be significantly related to BMD at several skeletal sites (24). More research is needed to understand fully the interactions of these nutrients in identifying preventative measures for bone loss and the implications in alveolar bone loss.
Other Nutritional Influences on Bone
Poor acid base homeostasis is often the result of a diet that contains an excess of acid forming foods. These foods are not necessarily acidic in themselves, but after metabolism they leave an ‘acid ash’ residue that needs to be buffered in order to avoid metabolic acidosis. Long-term exposure to excess acid forming foods leaves the body deficient in alkaline minerals and Ca+ are liberated from bone to buffer acidity.
There is growing evidence of a positive link between fruit and vegetable intake, acid base homeostasis and bone health. New (25) has demonstrated a significant positive effect of increased fruit and vegetable consumption on axial and peripheral bone mass and markers of bone metabolism. Tucker et al (26). have also suggested that excess protein reduces bone density and is associated with an increased acid base ratio The Framingham Study(27) also revealed magnesium, potassium and fruit and vegetables as base components of the diet associated with increased BMD. New et al (28) have shown that women who had the most ‘acidic’ diets (as assessed by ‘no endogenous acid production’) had the poorest bone density (both in axial and peripheral skeleton) and the highest level of bone resorption.
The World Health Organization recommends that only 0.5g of protein per kilo of body weight is needed for skeletal repair and maintenance. Varying choices of protein with vegetarian sources is also recommended, as this appears to have less effect on bone mineral density (29).
Caffeine, Cola and Alcohol
A possible link between poor BMD and caffeine and cola consumption was suggested in a piece of research published in the American Journal of Clinical Nutrition. (30) The research suggested that women who regularly drink caffeinated cola may be at greater risk of fractures and low BMD. The research looked at the effects of a range of drinks on a group of 30 women. A small but significant level of calcium was excreted after the women drank caffeinated cola. So-called ‘energy drinks’ have also been under the spotlight recently, with concern expressed by the American Dietetic Association (31) over their high caffeine content. Some of the drinks contain high quantities of ginseng, an adrenal stimulant similar to caffeine.
The evidence for the relationship between caffeine consumption and bone mineral density is mixed. A study conducted in Italy(32) concluded neither caffeine nor alcohol were implicated in low bone density and smoking 15 or more cigarettes per day provided only a small increased risk in low bone density. Lloyd (33) also assessed caffeine intake and bone status in 138 post-menopausal women and found no correlation between bone mineral density and caffeine consumption.
Barrett et al(34) studied 980 postmenopausal women aged 50-98 (mean age 72.7 years) between 1988 and 1991. They concluded that lifetime caffeinated coffee consumption equivalent to two cups per day is associated with decreased bone density in older women, but women who reported drinking at least one glass of milk per day were not affected. This study, however, was part of a much larger study conducted over a period of years. Almost 1,000 women were studied in contrast to 138 in the Lloyd study, some of which had been using HRT for a short period of time. What both studies failed to consider was that tea is also a considerable source of caffeine, with 100mg to coffee’s 120mg per average cup. The effect of caffeine and cola on alveolar bone is yet to be established. It is likely that caffeine and cola may provide an increased risk of low bone density in association with other risk factors, rather than being a deciding factor on their own.
Whether from specific alcohol toxicity, magnesium loss or nutrient deficiency, osteoporosis is rampant in alcoholics. Klein(35) noted that even moderate consumption of alcohol (one to two glasses per day) is clearly linked with reduced bone mass. Patients with alcoholic bone disease reveal a marked impairment in bone formation. Ethanol has been shown to reduce proliferation of osteoblasts. The consequences of alcohol intake during adolescence is particularly damaging, as peak bone mass is determined at this time. Alcohol also increases blood acidity, which leaches calcium ions from bone to buffer possible acidosis. Combined with smoking and caffeine intake which are often related, alcohol may be seen as a risk factor for low bone density.
Conclusion
The success of conventional periodontal treatment is well documented, and for many people provides all the treatment they may need to combat their periodontal disease and bone loss. There is, however, a section of the population who show an increased susceptibility to bone loss and periodontal breakdown. These facts alone give us the impetus to continue to research the complex aetiology of this multi-factoral disease and to embrace a multi-disciplinary approach in the treatment and prevention of periodontal disease. The research and trials reviewed show how inadequate nutrition and micronutrient status can be risk factors for both low skeletal and low alveolar bone density.
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