Osteoporosis

Primary osteoporosis
Secondary osteoporosis
• Advanced age
• Hypogonadism (male and female)
• Female sex
• Use of glucocorticoid or anticonvulsant medication
• Postmenopause
• Excess thyroid hormone
• White or Asian ethnicity
• Rheumatoid arthritis
• Family history of osteoporosis or low-trauma fracture
• Alcoholism
• Low body weight
 
• Low dietary intakes of calcium and vitamin D
• Low physical activity level
• Cigarette smoking

Effects of Osteopenia and Osteoporosis on the Oral Cavity

It has been hypothesized that osteopenia and osteoporosis confer an increased risk of periodontal disease and tooth loss [7, 15]. While many published studies demonstrate statistically significant associations, the evidence is not strong enough to conclude that low BMD is a causal determinant of periodontal disease or a reflection of shared risk factors [7]. A major limitation to reaching a consensus on the nature of the osteoporosis-periodontitis link is the lack of cohort studies in the literature and abundance of those with a cross-sectional design. In the hierarchy of study designs for establishing causality, cross-sectional designs deliver lower quality evidence than do cohort studies for several reasons. Cross-sectional surveys and case-control designs do not clearly establish which condition preceded the other or how long each condition has been present. In addition, when the outcome is radiographic or clinical periodontal disease, one may not know the status of the teeth that have been lost. Teeth that remain are likely to be healthier than those that are missing, creating a false inverse relationship. Another limitation is the fact that many studies were conducted with small sample sizes. Given the complex causes of oral and systemic bone loss, associations between the two are likely to be moderate or weak, and large sample sizes are needed to ensure adequate statistical power. Most studies excluded men. An evaluation of the evidence for causality must also take into account whether analytic methods controlled for important confounders such as age, years since menopause, smoking, and hormone replacement use.

Periodontal Diseases: Alveolar Bone Loss

Alveolar bone loss (ABL) often precedes tooth loss and is a key outcome in periodontal disease, thus alveolar bone is labile and has a principal role in support of the dentition. In periodontal disease, bacteria lead to initiation of the host inflammatory response that leads to ABL. It has been speculated that osteoporosis reduces alveolar bone quantity and quality, thereby exacerbating the periodontal disease process. A 5-year cohort study of 1,025 women reported that women with osteoporosis at any site (forearm, spine, hip) experienced greater loss of alveolar crest height compared to women with normal systemic bone status [16]. Another cohort study found that concurrent 5- and 10-year changes in alveolar bone mass and trabecular pattern—a qualitative assessment of overall quality of jawbone structure [17]—were correlated with changes in BMD at the forearm and hip [18, 19]. These studies are consistent with a study by Payne et al. [20], who found that osteoporotic women exhibited significantly more sites with ABL than women with normal spine BMD.
Cross-sectional and case-control studies also report significant positive associations between systemic bone and alveolar bone level [15, 2125]. However, limitations of several of those studies include lack of control for confounders [23, 25] and small sample size [23]. The largest cross-sectional studies of ABL describe results from over 1,200 participants in an ancillary component of the Women’s Health Initiative Observational Study [15, 22]. Severe periodontal disease was defined as mean alveolar crest height (ACH) loss ≥3 mm, or ≥2 sites with ≥4 mm ACH loss, or tooth loss related to periodontal disease. The overall adjusted odds of severe periodontal disease were approximately doubled in women with osteoporosis relative to those with normal BMD (15), but this association was age dependent. Among women age 70 or older, the odds ratio was 3.6 while in women under 70, it was 1.6.

Clinical Measures of Periodontal Disease

In the absence of radiographs, periodontal disease status is defined on the basis of clinical parameters such as probing pocket depth (PPD), clinical attachment loss (CAL), gingival recession, gingival bleeding, and tooth mobility. The use of different indices and cut-offs to designate periodontal disease yields varying estimates of periodontal disease prevalence and makes it difficult to compare the outcome of studies relating it to systemic bone status. Two of the five prospective studies published between 2001 and 2013 found significant associations between systemic BMD and clinical measures of periodontal disease. In a study of 179 men and women aged 70 years old, those with osteoporosis exhibited more sites with progression of CAL (after 3 years, the site was at least 3 mm worse than the baseline value) than persons with normal BMD [26]. These results were adjusted for gender, baseline CAL, body mass index, serum albumin, total cholesterol, and hand grip strength. In a 7-year observational study, 34 periodontal disease patients of both sexes were characterized by their pattern of changes in CAL and PPD [27]. Active disease was defined as an increase in percent of sites with CAL ≥5 mm over 5 years and 5 or more teeth with PPD ≥5 mm after another 2 years of follow-up, while stable disease was defined as a decreasing percent of sites with CAL and <5 teeth with deep pockets. More than half of the active periodontitis group reported having osteoporosis compared to 8% of patients whose periodontal disease was stable [27].
In contrast to those findings, Famili et al. found no difference in baseline BMD nor 2-year rates of BMD loss [28] between women with periodontal disease at baseline (CAL >4 mm on 12 or more teeth, n = 163) and those who were disease-free (n = 39). However, it is not clear if periodontal disease status remained the same in both groups over the follow-up period. Following 1,210 men for an average of 2.7 years, Phipps et al. [29] found no differences in percent of sites with CAL ≥5 mm, PPD ≥6 mm, or progression of periodontal disease (2 or more teeth with incident loss of attachment ≥3 mm) among baseline quartiles of total femur BMD. Although the follow-up study of participants at in the Women’s Health Initiative Observational Study reported more rapid loss of ACH in women with poor systemic bone status, it did not find that changes in CAL and PPD were related to baseline BMD [16].
Findings from cross-sectional and case-control studies of clinical periodontal measures are also mixed. Brennan et al. [22] studied 1,329 postmenopausal women and found that overall, mean CAL increased as BMD at several skeletal sites decreased. The relationship was evident only among women with no subgingival calculus and remained after adjustment for age, cigarette smoking, education, and time since last dental cleaning. These findings contradict an analysis of the third National Health and Nutrition Examination Survey (NHANES III) data in which women with low BMD of the total femur and high mean calculus index scores had up to 2.5 times as many sites with CAL greater than 7 mm as women with comparable calculus but normal BMD [30]. Differences in methodologies were cited in an effort reconcile these discrepant findings [22]. Numerous studies reported associations between worse clinical periodontal parameters and poor BMD status in women [21, 23, 25, 3137] and men [38]. Once again, lack of control for confounders [23, 25] and small sample size [23, 33, 34] limit the interpretation and generalizability of some findings. After controlling for covariates, Jabbar et al. found that BMD was no longer a significant predictor of periodontal disease [39].

Tooth Loss

Periodontal disease is a common reason for tooth loss in older adults [40, 41]. This provides a rationale for using tooth loss as a surrogate measure of past periodontal disease activity. There are a limited number of prospective studies that examine change in BMD and loss of teeth. In a 5-year follow-up study, Iwasaki et al. [42] categorized the rates of BMD loss for 404 women into tertiles and compared rates of tooth loss among them. Women with the fastest rate of systemic bone loss were at 1.27–1.38 greater risk (depending on the systemic site) of tooth loss than those with the slowest bone loss. These findings support a previous study which reported higher rates of bone loss at the hip, spine, and total body over a 7-year period in postmenopausal women who concurrently lost teeth relative to women who lost no teeth [43]. In a cohort of healthy men and women, all age 70 years and with at least 20 teeth remaining at baseline, there were no significant differences between persons with osteoporosis and a healthy group with regard to number of teeth present at baseline or number lost during 3 years of follow-up [26]. The requirement that 20 teeth be present at baseline may have resulted in selection of subjects with better oral health.
In general, cross-sectional studies with elderly subjects or a wide age range have found correlations between BMD and number of teeth remaining [4447] or edentulism [48], while the association was not evident when fragility fracture was the measure of systemic bone quality [49].

Summary of the Evidence for an Association Between Osteoporosis and Periodontal Disease or Tooth Loss

The question of whether low BMD and osteoporosis independently increase the risk of periodontal disease onset or progression remains unanswered despite the large number of studies that have been conducted. Interpretation of the findings is complicated not only by study design features and various definitions of periodontal disease, but also the fact that, within a single study, statistically significant results may be observed for some skeletal sites and periodontal disease/tooth loss indices but not others [16, 22, 24, 33, 46], or for one sex [32] or age group [22] but not another. Such discrepancies have been attributed to variation in percentages of cortical and trabecular bone and in prevalence of either disease in the study populations.
Therefore, there is a lack of evidence for a causal association and lack of agreement as to clinical significance when associations are found. A weak association can still be meaningful if the conditions are highly prevalent in a population. In the US population age 50 and older, osteoporosis and osteopenia affect approximately 44 million people, while periodontal disease affects approximately half of US adults aged 30 and older [50]. Even if osteoporosis and osteopenia were to cause only a small increase in the risk of periodontal disease, a reduction in the incidence of these risk factors could potentially eliminate hundreds of thousands of cases of periodontal disease each year. Therefore, examination of the effects of osteoporosis therapies on periodontal disease and tooth loss is warranted.

Effects of Osteoporosis Prevention and Treatment Strategies on the Oral Cavity

Medications for the Treatment of Osteoporosis

Approved treatments for osteoporosis include hormone replacement therapy (HRT), the selective estrogen receptor modulator raloxifene, the hormone calcitonin, recombinant human parathyroid hormone (PTH), and antiresorptives such as bisphosphonate. Bisphosphonate has been shown to reduce CAL, PD and gingival bleeding, and distance between the alveolar bone crest and cemento-enamel junction [5153]. However, incidents of osteonecrosis of the jaw (ONJ) after invasive dental procedures among women given high-potency intravenous bisphosphonate for cancer [54] raise concerns about its use. Among patients taking lower dose oral antiresorptive medications for osteoporosis, the prevalence of ONJ is low [55]. New agents are becoming available for management of cancer involving bone and osteoporosis. Denosumab is a monoclonal antibody directed against the cell surface receptor (receptor activator of nuclear factor ligand; RANK-L) affecting osteoclast differentiation and function that is now FDA approved for bone cancer [56, 57]; other agents are in clinical trial and are expected to become available in the future. RANK-L inhibitor and bisphosphonate drugs increase the risk of osteonecrosis, primarily when used as part of cancer therapy but rarely in osteoporosis. ONJ risk is related to cumulative drug dose and the medical condition being treated. Oral Health Care Professionals (OHCPs) must be aware of the use, schedule and doses of these agents so that the patient’s dental care is managed appropriately.
HRT studies utilized supplements of either estrogen alone or a combination of estrogen and progestin. A 3-year randomized controlled trial of HRT found a significant increase in alveolar bone mass in the treated group compared to a group given only calcium and vitamin D supplements [58]. Payne, Reinhardt, and colleagues reported that estrogen sufficiency is associated with preservation of alveolar bone density and less frequent CAL [20, 5961]. Postmenopausal women who never used estrogen were twice as likely as premenopausal women to have periodontal disease (≥30% teeth with at least one site with CAL ≥5 mm), whereas the odds of disease among postmenopausal estrogen users were not significantly elevated [62]. In NHANES III, postmenopausal women who used estrogen for at least 2 years had lower mean CAL values than women who never used it [30].
Several large population-based studies of postmenopausal women also concluded that women who have ever used HRT retain more teeth than nonusers and have a lower likelihood of being edentate [6365] independent of age, smoking, and other factors. Duration of HRT use was also related to tooth retention. But a study of individuals seen in a dental school reported no association between HRT and number of teeth [49]. Long-term HRT also has significant adverse health effects which led to a decline in its use [66]. Thus, nutritional approaches to osteoporosis prevention appear to be safer alternatives.

Nutritional Approaches to Osteoporosis Prevention

Calcium and Vitamin D

Calcium is one of the major components of bone’s hard tissue. It also has numerous other functions in the body. Vitamin D plays a critical role in calcium homeostasis by aiding calcium absorption from the gut, and along with PTH, is one of the primary hormones that regulates mineral deposition and release from bone and excretion via the kidney. Inadequate dietary calcium intake and/or vitamin D status result in a negative calcium balance and the body will then use calcium stored in the skeleton for its immediate needs. Eventually, this loss of mineral contributes to decreased BMD. Other factors such as smoking [67] and thyroid and kidney function [68] affect calcium homeostasis, but correction of calcium and vitamin D intakes is one of the more easily modifiable approaches to restore balance. Raising calcium and vitamin D intakes, typically with supplements, slows the rate of bone loss [69, 70], but there is inconsistent evidence of a benefit on fracture risk [7173]. However, calcium and vitamin D supplements are important adjuncts to drug therapies for osteoporosis.
Few studies have examined the effect of calcium and vitamin D intakes or supplements on periodontal disease or tooth loss. Hildebolt et al. [74] reported a 0.74% per year increase in mandibular bone mass over a 3-year period with administration of 1,000 mg calcium and 400 IU vitamin D. The magnitude of the increase was similar to that seen in women given calcium and vitamin D plus estrogen; however, there was no true placebo group. In a study of 51 patients receiving periodontal maintenance, there were no significant differences in mean levels of mean PPD, CAL, and alveolar height loss among those who elected to use calcium and vitamin D supplements and patients who did not [75]. After 6 months of follow-up, the supplement users displayed less periodontal disease but the benefit did not persist at 1 year [76]. In a randomized placebo-controlled trial to study the effects of 500 mg/day calcium and 700 IU/day vitamin D supplementation on systemic bone loss in elderly men and women, the supplemented group showed an approximate 50% reduction in the risk of tooth loss over 3 years [77].

Calcium Alone

A calcium intake that was below recommendations (1,000 mg/day for <50 years, 1,200 mg/day for age 50+) was associated with an increased incidence of tooth loss in men but not in women [78]. However, calcium intake from dairy foods was associated with fewer teeth with CAL ≥3 mm [79] and had a protective effect on tooth loss incidence in both men and women [80]. A prospective study of 552 older men suggested that calcium intakes above 1,000 mg/day may be beneficial in slowing ABL progression, independently of age, initial number of teeth, smoking status, vitamin D intake, caries status, and clinical periodontal disease status [81]. A calcium supplement trial conducted in men concluded that added calcium, either 600 or 1,200 mg/day, had no effect on tooth loss risk; however, only 2 men lost any teeth during the 2-year study [82]. Nishida et al. [83] analyzed dietary intake surveys and periodontal data in more than 12,000 adults from NHANES III. After controlling for age and smoking status, the odds of having periodontal disease (mean periodontal attachment loss ≥1.5 mm) were nearly double in younger men and women whose calcium intake was below 800 mg/day relative to ≥800.

Vitamin D Alone

Vitamin D status is determined by the level of serum 25-hydroxyvitamin D (25(OH)D), which reflects both the contribution from diet and from the conversion of 7-dehydrocholesterol in the skin into pre-vitamin D after exposure to the sun. Optimal serum levels are 25 ng/ml or higher. Mild to moderate vitamin D deficiency is indicated when levels are less than 25 ng/mL and severe deficiency when <10 ng/ml. Vitamin D deficiency is common in the US, affecting 42% of adults [84]. Persons at greater risk include nonwhites, the obese, and those in poor health, without a college education, or no daily milk consumption [84]. Daily supplementation with 800–1,000 IU/d of vitamin D or up to 50,000 IU monthly is considered safe and sufficient to maintain serum 25(OH)D at optimal levels [85]. Correction of vitamin D deficiency requires supplements at higher doses than typically found in over-the-counter preparations.
In NHANES III participants, low levels of serum 25(OH)D were associated with a greater extent of CAL in older individuals [86], and with gingival bleeding at sites without attachment loss [87]. Because many individuals do not routinely have serum 25(OH)D measured and do not know their vitamin D status, studies are needed of periodontal disease and dietary and supplemental vitamin D intake—sources of vitamin D that can readily be monitored.

Summary of the Evidence for an Association Between Osteoporosis Therapies and Periodontal Disease or Tooth Loss

HRT and antiresorptive agents may be effective in reducing periodontal disease and tooth loss, but have serious side effects. The studies using nutritional approaches to reduce periodontal disease have several limitations, including many with a cross-sectional design [75, 83, 86, 87], lack of data on supplement use to complement dietary intake estimates [83], small sample size [75, 76], and secondary data analyses of randomized trials [77, 82]. There is a need for more prospective studies of the effects of calcium, vitamin D, and other nutrients on periodontal disease and tooth loss.

Professional and Practice Issues

The OHCP can increase a patient’s knowledge of risk factors, especially poor nutrition and smoking, that affect both oral and systemic bone health. It is important to stress good nutrition and lifestyle habits in childhood and early adulthood before the signs of osteoporosis become evident.
Recommended intake levels for calcium and vitamin D in the United States [88] are given in Table 16.2 and major food sources of these nutrients are shown in Fig. 16.1. Nutritional guidance should emphasize a balanced overall diet and use of food as primary sources of calcium and vitamin D rather than supplements. Foods supply additional nutrients that are essential for bone health, including magnesium, phosphorus, selenium, B vitamins, and vitamin A. Quality of the total diet is important too because extreme intakes of nutrients such as protein, phosphorus, sodium, and caffeine can alter calcium absorption and excretion, particularly when calcium intake is marginal [68]. By obtaining nutrients from foods instead of supplements, one is less likely to take in extreme levels. Furthermore, the US Preventive Services Task Force concluded that the amounts of calcium and vitamin D in many over-the-counter supplements (400 IU vitamin D or less, 1,000 mg calcium or less) are not effective in preventing osteoporotic fractures [71]. Calcium supplements have been cautiously linked to adverse outcomes such as kidney stones [71] and myocardial infarction [89].

Table 16.2

Adult dietary reference intake values (recommended dietary allowances or adequate intake) of calcium and vitamin D in the United States [88]
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Age
Calcium (mg/d)
Vitamin D
 
IU/d
μg/d
0–6 months
200a
400
10a
6–12 months
260a
400
10a
1–3 years
700
600
15
4–8 years
1,000
600
15
9–13 years
1,300
600
15
14–18 years
1,300
600
15
19–30 years
1,000
600
15
31–50 years
1,000
600
15
51–70 years (Males)
1,000
600
15
51–70 years (Females)
Nov 4, 2015 | Posted by in General Dentistry | Comments Off on Osteoporosis
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