Background
Periodontal therapy is aimed to provide functional dentition and comfort for patients [
1] with periodontitis. Non–surgical periodontal therapy (NSPT) focuses on elimination of bacterial plaque on the root surface by means of scaling and root surface debridement and preparing the root surface for healing. NSPT has been shown to provide improvement in clinical parameters namely, Visible Plaque Index (VPI), Gingival Bleeding Index (GBI), Probing Pocket Depth (PPD), Clinical Attachment Level (CAL), as well as reduction inflammation and in periodontal pathogens. NSPT was shown to induce a shift from a pre-dominant Gram negative to a Gram positive subgingival microbiota in the general population [
2] and to significantly reduce total bacteria counts and positive sites of
P. gingivalis and
T. forsythia [
3,
4]. NSPT is also expected to reduce the serum resistin level, which otherwise is present in higher amount in case of periodontal inflammation with periodontitis patients as compared to healthy individuals [
5].
The outcome of the NSPT might vary depending on the severity of the disease as well as the other health complications of the patients such as obesity [
6,
7]. Previous research showed that mean serum resistin was higher in obese subjects with periodontitis followed by non-obese periodontitis and non-obese healthy [
8]. Following 2 months post-NSPT, greater reduction in resistin was observed in normal weight with periodontitis than obese periodontitis subjects [
9]. In contrast, previous studies which compared obese and non-obese subjects with periodontitis following NSPT showed no significant difference in terms of serum levels of resistin at baseline and 3 months post-NSPT [
5,
10]. Similarly, obesity condition could enhance the risk of patients to exhibit periodontitis by having high numbers of pathogenic subgingival species. Previous studies demonstrated that mean counts of
P. gingivalis and
T. forsythia were higher in obese with periodontitis [
11,
12].
Resistin is a 12.5 kDA cysteine-rich secretory protein with mature sequence consists of 108 amino acids. Resistin has been expressed in macrophages, neutrophils and lymphocytes, and play various regulatory roles in biological processes including inflammation [
13]. The role of resistin in the inflammatory pathway has been suggested through a nuclear factor NF-κB pathway [
14]. Systematic and meta-analysis study reported high level of serum resistin observed in periodontitis patients as compared to healthy individuals [
15]. This could be explained by the increased local pro-inflammatory cytokine levels in patients with periodontal inflammation, which is also associated with a state of elevated localized inflammatory burden. On the same note, obese subjects also showed elevated levels of serum inflammatory biomarkers (secreted from adipocytes), which modulate inflammatory responses indicating its possible inflammatory role in periodontitis.
The lack of evidence in this area and conflicting outcomes from previous studies warrant further investigations. More specifically, studies on the potential outcome of NSPT on the periodontal parameters, serum resistin level, and periodontal pathogens counts in periodontitis with obesity remains largely scanty. Thus, it remains unclear whether NSPT has a significant impact on these obese patients and normal weight patients, with periodontitis. Therefore, this study was aimed to evaluate the impact of NSPT on clinical parameters, serum resistin level and periodontal pathogen count in periodontitis patients with obesity and with normal weight.
Discussion
Periodontitis is a chronic inflammatory response that causes gingival inflammation and destruction of hard tissues [
25]; with 30 to 35% prevalence in the general population worldwide [
26]. Interestingly, the prevalence of periodontitis among obese populations worldwide has been reported between 47 to 74% [
16,
27,
28]. Clinical conditions of periodontitis might aggravate in patients with other health complication such as obesity [
29]. A positive but weak association between obesity and periodontitis has been reported [
30], with unclear underlying biological mechanisms.
The present study reported no significant difference in mean serum resistin levels between baseline and 12 weeks after NSPT in both obese and normal weight groups. The current study findings contradicted other short-term studies, with a gap of 10–12 weeks to measure serum resistin following NSPT [
31,
32]. Suresh and co-workers (2018) reported greater reduction in resistin which was observed in normal weight periodontitis than obese periodontitis at 8 weeks post-NSPT [
9]. Even though short-term studies can demonstrate improvements of clinical parameters; however, it is not the same with serum level of cytokines and resistin. This notion is supported by Ide et al. (2003), who reported that short term study of 12 week duration could be insufficient to establish any biochemical changes following NSPT [
32]. Thus, a study with a longer duration is recommended to observe meaningful changes in biochemical parameters. Tonetti and colleagues (2007) showed that systemic biomarkers were reduced at 6 months following NSPT [
33]. Although these findings were observed at day 1 following NSPT; the levels of systemic biomarkers continued to be more regular after 6 months. D’Aiuto et al. (2005) in a systematic review suggested that NSPT could trigger a short term inflammatory response which was followed by a consistent progressive reduction in systemic inflammation and an improvement in endothelial function [
34]. The obese individuals showed exaggerated inflammatory response [
35]. However, a single-round of intensive NSPT could have triggered a short-term acute inflammatory response, resembling acute changes in the oxidative stress following NSPT [
34]. A significant increase in diacron reactive oxygen metabolites (D-ROM) after NSPT has been reported, with a positive linear correlation between D-ROM levels and systemic inflammation biomarkers. The acute inflammatory response may have been triggered by the inevitable periodontal tissue damage during the procedure. Thus, the acute inflammatory findings in relation to oxidative stress could be explained by the increase in serum resistin in the obese group following NSPT in the present study.
In the current study, there were non-significant changes in mean count of
P. gingivalis,
T. forsythia and
P. intermedia following NSPT in both groups (Table
5). It is to be noted that there is no report on the changes of periodontal pathogens count before and after NSPT in periodontitis with obesity. Previous studies showed that mean count of
P. gingivalis,
T. forsythia and
P. intermedia could be reduced by 7–45% [
36,
37] at 12 weeks post-NSPT in CP. However, the reductions of the similar bacterial flora were ranged between 18 to 99% after NSPT in periodontitis with diabetes [
38,
39]. The findings from these studies were consistent with the present study in which NSPT is effective at reducing periodontal pathogens in normal weight subjects.
The study design was developed before 2017 Classification for Periodontal Disease and Peri-implant Disease and Conditions, thus the earlier case definition by Eke et al. (2012) was used [
16]. At baseline, the obese group had almost double mean values of VPI and GBI, reflective of its inflammatory condition (Table
2). This concurs with current understanding that obese is a chronic inflammatory condition, which could contribute to an increase in the existing inflammatory burden associated with periodontitis [
40]. This notion is further supported by Suvan et al., (2014) [
41] who suggested obesity could have triggered greater inflammatory burden in other co–morbidities including periodontitis. This could imply that obesity condition may compromise the healing efficiency in those with periodontitis.
In addition, the obese group had lesser severity of periodontitis (lower means PPD and CAL) compared to normal weight group (Table
2). This could be explained by the fact that the normal weight group had significantly higher number of smokers (Table
1). It is well established that cigarette smoking remains an independent risk factor for development and progression of periodontitis, even after controlling for variables such as oral hygiene, plaque, calculus, socio-economic and demographical factors. Smoking has been associated with increasing host susceptibility towards periodontitis; as well as increasing periodontitis severity, by influencing the healing potential following treatment by means of its reduced angiogenesis nature. The risk associated was estimated with odd ratios of 2.5 to 6.0 [
42‐
44]. It is worth mentioning that majority of the PPD were measured as less than 4 mm indicating a mild periodontitis among the participants of the study.
NSPT has been reported as an effective treatment to reduce local inflammatory burden [
34]. In this study, the means of VPI, GBI and PPD were significantly reduced after NSPT. The findings were in line with other previous studies [
18,
45]. It is important to note that, clinical parameters such as VPI, GBI and PPD are associated with active diseased state. Thus, it was expected that participants in both groups would have responded to NSPT (as a mean of managing active disease) by means of improvement in means VPI, GBI and PPD. However, NSPT did not result in significant reduction in mean CAL, and that could be explained by the fact that CAL accumulation is more influenced by the past disease experience rather than the current periodontitis status. CAL is also an estimate of accumulative periodontal tissue destruction [
46,
47]. The extent of the disease would depend on how long the investigated population has been exposed to the disease.
When compared between groups, the obese group showed higher mean changes of VPI and GBI compared to the normal weight group, with statistical significant differences following NSPT (Table
2). This finding was contradictory to previous studies which reported reduction in the mean changes of VPI and GBI, but of no statistically significant difference [
45]. Other study reported significant difference in mean change of CAL at 3 months following NSPT; however no significant difference in other parameters was identified [
18]. The authors deduced that obesity does not contribute to the total burden of inflammation and suggested both obese and non-obese participants may have responded equally well to NSPT based on the intragroup results [
18,
45].
We carried out linear (multiple) regression analysis (Table
3) to find out whether obesity could be a predictor for mean changes in VPI and GBI. After adjusting for smoking habit, obesity was found to be a significant predictor for VPI and GBI (
p < 0.05). Obese participants were shown to have 54.3 and 43.9% time higher mean changes of VPI and GBI respectively compared to their normal weight counterpart with similar anthropometric profile. Clearly, NSPT is effective in reducing local inflammation in periodontitis obese and normal weight. However, cigarette smoking might have compromised the host healing potential resulting in relatively lower mean changes of VPI and GBI in the normal weight group following NSPT. It is worth to note that the majority of participants (Table
1) in this study were non diabetic, which is another risk factor for periodontitis.
Post hoc sample size calculation was carried out using G*Power software version 3.1 [
19]. The calculation was based on detectable mean difference CAL between 2 groups obtained from this study. With a standard error of 5% (
p = 0.05), it demonstrated the power of 43% (0.43). In view of medium mean difference CAL (0.71 mm) obtained from the study, the 18 obese and 30 normal weight should be acceptable. The results were deemed acceptable for the sample size used.
Limitations in this study include (i) most of the participant had mild periodontitis and (ii) short time monitoring. Future study should include involvement of obese with moderate to severe periodontis participants. Hopefully, this could be useful to evaluate the potential outcome of NSPT and bring about conclusive outcomes, especially to rule out the true effects of obesity and periodontis. At the same time, further consideration should be given on the length of the study period with increased frequency of monitioring the other clinical parameters.
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