We have read with great interest the published article by Gümüş et al.1 They have evaluated saliva and serum levels of pentraxin-3 (PTX3) and interleukin-1β (IL-1β) in patients with generalized chronic periodontitis (CP) or aggressive periodontitis (AgP) and periodontally healthy individuals and concluded that salivary PTX3 might be suggested to be related to periodontal tissue inflammation. However, there are some points that need to be clarified.
PTX3 is an acute-phase protein and produced in response to inflammatory conditions in vivo.2 There are various situations that likely affect PTX3 levels. The authors defined exclusion criteria as individuals with medical disorders, such as diabetes mellitus, and immunologic disorders and those who had received antibiotic or periodontal treatment in the last 6 months. In addition to these conditions, PTX3 levels vary in several inflammatory or infectious diseases such as rheumatologic diseases, vasculitis, chronic obstructive pulmonary disease, asthma, pneumonia, and ulcerative colitis.3 In this regard, simple laboratory tests such as C-reactive protein, erythrocyte sedimentation rate, complete blood count, and routine biochemistry tests could have been performed in addition to PTX3 and IL-1β evaluation to make selection of participants for the study more reliable.
Previous studies showed that angiotensin-converting enzyme inhibitors, glucocorticoids, and statins affect serum PTX3 levels.4 In addition, dietary supplements such as omega-3 fatty acid, vitamin D, vitamin A, and vitamin E could affect PTX3 levels.5 Bailey et al. reported that supplement use was reported by 49% of the United States population.6 In this regard, the authors should state whether the participants use these kinds of dietary supplements.
Obesity is another confounding factor for PTX3 measurement. Witasp et al.7 reported that PTX3 levels positively correlate with obesity. Therefore, body mass indexes of participants should be defined.
Lastly, although the authors expressed that not selecting sex-matched individuals was a limitation, we would go further in stating that it is not acceptable. Yamasaki et al.8 showed that there was a significant difference between the sexes in terms of PTX3. Also, we wonder if there is a plausible explanation as to why the authors did not obtain serum samples of control groups. This situation leads to lack of strength of the study.
In conclusion, we believe this study contributes valuable information to the medical literature. However, the explanation of our concerns will certainly provide clearer information for readers.
The authors report no conflicts of interest related to this letter.
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