Association between osteoporosis and periodontitis

 

Xanthippi E. Dereka

Lecturer

Department of Periodontology, School of Dentistry, University of Athens, Athens, Greece

 

Abstract

Research interest has recently been focused on the association between chronic periodontitis and osteoporosis. Periodontitis is an inflammatory disease of tooth-supporting tissues resulting from the interactions between bacterial biofilms and the host’s immuno-inflammatory response, leading to bone resorption. Specific periodontal microorganisms, smoking, and diabetes mellitus are the risk factors most strongly related to the induction and progression of periodontitis. Osteoporosis is a severe systemic bone disease affecting a significant percentage of people worldwide. It is associated with ageing and characterized by low bone mass and impairment of bone architecture, which increases susceptibility to bone fracture. Early detection of osteoporosis is possible with accurate diagnostic methods that measure bone mineral density (BMD). Several major or minor, modifiable or nonmodifiable risk factors for osteoporosis heve been identified, including low BMD, family history, previous fracture, low body weight, and smoking. Low BMD is considered the best predictor of fracture risk in postmenopausal women.

The aim of the present paper is to review the literature concerning the possible interactions between periodontitis and osteoporosis and to determine the underlying biological mechanisms. The findings indicate that low systemic bone mass in estrogen-deficient women probably affects alveolar bone density, which could constitute an important factor for the progression of periodontitis. Despite these findings, reviewers seem to agree that additional studies are needed to assess the role of osteopenia/osteoporosis in the induction and progression of periodontal disease.

Analecta Periodontologica 2009; 20:115-133

Researchers have recently focused on the association between osteoporosis and chronic periodontitis. In considering two patients, the first with a history of alveolar bone loss due to periodontitis and the second with systemic bone loss due to osteoporosis, one can assume that the two diseases share common features (Reddy 2001).

Periodontitis is an inflammatory disease of tooth-supporting tissues involving interactions between biofilms containing bacteria and other virulence factors and the host’s immuno-inflammatory response, leading to connective tissue alterations and bone resorption (Kornman 2008). Several bacteria, including Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, and Aggregatibacter actinomycetemcomitans, have been identified as etiologic agents in periodontal disease (Socransky and Haffajee 1997). Microorganisms are attached to the tooth surface, forming biofilms that have been defined as highly organized microbial communities embedded in an organic matrix (Marsh 2005). Periodontal tissue health depends on the balance between microbiota and the host immune system. During periodontal infection, microbial by-products penetrate the gingival connective tissue, inducing the host’s immune response, which provokes a varied degree of bone destruction.

Osteoporosis is one of the most common skeletal disorders, affecting a significant percentage of people worldwide. It is a severe systemic bone metabolic disease associated with ageing and is characterized by low bone mass and impairment of bone architecture, which increases susceptibility to bone fracture. An increasing percentage of women and men will be affected by osteoporosis, as the population ages (Kuo et al. 2008). Furthermore, the economic impact of osteoporotic fractures is increasing as the world population continues to age (Lips 1997, Delmas et al. 2005). The occurrence of fractures has increased in both sexes (Pietschmann et al. 2008). Approximately 30-50% of women and 15-30% of men will confront a fracture related to osteoporosis within their lifetime (Randell et al. 1995, Geurs 2007). Epidemiological data have established that the prevalence of the disease is constantly increasing; in the next years the number of osteoporotic fractures is expected to double. Bone loss progresses rapidly in women after menopause, as estrogen levels are reduced. Although bone loss rates may differ among populations and by evaluation method, some reports state that the decline in postmenopausal bone mass is 0.5-1.0% per year (Jeffcoat 2005).

Bone strength is determined by bone quality and bone density. Early detection of osteoporosis is possible with an accurate diagnostic method that measures bone mineral density (BMD). This measurement is the most readily quantifiable predictor of fracture risk for individuals who have not yet had a fragility fracture, and this risk should always be viewed in the context of the person’s age (Brown and Josse 2002). Dual energy X-ray absorption (DXA) was introduced in 1987 to measure systemic bone loss. DXA measures bone density as ‘area density’ in gram/cm2. The interpretation of results is based on two scores: the T-score, which is derived by subtracting the BMD of young normal persons from the BMD of an individual and then dividing the difference by the normal population standard deviation (SD), and the Z-score, which compares the BMD of the patient to a race-, gender-, and age-matched population (Jeffcoat 2005). According to the World Health Organization (WHO), a person is considered as osteoporotic when the BMD is 2.5 SD below the mean for young healthy adults (Τ-score < –2.5). A BMD between 1 and 2.5 SD below the mean (–1.0 < Τ-score < –2.5) is classified as osteopenia (WHO 1994, Brown and Josse 2002).

Digital radiography that monitors alveolar bone height and density changes has recently been modified to quantitatively estimate bone loss in dental X-rays (Jeffcoat et al. 1996). Moreover, computer-assisted densitometric image analysis (CADIA) is applied to estimate changes in bone density at crestal and subcrestal regions of interproximal bone using algorithms to interpret the results (Payne et al. 1999, Jeffcoat 2005).

 

Risk factors for periodontitis

The effectiveness of the host immune system depends on several internal and external factors. Νonmodifiable risk factors that have been related to periodontitis (Table 1) include (1) age, although the relation to periodontitis is not well clarified; (2) gender, because men have poorer periodontal health compared with women; (3) race/ethnicity, mainly because of the variety of socioeconomic opportunities among different groups; and (4) gene polymorphisms, although these cannot be characterized as true risk factors because of inadequate epidemiological data.

Furthermore, several environmental and acquired factors (Table 1) may contribute to the induction of periodontitis and the progression of the disease, including (1) socio-economic status, which may affect a person’s periodontal health; (2) specific periodontal microorganisms that are associated with different forms and stages of periodontal disease; (3) cigarette smoking, which has been proven to be related to the prevalence and severity of periodontitis; (4) diabetes mellitus, which is strongly associated with periodontitis; (5) osteopenia and osteoporosis; (6) HIV infection, for which the evidence concerning its relationship with periodontitis is rather contradictory; and (7) psychosocial factors, which are not strongly associated with periodontitis (Borrell and Papapanou 2005).

 

Risk factors for osteoporosis

Several major or minor, modifiable or nonmodifiable risk factors for osteoporosis have been identified (Table 2), including low BMD, family history, previous fracture, low body weight, and smoking (Brown and Josse 2002, Jeffcoat 2005, Geurs 2007). Of these factors, low BMD is considered the best predictor of fracture risk in postmenopausal women who do not have any other signs or symptoms of the disease. Moreover, age can be used as predictor of fracture risk independently of BMD in individuals who are over 65 years old.

Long-term, high-dose glucocorticosteroid treatment as a cause of bone destruction was examined by von Wowern et al. (1992). Loss of mandibular and forearm bone mineral content was analyzed in relation to periodontal indices such as dental plaque, gingival bleeding, and loss of attachment in 17 patients under going high-dose glucocorticosteroid treatment for 12 months. A 5.6%/year bone loss occured at both sites, although no significant changes could be demonstrated in the periodontal indices (von Wowern et al. 1992).

Genetic factors play an important role in the regulation of bone density, skeletal geometry, and the bone remodeling process (Jin and Ralston 2005). Multiple genes and their associated phenotypes controlling BMD and bone mass have been identified as responsible. The associated phenotypes studied are 50-80% inheritable and a large number of genes exhibit the potential to be involved in the pathogenesis of osteoporosis (Williams and Spector 2006).

 

Studies on the relationship between osteoporosis and periodontitis

Clinical studies have demonstrated the relationship among osteoporosis, bone destruction and tooth loss (Krall et al. 1996, Payne et al. 1999), although a strong statistical relationship between systemic and oral osteopenia (jawbone loss) has not yet been well clarified. Recent data indicate that individuals with systemic osteopenia/osteoporosis may be at increased risk for oral osteopenia symptoms, but this has not been definitively proven (Chesnut 2001). Research evidence mainly supports the association of osteoporosis with the initiation and progression of periodontal disease, although most studies have small sample sizes and are cross-sectional, uncontrolled, and restricted to postmenopausal women (Wactawski-Wende 2001). Furthermore, the results of published studies are often conflicting.

Kribbs et al. (1989) investigated the relationship between mandibular and skeletal bone mass in a group of 85 postmenopausal women with osteoporosis and reported that most of the edentulous patients had extremely resorbed ridges. The same research group (Kribbs et al. 1990) measured the mandibular bone mass and density, as well as cortical thickness at the gonion in 50 normal women (20-90 years of age). The researchers concluded that mandibular bone mass was significantly correlated with skeletal bone mass but was not affected by age, whereas cortical thickness at the gonion decreased with age (Kribbs et al. 1990).

In a relevant report, the possible relationship between periodontitis and systemic bone mass was evaluated in 286 female volunteers (46-55 years of age) by measuring alveolar bone height, lumbar BMD and metacarpal cortical thickness (Elders et al. 1992). No significant correlation between periodontal clinical parameters and bone mass parameters was found; therefore, systemic bone mass was not suggested as an important factor in the pathogenesis of periodontitis (Elders et al. 1992).

Hirai et al. (1993) reported that the reduction of the residual alveolar ridge is affected by osteoporosis, as well as by the gender and age of the patient. Βone mineral content, with advancing age, tended to increase slightly in the men's mandibles, whereas it tended to decrease in the women's mandibles (Solar et al. 1994). The relationship between self-reported tooth loss and BMD at the hip and spine in 608 men and 874 women (65-76 years old) was examined in a cross-sectional study (May et al. 1995). Α consistent decrease in BMD with increasing number of lost teeth was observed in men, a decrease that was irrelevant to age, body mass index, and smoking, whereas no significant association was found between tooth loss and BMD in women (May et al. 1995).

The association between dental status and skeletal bone density was investigated in 329 healthy postmenopausal women with normal bone density and the results showed that systemic bone loss may contribute to tooth loss (Krall et al. 1994). Moreover, the correlation between advanced periodontitis and bone mineral status of the skeleton and mandibular cortical bone was determined in a group of 227 healthy postmenopausal women aged 48-56 years old (Klemetti et al. 1994). Data analysis suggested that individuals with high mineral values in the skeleton seem to retain their teeth with deep periodontal pockets more easily than did individuals with osteoporosis (Klemetti et al. 1994).

Moreover, researchers proposed that periodontal disease may be an early manifestation of severe bone metabolic disorder (Whalen and Krook 1996, Kuo et al. 2008). Bando et al. (1998) reported that sufficient masticatory function with periodontally healthy dentition may inhibit or delay the progress of osteoporotic changes in skeletal bone and that edentulous women may be more susceptible to osteoporosis. The loss of posterior teeth in elderly Japanese women has been associated with a decrease in alveolar bone height and mineral density (Taguchi et al. 1999). Conversely, Weyant et al. (1999) evaluated the association between systemic BMD and the clinical signs of periodontal tissue destruction in a cross-sectional study of 292 dentate women with an average age of 75.5 years. Data analysis indicated that there was no statistically significant association between the clinical parameters of periodontal disease and systemic BMD, and the authors concluded that systemic osteopenia could be considered only as a weak risk factor for periodontal disease in older women (Weyant et al. 1999).

Smoking is considered as a major but modifiable risk factor for osteoporosis. Therefore, the impact of smoking on alveolar bone height and density changes has also been investigated. In a cross-sectional study of 135 postmenopausal women (41-70 years old), clinical attachment loss was correlated with tooth loss, but not with vertebral or proximal femur bone density; current smoking, years since menopause, and interaction of age and smoking were statistically significant predictors of attachment loss (Hildebolt et al. 1997). In a similar study, 59 postmenopausal women with periodontitis were followed for 2 years (Payne et al. 2000). Females with systemic osteoporosis/osteopenia manifested net alveolar bone density loss, although their dental plaque levels did not differ from nonsmoking subjects with normal BMD. The authors concluded that smoking is associated with a higher frequency of alveolar bone height and density loss in postmenopausal women (Payne et al. 2000).

Clinical data indicate that postmenopausal women with low BMD are more likely to have clinical attachment loss, gingival recession, and inflammation (von Wowern et al. 1994, Mohammad et al. 1996, 1997, Tezal et al. 2000). However, several studies failed to identify a significant correlation (Weyant et al. 1999, Lundstrom et al. 2001) and noted that an increased incidence of progressive periodontitis based on clinical attachment changes is not associated with estrogen deficiency alone (Reinhardt et al. 1999).

Tezal et al. (2000) evaluated the relation between systemic BMD and periodontal disease in 70 postmenopausal Caucasian women (51-78 years of age). The results implied that osteopenia could be a risk indicator for periodontal disease in postmenopausal women because skeletal BMD was found to be related to interproximal alveolar bone loss and, to a lesser extent, to clinical attachment loss (Tezal et al. 2000). In another study evaluating the periodontal status of 89 premenopausal and 101 postmenopausal Japanese women, low metacarpal BMD was associated with periodontitis and tooth loss after menopause (Inagaki et al. 2001).

The association between BMD and clinical attachment level is not well proven. Pilgram et al. (2002) investigated in a cross-sectional study the possible association between BMD of the spine and hip and clinical attachment loss in 135 healthy postmenopausal women. The results revealed a weak correlation between clinical attachment level and BMD (Pilgram et al. 2002). However, decreasing BMD of the os calcis was associated with increased clinical attachment loss and tooth loss in a cross-sectional study of 30 postmenopausal Asian-American women (Mohammad et al. 2003). A significant association between BMD and sites with progressive attachment loss was detected in 179 older Japanese (over 70 years old) who were followed for 3 years (Yoshihara et al. 2004). In another 2-year study, no association among edentulousness, clinical attachment loss, and longitudinal changes in BMD was reported in 398 women with a mean age of 75.5 years (Famili et al. 2005). Yet clinical evidence supported a strong association between systemic BMD and clinical attachment loss in a cross-sectional study of 1,329 postmenopausal women, whereas the presence or absence of subgingival calculus seemed to act as an effect modifier (Brennan et al. 2007a).

Furthermore, the presence of specific subgingival bacterial species was investigated in a cross-sectional study of oral health and osteoporosis in 1,256 postmenopausal women (Brennan et al. 2007b). The results revealed that the most prevalent species was Streptococcus sanguis, followed by Prevotella intermedia, Tannerella forsythia, Capnocytophaga sp., Eubacterium saburreum, Campylobacter rectus, Porphyromonas gingivalis, and Fusobacterium nucleatum. Infections with P. gingivalis, T. forsythia, P. intermedia, and C. rectus were associated with an increased possibility of alveolar bone loss (Brennan et al. 2007b). The influence of oral infection and age on the association between osteoporosis and oral bone loss was further evaluated by the same research group. In a cross-sectional study of 1,256 postmenopausal women, oral infection was assessed in subgingival plaque samples, systemic BMD was measured by DXA, and alveolar crest height was calculated on standardized dental radiographs (Brennan-Calanan et al. 2008). Older women (>70 years old) presented with more jawbone loss, but BMD and oral infection were not significantly associated with mean alveolar height. However, BMD and bacterial infection were independently associated with alveolar bone loss in younger postmenopausal women (<70 years old). The researchers concluded that bacterial infection was not a confounder or effect modifier of the associations between systemic bone density and oral bone loss (Brennan-Calanan et al. 2008).

 

Interactions between osteoporosis and periodontitis: underlying biological mechanisms

Osteoporosis and periodontitis are chronic diseases characterized by bone resorption. Bone homeostasis results from the coordinated interaction between bone-forming and bone-resorbing cells, and the imbalance of the activity between these two cell types leads to gradual bone degradation and osteoporosis (Pietschmann et al. 2008). Estrogen deficiency in the postmenopausal female is the major cause of osteoporosis which could also contribute to periodontal disease characterized by increased alveolar bone destruction and tooth loss. The mechanism of bone loss for both bone disorders is systemic or local increased bone resorption due to increased osteoclastic activity and to local cellular or cytokine effects (Chesnut 2001). Multiple underlying mechanisms involved in the interactions between these two diseases have been considered.

Estrogen decline during menopause is associated with an increased potential for human bone marrow cells to release bone-resorbing cytokines, which may play an important role in accelerated bone resorption (Bismar et al. 1995). Estrogen activity is affected and regulated by multiple cytokines that stimulate a large number of target cells, but increased bone resorption may occur from relative elevation of only a few factors in the microenvironment of the bone (Pacifici 1996). Interleukin (IL)-1 and tumor necrosis factor (TNF) play an important causal role in the bone loss process. These cytokines are produced in bone and bone marrow and are released in large amounts in estrogen-deficient subjects. Estrogen deficiency increases osteoclastogenesis via IL-1 and TNF-mediated stimulation of macrophage colony-stimulating factor production by stromal bone marrow cells (Kimble et al. 1996).

The concentration of IL-1, a potent stimulator of osteoclastic bone resorption, is elevated in estrogen deficiency by increased production of IL-1 and concurrent inhibition of the IL-1 receptor antagonist (IL-1ra). Keen et al. (1998) examined the relationship between annual rates of BMD changes over 5 years and the IL-1 receptor antagonist gene (IL-1RN), which is a potential candidate gene for the regulation of postmenopausal bone loss. Three alleles with five genotypes were identified and the allelic variation at the IL-1RN locus was associated with differential rates of early postmenopausal bone loss (Keen et al. 1998). In addition, low concentrations of estradiol and progesterone were proposed as risk factors for periodontitis because, under these conditions, monocytes respond directly to bacterial lipopolysaccharide stimuli by producing high levels of IL-1α and IL-1β (Morishita et al. 1999).

The potential common pathways between osteoporosis and periodontal disease were thoroughly studied in an animal model of postmenopausal osteoporosis (Golub et al. 1999). In the ovariectomized aged rat, local alveolar bone loss and systemic loss of bone density were accompanied by increased gingival collagenase activity. Interestingly, the severity of both osteoporosis and bone destruction was reduced when a nonantimicrobial, chemically modified tetracycline was administered to these rats (Golub et al. 1999).

Furthermore, IL-6, a potent mediator of inflammatory processes, may be involved in the pathogenesis of both osteoporosis and periodontal disease because of the observed age-related increased IL-6 levels (Ershler and Keller 2000). However, Keller et al. (2000) demonstrated that modulation of IL-6 levels is not the key mechanism through which estrogen deprivation mediates bone loss. Serum IL-6 levels were tested as a predictor of bone loss in a longitudinal study of 137 postmenopausal German women (Scheidt-Nave et al. 2001). The epidemiological data indicated that serum IL-6 was predictive of femoral bone loss in postmenopausal women but that this predictive effect was restricted to the first 10 years after menopause (Scheidt-Nave et al. 2001).

The initiation and progression of periodontal diseases may be influenced by an increased host susceptibility to infectious challenges (Wactawski-Wende 2001). It is biologically plausible that part of the periodontal destruction is influenced by systemic bone loss. The following potential mechanisms by which osteoporosis may be associated with periodontal diseases have been presented:

1. Low BMD in the oral cavity associated with low systemic bone mass leads to more rapid alveolar bone resorption as an inflammatory response to infection.

2. Systemic factors of bone remodeling may modify the local response of periodontal tissues to infection.

3. Genetic factors that predispose a person to systemic bone loss may also predispose the individual to more pronounced periodontal damage.

4. Certain lifestyle factors could act as risk factors for the development of osteopenia and periodontal disease (Tezal et al. 2000).

Golub et al. (2006) proposed a “two-hit” model that linked osteoporosis, among other systemic diseases, and periodontal bone loss. Briefly, periopathogenic microorganisms provide one “hit” in the cascade of destructive events of periodontitis, and the second “hit” comes from a systemic inflammatory response that is induced by various medical disorders. Even a small increase in the circulating serum levels of IL-1, IL-6, and TNF may initiate the cytokine/prostaglandin/matrix metalloproteinase/receptor activator of nuclear factor-kappa B ligand (RANKL) cascade in the periodontal tissues (Golub et al. 2006).

Bone mass decreases during menopause and bone strength is reduced because of the increased frequency of bone resorption activation and the decreased ability of osteoblasts to produce new bone. Recent data support the principal role of estrogen in controlling bone resorption by the estrogen receptors ERα and ERβ in the cytoplasm of osteoblasts and osteoclasts. These receptors restrict the osteoclast activation pathway in osteoblasts, decrease the osteoclast formation from the progenitor osteoclasts, and inhibit the osteoclastic activity of osteoclasts (Lerner 2006a). Furthermore, estrogen may control the function of prostaglandin E2, which is a potent stimulator of bone resorption and osteoclast formation, through the inhibition of the cytokines that stimulate cyclooxygenase-2. Even though estrogen deficiency enhances expression of IL-1 and TNF, efforts to correlate serum levels of these cytokines with osteoporosis resulted in contradictory findings (Lerner 2006a).

The key cytokine system that regulates the bone remodeling process depends on the differentiation and activation of osteoclasts, RANKL, and its soluble decoy receptor osteoprotegerin (OPG) balance (Kong et al. 1999, Hofbauer and Heufelder 2001). Recent research evidence shows that the RANKL/OPG pathway plays the most important role in osteoclastogenesis and inflammatory bone loss in periodontitis (Taubman et al. 2005, Wada et al. 2006, Leibbrandt and Penninger 2008). OPG binds to RANKL and prevents the interaction between RANK and RANKL and thus the formation of osteoclasts. TNF-α stimulates IL-1 production from osteoblasts and stromal cells in the presence of certain levels of RANKL, as well as from osteoclasts in the presence of RANK (Lerner 2006a). In addition, activated T cells express RANKL, which binds to RANK on dendritic cells and enhances their activation and survival. On the other hand, T cells produce inflammatory cytokines (IL-1, IL-6, and TNF) that stimulate RANKL expression in osteoblasts. Thus, activated T cells and osteoblasts stimulate the differentiation of osteoclasts via the RANK/RANKL pathway, resulting in bone resorption. Osteoclast differentiation is balanced by OPG secreted from osteoblasts and by IL-4 and TNF produced by T cells (Leibbrandt and Penninger 2008).

Estrogen deficiency diminishes the expression of OPG (Saika et al. 2001), upregulates the RANKL/OPG system, and dysregulates T cell function and antigen presentation (Pietschmann et al. 2008). Moreover, in the presence of Gram-negative bacterial infection, estrogen deficiency has been shown to exhibit synergistic effects on bone metabolism with lipopolysaccharide, leading to enhanced bone resorption in female mice (Fujita et al. 2008).

Recent research evidence has suggested that periodontal status is associated with osteoporosis, ethnicity, probing depth, gender, serum C-reactive protein, and levels of Parvimonas micra, Prevotella intermedia, Tannerella forsythia, and Streptococcus mutans (Swoboda et al. 2008). Furthermore, in an animal model study, the elevated expression of IL-6, nuclear factor-kappa B, bone-specific alkaline phosphatase, and bone osteocalcin implied the potential role of these molecules in the pathogenesis of osteoporosis (Zhu et al. 2008).

 

Hormone replacement therapy and perio-dontal status

Hormone replacement therapy is commonly used to prevent bone loss and other signs and symptoms in osteoporotic women. Estrogen supplementation has been associated with reduced gingival bleeding compared with a control group (Norderyd et al. 1993) and has been proven beneficial in preventing tooth loss, although not without risk for other systemic disorders (Paganini-Hill 1995a, 1995b). In addition, women who underwent this treatment experienced positive effects on the bone mass of the mandible and lumbar spine (Jacobs et al. 1996).

The influence of estrogen status on alveolar bone changes was addressed in a 1-year longitudinal study in which estrogen-sufficient postmenopausal women displayed a gain of alveolar bone density, whereas estrogen-deficient women exhibited bone loss (Payne et al. 1997). However, Streckfus et al. (1997) reported that postmenopausal women receiving estrogen therapy had higher salivary IL-6 concentrations, more alveolar bone loss, more missing teeth, and reduced alveolar bone density than did premenopausal women. Estrogen replacement therapy has also been associated with reduced gingival inflammation and reduced frequency of clinical attachment loss in osteoporotic women in early menopause (Reinhardt et al. 1999) and with increased alveolar bone density and improvement of dental health (Civitelli et al. 2002, Hildebolt et al. 2002). Finally, Hildebolt et al. (2004) reported that osteoporotic women receiving estrogen replacement treatment and/or calcium and vitamin D supplementation exhibited significant increases in oral bone density, which were greatest during the first 3 years in a 5-year treatment period.

 

Conclusions

Reviewers seem to agree that, to assess the role of osteopenia/osteoporosis in the induction and progression of periodontal disease additional studies are needed: well-designed large-scale studies to determine the role of osteopenia on the prevalence and severity of periodontal disease and prospective studies controlling the confounding variables to determine whether osteopenia is associated with the incidence and progression of periodontal diseases. Intervention studies may be helpful to justify modification of BMD as an approach for the management of periodontal disease (Tezal et al. 2000, Wactawski-Wende 2001, Borrell and Papapanou 2005).

Research data do not strictly correlate alveolar bone mass with osteoporosis, although the findings of several studies indicate that low systemic bone mass in estrogen-deficient women probably affects alveolar bone density. Furthermore, estrogen replacement therapy in postmenopausal women seems to positively affect jawbones, suggesting that oral bone could be susceptible to osteoporosis (Lerner 2006b).

 

Acknowledgments

 

The author declares that there are no financial or other conflicts of interest related to this publication.