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Osteoporosis and periodontitis are diseases associated with altered bone structure and decreased bone mass. As well as similar disease characteristics, they also share risk factors and biological markers. Investigations have thus been carried out to determine whether the two diseases are linked. The epidemiology, current research and potential mechanisms linking the two conditions as well as the implications for the management of periodontal disease will be discussed.
Epidemiology of Periodontitis
A study by ARCPOH (2009) regarding periodontal diseases in the Australian population found that overall prevalence of mild periodontitis was 22.9%. Rates are higher for men at 26.8% than for women with a rate of 19.0%. Although mild periodontitis is very common amongst the Australian population, severe periodontitis affects less than 5% of people (Hirsch 2004). Periodontitis can begin in people as young as 15 but prevalence is strongly associated with age, with disease rates in the 75+ category being over 8 times higher than the 15-34 age group (ARCPOH 2009). Other significant risk factors include smoking, diabetes, stress, genetic predisposition, poor nutrition and low physical activity.
Graph 1 - Prevalence of Periodontitis in the Australian Population According to Age
Percentage of Australians with the Disease
Epidemiology of Osteoporosis
Osteoporosis is a skeletal condition characterised by reduced bone mineral density (BMD) and structural changes to bone (Kim et al 2006). It is caused by an imbalance between bone formation and bone resorption resulting in an overall loss of bone mineral and altered bone microarchitecture (Wactawski-Wende 2001). The changes that occur to the structure of the bones cause weakened trabecular and cortical structures, predisposing patients to fracture and deformity (Gomes-Filho et al 2007).
Like periodontitis, osteoporosis is a very common disease with approximately 1 in 10 Australians affected by osteoporosis in 2001. However, unlike periodontitis, prevalence is over three times higher for women than men. Apart from this difference, there are many common risk factors for osteoporosis and periodontitis. Higher rates are strongly associated with increasing age (Access Economics 2001). Smoking is also implicated in lower bone mineral density as is low physical activity and poor nutritional intake (Lorentzon et al 2007; Miyabara et al 2007). Other important risk factors include, Caucasian race, alcohol use (>2 drinks per day), medical conditions (eg. hyperparathyroidism, diabetes), intake of certain medications (eg. glucocorticoids, anticonvulsants), low body mass index, anorexia nervosa and hormone levels (especially decreased oestrogen levels) (Dervis 2005; Wactawski-Wende 2001). Due to the nature of many of these risk factors, osteoporosis is most common in post-menopausal women (Dervis 2005).
Graph 2 - Prevalence of Osteoporosis in the Australian Population According to Age
(Access Economics 2001)
Percentage of Australians with the Disease
Figure 1 - Risk Factors for Osteoporosis and Periodontitis
Low Body Weight
Low Peak Bone Mass
Race (Caucasian or Asian)
Hyperparathyroidism & Hyperthyroidism
Heavy Alcohol Consumption
Poor Immune Function
Low Physical Activity
Review of Current Literature
Clinical trials investigating periodontitis as a manifestation of systemic osteoporosis are compared in the systematic review by Martinez-Maestre et al (2010). The review identified randomised controlled trials relating osteoporosis and periodontitis through Internet search engines, the MEDLINE database and the Cochrane Controlled Trials Register, identifying 145 publications. The literature was then screened to exclude references that assessed treatment outcomes, diagnostic procedures, literature reviews and those that used invalid diagnostic criteria to identify either disease. Thirty-five trials remained and were compared independently by one examiner based on characteristics of the participants, interventions and how results were measured in each trial. The findings of each study were classified as observing either a positive or negative correlation between periodontitis and osteoporosis incidences in individuals. The results are summarised in Table 1. (Martinez-Maestre's et al 2010).
Table 1 - Comparison of Literature Associating Osteoporosis and Periodontitis
Criteria assessed in study
Number of studies
Systemic osteoporosis vs. periodontitis
Systemic osteoporosis vs. mandibular osteoporosis
Systemic osteoporosis vs. tooth loss
Osteoporotic fracture vs. tooth loss
Osteoporotic fracture vs. mandibular osteoporosis
Osteoporotic fracture vs. tooth loss
The large number of excluded references demonstrates the high proportion of studies on the subject that possess methodological drawbacks. The majority of the included studies were also unable to provide conclusive (as opposed to suggestive) results, due to small sample sizes, limited control of confounding factors and inconsistent diagnostic criteria used to identify periodontitis and osteoporosis. Furthermore, variability in diagnostic criteria and definitions of osteoporosis make comparisons between references difficult. For example, systemic osteoporosis, as determined by dual photon or x-ray absorptiometrical analyses of the spine, hip, femur or forearm, is differentiated from osteoporotic fracture, that is determined by cortical bone thickness and trabecular bone pattern. Similarly, mandibular osteoporosis (analysed by dual photon absorptiometry of the mandible, residual ridge resorption and microdensitometrical analyses of occlusal, periapical and panoramic radiographs) is differentiated from periodontitis, which is diagnosed according to alveolar bone loss, probing depth, clinical attachment loss (CAL), tooth loss and plaque index clinically and/or radiographically (Martinez-Maestre's et al 2010).
Direct comparisons between the literature are also limited by differences in study methods and diagnostic criteria. For example, the degree of bone and attachment loss, cause of tooth loss, plaque index thresholds and radiographic analyses used to diagnose periodontitis, and whether these diagnoses correlate between studies is not discussed in the systematic review and only assumed to be equal across studies (Martinez-Maestre's et al 2010).
The effectiveness of the diagnostic criteria may also affect results of individual studies. Martinez-Maestre's et al (2010) found that trials based on radiological diagnoses of periodontitis identified a positive relationship with osteoporosis at a higher incidence than diagnoses based on clinical examination (Martinez-Maestre's et al 2010). Similarly, it has been suggested, and is currently controversial whether lumbar spine and femur BMD are accurate measures of systemic bone health (Megson et al 2010).
The majority of studies are cross-sectional and based on small sample sizes, which may add to the controversial nature of current evidence. Cross-sectional analyses do not control for potential confounding factors such as smoking and the temporality of results is not reflective of the course of either disease (Wactawski-Wende 2001).
Although the review of current literature by Martinez-Maestre's et al (2010) implies a positive association between the two diseases (that periodontitis is a local manifestation of systemic osteoporosis) the controversial nature of the included cross-sectional studies indicate that current evidence is equivocal. All studies included in the analysis support the need for further investigation of the relationship (Martinez-Maestre's et al 2010).
In addition to inconclusive results, literature negating the role of systemic osteoporosis on periodontitis is also available. Cross-sectional analyses of CAL and BMD by Pilgram et al (2002) produced no statistically significant findings. Longitudinal measurements conducted by the same authors implicated only a weak association between increased BMD and decreased attachment loss. The minor and inconsistent relationship between systemic bone health and periodontal status established in this study suggests that the investigated association may only involve both diseases being influenced by general health (Pilgram et al 2002). The legitimacy of these results is also limited by small sample size and poor control of potential confounding factors.
Nicopoulou-Karayianni et al (2009) also found that after adjusting for age and smoking, no association between CAL and tooth loss with systemic bone loss was evident. Controlling potential confounding factors (particularly increasing age and smoking) is essential for determining a causal relationship as increasing age, for example, affects both systemic BMD and is associated with increased numbers of missing teeth without any correlation to osteoporosis and periodontitis respectively.
It is possible that controlling shared risk factors of periodontitis and osteoporosis (Figure 1) will decrease the number of statistically significant positive results. This would indicate the two diseases are independent processes, linked only by common risk factors that influence bone resorption. Such a casual association would also explain epidemiological differences between osteoporosis and periodontitis as well as the presence of some contraindicating risk factors. In Australia, periodontitis is more prevalent in men, compared to the significantly increased prevalence of osteoporosis in women (ARCPOH 2009; Access Economics 2001). Similarly, low body mass index is reported to be a risk factor in osteoporosis, compared to diabetes implicated in periodontitis (Palomo et al 2007).
Mechanisms of Association
There are several possible mechanisms that may be responsible for the association between osteoporosis and periodontitis.
Firstly, decreased bone mineral density associated with osteoporosis increases the ability of the host immune response to resorb alveolar crestal bone in periodontitis, since bone is more porous which allows destructive inflammatory mediators to better penetrate bone structure (Wactawski-Wende 2001). This mechanism would therefore facilitate initiation of periodontitis and exacerbate progression of periodontitis following initiation.
Secondly, osteoporosis causes an increase in systemic levels of cytokines, particularly interleukin-1 and interleukin-6, which increases systemic bone resorption (Wactawski-Wende 2001). This includes increased resorption of craniofacial and oral bones, and it has been found that mandibular BMD can be correlated with skeletal BMD (Dervis 2005).
Thirdly, there are several common genetic and environmental factors that predispose people to both osteoporosis and periodontitis (Wactawski-Wende 2001). Common risk factors include genetics, malnutrition, and certain systemic diseases such as diabetes. These risk factors are assessed in Table 2.
Table 2 - Common Risk Factors in Osteoporosis and Periodontitis
Evidence - Examples of Studies
Mechanism of Action
Slemenda et al (1991) - comparing bone mass in monozygotic twins correlates better than comparing bone mass in dizygotic twins.
Geurs (2007) - bone mineral density has familial links.
Baldi et al (2009) - genetic polymorphisms, in combination with environmental influences, increase susceptibility to periodontitis.
Geurs (2007) - regulation of bone density is partially determined by genetic factors.
Baldi et al (2009) - structural alterations in particular enzymes, eg. metalloproteinases, alter their function.
Davies et al (2000) - dietary calcium supplements can slow the rate of bone resorption in post-menopausal women.
Kulie et al (2009) - vitamin D is essential for calcium absorption, hence deficiency can lead to a negative calcium balance, which compromises bone strength.
Amaliya (2007) - vitamin C is required for normal collagen formation, hence deficiency reduces bone strength and integrity of gingival tissues.
Kaye (2007) - bone has both mineral and organic components, and intake of dietary calcium, vitamin D and vitamin C are needed for normal bone formation.
Rothem et al (2009) - smokers have 4-5% lower bone mineral density values than non-smokers.
Stabholz et al (2010) - smokers have a dose-dependent increase in the incidence and severity of periodontitis and tooth loss.
Rothem et al (2009) - high nicotine intake suppresses osteoblast proliferation and increases bone metabolism.
Decreased physical activity
McKay et al (2010) - weight-bearing impact exercise leads to increased bone strength and improved bone architecture in adolescents.
Geurs (2007) - decreased weight-bearing activities and reduced muscular strain on bone structure lead to decreased stimulation of bone formation.
Heavy alcohol consumption
Hannan et al (2000) - women aged 67 to 90 who consumed more than 6 alcoholic beverages per day had increased bone resorption.
Geurs (2007) - ethanol directly decreases osteoblast function, causing a decrease in bone deposition.
There are several risk factors unique to osteoporosis, including:
Hormones - as demonstrated by the higher incidence of osteoporosis in menopausal women, oestrogen deficiency is a significant risk factor since menopause results in decreased levels of oestrogen production and secretion (Geurs 2007). Oestrogen plays an important role in maintaining bone mineral density, so deficiency results in accelerated bone resorption (Geurs 2007). This also accounts for the increased risk in females of developing osteoporosis.
Low body weight - leads to an increased rate of bone loss (Geurs 2007).
Low peak bone mass - reduced bone mass leading into later life reduces the bone mineral content available for resorption (Kaye 2007).
Implications for the Management of Patients with Periodontitis and Osteoporosis
Treatments used for osteoporosis may have an effect on alveolar bone as well, thus lessening the effects of periodontitis. However, the exact effect of osteoporosis medications on oral bone structure requires confirmation through further studies (Dervis 2005).
Hormone Replacement Therapy
The principle of hormone replacement therapy is to replenish systemic oestrogen levels to reduce the rate of bone loss, particularly in post-menopausal women. Most studies indicate that oestrogen and/or hormone replacement therapy can reduce tooth loss, increase mandibular bone density and reduce gingival bleeding (Dervis 2005). These improvements, however, tend to be relatively small and questionable in terms of clinical significance (Bartold et al 2010). The side-effects of hormone replacement therapy can also be significant, hence this course of treatment is not recommended for the management of bone loss in periodontitis (Bartold et al 2010).
Insufficient calcium and vitamin D has been shown to be associated with poorer bone health. Mineral supplements can be taken by osteoporosis patients to increase their calcium and vitamin D levels. Calcium supplementation has been shown to improve the health of patients with osteoporosis by reducing bone loss (Nordin 2009). Increased BMD has also been attributed to taking supplementary vitamin D (Jackson 2006). It has been suggested that patients with periodontitis should also take calcium and vitamin D supplements to improve their bone health. A study by Garcia et al (2010) showed that patients who took additional calcium and vitamin D had less periodontal disease than patients who did not take supplements. Therefore, patients who are taking mineral supplements to improve their osteoporosis may see additional benefits for their periodontal health. With further research to verify the benefits of calcium and vitamin D supplements for periodontal health, it may also be advisable that dentists recommend their patients take calcium supplements to reduce bone loss associated with periodontitis.
Dentists can play an important role in improving the nutritional intake of their patients (Palacios et al 2009). When addressing a patient's dietary habits in their medical history, calcium and vitamin D intake should be discussed. If a patient indicates that their consumption is insufficient, it could be an indication they are at greater risk of poor periodontal health as well as osteoporosis. Poor nutrition is becoming more prevalent in the Australian community, for example, many Australians have deficient levels of serum vitamin D (Shrapnel et al 2006). Therefore, periodontal disease and osteoporosis may become more common in the future and addressing nutritional problems will be an important aspect of general dental practice.
Bisphosphonate therapy interferes with osteoclast activity, leading to decreased systemic bone resorption (Palomo et al 2007). Bisphosphonates are pyrophosphate analogues which selectively adsorb to hydroxyapatite in bone, thus preventing bone mineral from undergoing enzymatic hydrolysis (Palomo et al 2007). Bisphosphonates used in the treatment of osteoporosis, such as alendronate and risedronate, could potentially be used for treatment of periodontitis due to the commonality of bone resorption mechanisms and the ability of bisphosphonates to modulate the host response to periodontopathogens (Palomo et al 2007). Many studies have indicated the benefits of bisphosphonate therapy with regards to alveolar bone levels and periodontal health, for example a study by Rocha et al (2004) showed that the rate of alveolar bone loss in periodontitis can be slowed with bisphosphonate therapy. Improvement in alveolar bone height is small, however, and the clinical significance of this improvement is debatable (Bartold et al 2010). Patients undertaking long-term high-dose bisphosphonate therapy are at risk for osteonecrosis of the jaw following tooth extraction (Kaye 2007). For these reasons bisphosphonate therapy is not recommended solely for the treatment of bone loss in periodontitis (Bartold et al 2010).
Many dentists do not address bone health as part of a standard medical history. If there is a link between osteoporosis and periodontitis, a greater focus could be placed on osteoporosis when assessing a patient's general health. If a patient reports having low BMD, it may indicate that periodontal health is at risk also. The same may be true for patients who present with periodontitis but have not been diagnosed with osteoporosis, particularly if they are females of menopausal age. For these patients, a referral to their general practitioner may be advisable. With greater collaboration between dentists and medical practitioners, the debilitating effects of bone fractures may be prevented (Edwards et al 2008).
Dental radiographs may be a useful tool for determining if a patient has low BMD. Analysis of trabecular density or cortex thickness can be used for the early detection of osteoporosis (Megson et al 2010). Patients with periodontitis have panoramic images taken to assess their periodontal health but these radiographs could also be used for the detection of low BMD. If a problem is detected, these patients could be referred to their general practitioner for further testing.
Further Research/Investigation Required
It is evident that the relationship between osteoporosis and periodontitis requires further investigation to determine conclusive results.
Such investigations should include prospective longitudinal studies that control for potential confounding factors (Lai 2004).
Large sample sizes are required for improved statistical significance and to accurately represent the population in race, gender and age. These studies should not be limited to post-menopausal women, despite the higher expected prevalence of osteoporosis in this population group. In fact, it is also suggested by Wactawski-Wende (2001) that as periodontal disease is more prevalent in males and African-American populations, further studies should focus in these groups for gender and race analyses. (Wactawski-Wende 2001)
Periodontitis and osteoporosis needs to be consistently defined in future studies and identified according to adequate and true diagnostic criteria (including both clinical and radiographic assessment). As well as improving study design, further randomised controlled trials should be conducted to assess the oral effects of osteoporosis therapies. This will assist in determining the clinical significance of a potential association for oral health professionals (Krall 2001).
Current evidence available exploring an association between periodontitis and osteoporosis is thus far inconclusive. This makes defining the nature of the relationship difficult and further research is required for clarification. The similar characteristics of the two diseases suggest that biological associations may exist through various mechanisms. However, the presence of similar risk factors indicates that this relationship may be casual, rather than causal. Although additional investigation is required, oral health professionals should be aware of the possible connection between periodontitis and osteoporosis.