The study included 33 aggressive periodontitis patients and 33 healthy individuals. Patient group included 24.4% male and 57.6 female, ranging in age from 16-47 years, with a mean equal to 26.3 years old. Regarding control group 24.4% were males and 57.6% were females, ranging in age from 16-44 years, with a mean equal to 29.1 years old (Table 1). In total, the mean ± SD of circular C-reactive protein was 4.67 ± 0.841 mg/l, with a mode equal to 4.9 mg/L, the median was 4.9 mg/L, and ranged from 2.8 to 6.1 mg/l with the 75% interquartile range (IQR) equal to 5.1 mg/l; the variance in all individual values was significantly distributed on the normal curve with t-test of 31.8 and p < 0.0001. For males the mean ± SD of circular C-reactive protein was 4.42 ± 0.57 mg/l, with a mode equal to 3.9 mg/L, the median was 4.33 mg/L, and ranged from 3.7 to 5.7 mg/l with the 75% interquartile range (IQR) equal to 4.9 mg/l; the variance in all individual values was significantly distributed on the normal curve with t-test of 28 and p < 0.0001. For females the mean ± SD of circular C-reactive protein was 4.85 ± 0.968 mg/l, with a mode equal to 5.1 mg/L, the median was 5.1 mg/L, and ranged from 2.8 to 6.1 mg/l with the 75% interquartile range (IQR) equal to 5.4 mg/l; the variance in all individual values was significantly distributed on the normal curve with t-test of 21.8 and p < 0.0001 (Table 2).

C-reactive protein concentrations (mg/l) for aggressive periodontitis total patients was as follow: the mean ± SD of circular C-reactive protein was 4.67 ± 0.841 mg/l, with a mode equal to 4.9 mg/L, the median was 4.9 mg/L, and ranged from 2.8 to 6.1 mg/l with the 75% interquartile range (IQR) equal to 5.1 mg/l; the variance in all individual values was significantly distributed on the normal curve with t-test of 31.8 and p < 0.0001.

While for healthy controls the C-reactive protein concentrations (mg/l) were lower than that of the patients in which the mean ± SD of circular C-reactive protein was 2.067 ± 0.387 mg/l, with a mode equal to 2.1 mg/L, the median was 2.1 mg/L, and ranged from 1.2 to 3.1 mg/l with the 75% interquartile range (IQR) equal to 2.2 mg/l; the variance in all individual values was significantly distributed on the normal curve with t-test of 30.6 and p < 0.0001 (Table 3). Considering age groups effects on the C-reactive protein concentrations (mg/l) for aggressive periodontitis patients, roughly equal levels values were occurred in all age groups (Table 4).

DISCUSSION

CRP represents a dependable marker of acute phase response to infectious burden and/or inflammation [35]. As a result of its kinetic possessions, C-reactive protein best illustrates the inflammatory state of the human [36]. Recent evidence indicated that patients with acute periodontitis had increased serum C-reactive protein levels compared to an unaffected control group [37]. We compared and evaluated systemic levels of CRP in peripheral blood samples of patients with aggressive periodontitis and healthy controls. CRP levels may fluctuate with various factors such as hypertension, alcohol use, smoking, diabetes, sleep disorders, chronic fatigue, depression, several other systemic diseases, and pregnancy or lactation [38]. Therefore, we established robust exclusion criteria (see Methods) for patients to be included in this study.

In the current study, the C-reactive protein (mg/L) concentrations of periodontitis patients were approximately 2.5 volumes higher than that of healthy controls (patients' mean ± SD = 4.67 ± 0.841 mg/L vs. 2.067 ± 0.387 mg/L of control). This underscores the fact that CRP levels correlate with severity of periodontal affection and aggressive periodontitis shows a stronger systemic inflammatory burden than the control group similar to that reported by Wohlfeil [39]. Also, our finding is similar to that study of Goyal [40] showed the highest CRP levels in patients with aggressive periodontitis and the lowest values in the group of healthy patients [40]. Other studies showed increased CRP levels in patients with chronic periodontitis compared to patients with gingivitis [41,42]. In a study by Podzimek [43] aggressive periodontitis patients had an average CRP of 2.8 mg/L below or levels of the same patient group (4.67 ± 0.841 mg/L). This difference may be explained by that, race has been found to influence CRP levels [44] and data in diverse populations are not comparable. A study from the USA reported C-reactive protein (CRP) levels of 2.05 mg/L in aggressive periodontitis patients with the generalized form and C-reactive protein (CRP) levels of 1.1 mg/L in patients with the localized form [45]. However, our result (4.67 ± 0.841 mg/L) is similar to another study from the USA that showed C-reactive protein (CRP) levels of 4.06 mg/L in subjects with high levels of clinical attachment loss mean [46].

While lower values were reported in a Swedish study showing an average CRP of 2 mg/L in periodontitis patients [47]. In the Netherlands, a study reported lower CRP levels than (1.45 mg/L) in patients with a generalized form of periodontitis and CRP levels of 1.30 mg/L in patients with the localized form [48]. Another study from India showed a higher level than our study where CRP levels of 7.49mg/L in aggressive periodontitis patients and CRP levels of 4.88mg/L in chronic periodontitis patients were found [49]. Therefore, in our study, only patients of Yemeni origin were included.

Regarding the statistical associations between male and female indices as well as ages with CRP levels determined in periodontitis patient groups, there were no significant differences with C-reactive protein concentrations (mg/L) for the comparison of aggressive periodontitis for males and females or for age groups (Tables 2 & 3). These results are similar to those previously reported in which no significant differences were found between sexes or between ages [43]. Thus, CRP increases with periodontal impairments. The CRP indicator is a very important issue. The observed association between periodontal conditions and systemic CRP demonstrated that periodontal affections may be a contributing factor to systemic inflammation. In the study by Beck [50]. CRP as a clinical parameter was more difficult to estimate the degree of systemic inflammation than traditional classifications of mild, moderate, and severe periodontitis or other measures of disease severity such as attachment loss [50]. The novelty of the results obtained was based on comparing one type of periodontal disease with healthy controls, as two or three types are usually compared, and on comparing various periodontal indices with subsequently determined CRP levels in the patient's peripheral blood.

CONCLUSION

Our study results show that CRP levels increase subsequently with the aggressive periodontitis patients, and there was no significant effect of sex or ages in the level. Further studies are needed to clarify this association and the associated confounding factors. In further research, other systemic markers that might be more specific to periodontal disease such as fibrinogen, leptin, white blood cell count, and interleukin-6 should be considered. Changes in their values during the treatment of periodontal disease could lead to improved monitoring of periodontal tissue status during therapy. Elevated levels of such markers of systemic inflammation are connected to both systemic diseases and periodontal diseases. Studying these markers would certainly be beneficial for monitoring periodontal disease therapy.

ACKNOWLEDGMENTS

The authors thank the Faculty of Dentistry, Sana'a University, Sana'a, and Yemen for their generous support.

CONFLICT OF INTEREST

No conflict of interest associated with this work.

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  Table 1
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  Table 2
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  Table 3
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  Table 4