Rker [33,34]. The combined assessment of CRP and purchase MK 8931 orosomucoid profiles can be used to diagnose, date and monitor the inflammatory JI 101 manufacturer syndrome: in an early onset reaction, only CRP increases; then both CRP and orosomucoid increase; and after a successful treatment, CRP decreases first. Since periodontitis is a chronic disease of infectious origin, orosomucoid 25033180 appears to be a better inflammatory marker than CRP in the morbidly obese, who display a chronic increase in CRP. Moreover, in obese patients, IL-6 synthesis is more the reflection of adipose tissue production itself than representative of systemic inflammation [35]. Therefore, IL-6 levels may correlate less with periodontal disease than CRP or orosomucoid. Indeed, the data of the present study do not show any association between CRP, IL-6, leptin or adiponectin with periodontitis in morbidly obese patients. This is 
in accordance with a case control study showing that periodontitis was not associated with decreased levels of adiponectin [36]. In this study, the association between severity of periodontitis and the orosomucoid levels failed to reach statistical significance after adjustment for diabetes (Table 3). A large cohort study has shown that orosomucoid levels were associated with the development of diabetes mellitus in middle-aged adults [37]. Recently, an animal study has suggested that orosomucoid may be involved in the reduction of neutrophil migration and increased susceptibility to sepsis in diabetic mice [38]. Diabetes could thus introduce a bias in the association between high orosomucoid levels and periodontitis in obese patients with impaired neutrophil function. Furthermore, orosomucoid is a marker of malnutrition. There is a link between nutritional status and periodontitis [39] which could explain the association between orosomucoid level and pocket depth in morbidly obese patients. Nevertheless, theOrosomucoid, Obesity and Periodontitisorosomucoid threshold to define malnutrition is 1.2 g/l and in this study none of the morbidly obese patients had orosomucoid plasma levels reaching that value. The present study has several strengths. First, it is the first study to deal with 
the association between periodontal parameters and systemic inflammation markers in a morbidly obese population. We chose morbid obesity as a model because it represents the most extreme condition of obese patients, i.e. the worst inflammatory condition. To our knowledge, this is the first clinical study demonstrating a systemic link among obesity, periodontitis, and systemic low-grade inflammation. Second, we do not use a specific classification for periodontal diseases. Instead, we use clinical periodontal parameters to enable comparisons with other available data. The definition of periodontitis varies considerably in epidemiological studies [22]. The use of a diagnostic classification may jeopardize the analysis by increasing the risk of finding spurious associations. Third, we included a full-mouth periodontal clinical examination at six sites per tooth, to obtain a detailed periodontal status of all individuals. Therefore, the sensitivity of our study may be higher than others which used partial recording and/or self-reported data. However, this study has limitations inherent to its cross-sectional design that cannot determine a causal relationship. It may also be assumed that our sample size is relatively small. Even if an increase in morbid obesity prevalence is observed in industrialize.Rker [33,34]. The combined assessment of CRP and orosomucoid profiles can be used to diagnose, date and monitor the inflammatory syndrome: in an early onset reaction, only CRP increases; then both CRP and orosomucoid increase; and after a successful treatment, CRP decreases first. Since periodontitis is a chronic disease of infectious origin, orosomucoid 25033180 appears to be a better inflammatory marker than CRP in the morbidly obese, who display a chronic increase in CRP. Moreover, in obese patients, IL-6 synthesis is more the reflection of adipose tissue production itself than representative of systemic inflammation [35]. Therefore, IL-6 levels may correlate less with periodontal disease than CRP or orosomucoid. Indeed, the data of the present study do not show any association between CRP, IL-6, leptin or adiponectin with periodontitis in morbidly obese patients. This is in accordance with a case control study showing that periodontitis was not associated with decreased levels of adiponectin [36]. In this study, the association between severity of periodontitis and the orosomucoid levels failed to reach statistical significance after adjustment for diabetes (Table 3). A large cohort study has shown that orosomucoid levels were associated with the development of diabetes mellitus in middle-aged adults [37]. Recently, an animal study has suggested that orosomucoid may be involved in the reduction of neutrophil migration and increased susceptibility to sepsis in diabetic mice [38]. Diabetes could thus introduce a bias in the association between high orosomucoid levels and periodontitis in obese patients with impaired neutrophil function. Furthermore, orosomucoid is a marker of malnutrition. There is a link between nutritional status and periodontitis [39] which could explain the association between orosomucoid level and pocket depth in morbidly obese patients. Nevertheless, theOrosomucoid, Obesity and Periodontitisorosomucoid threshold to define malnutrition is 1.2 g/l and in this study none of the morbidly obese patients had orosomucoid plasma levels reaching that value. The present study has several strengths. First, it is the first study to deal with the association between periodontal parameters and systemic inflammation markers in a morbidly obese population. We chose morbid obesity as a model because it represents the most extreme condition of obese patients, i.e. the worst inflammatory condition. To our knowledge, this is the first clinical study demonstrating a systemic link among obesity, periodontitis, and systemic low-grade inflammation. Second, we do not use a specific classification for periodontal diseases. Instead, we use clinical periodontal parameters to enable comparisons with other available data. The definition of periodontitis varies considerably in epidemiological studies [22]. The use of a diagnostic classification may jeopardize the analysis by increasing the risk of finding spurious associations. Third, we included a full-mouth periodontal clinical examination at six sites per tooth, to obtain a detailed periodontal status of all individuals. Therefore, the sensitivity of our study may be higher than others which used partial recording and/or self-reported data. However, this study has limitations inherent to its cross-sectional design that cannot determine a causal relationship. It may also be assumed that our sample size is relatively small. Even if an increase in morbid obesity prevalence is observed in industrialize.
