ASSOCIATION BETWEEN SERUM RESISTIN LEVEL AND PERIODONTAL CONDITION CHANGE
AMONG ELDERLY PEOPLE
28
serum resistin levels is related to the inhibition of the
parasympathetic nervous system [32]. To date, there is
still a lack of promising data in humans. This is because
there is a striking difference in terms of biological
responses between humans and rodents. Hence,
we postulated that high serum resistin at baseline in
our subjects might be a signaling factor to activate
the central nervous system regulating an extensive
amelioration of the local inflammation. In contrast, a
low serum resistin level might not provide an adequate
signal to stimulate the reduction of the peripheral
inflammation. The exact mechanism to explain this
finding, however, has not yet been fully elucidate.
Furthermore, resistin may respond differently
depending on the age of the patients because it was
found that resistin levels in children had no correlation
with metabolic parameters. However, they correlated
only with the onset of pubertal development [33].
Thus, resistin in the elderly probably exerts different
effects than in the adults. Additionally, the serum resistin
level is also affected by many other factors such as
lipopolysaccharides form oral pathogens [13], insulin
level [10,34], cardiovascular disease condition [35], and
chronic kidney disease [36]. All these factors might
exert an effect on serum resistin levels more than local
inflammation occurring in mild/moderate periodontitis.
Conversely to the effect of serum resistin on the
alteration of the periodontal condition, serum IL-6
and adiponectin level were hardly associated with the
change of the periodontal condition (data not shown).
For IL-6, the results are somewhat supported by the
previous reports [37-39] in which these molecules were
produced mainly only during the early inflammation
event and were probably synthesized only in low level in
elderly. Therefore, in the long-term observation and with
a relatively low level of localized inflammation such as in
the present study, we could not observe any effect of IL-6
on the periodontal condition changes. For adiponectin,
previous studies suggested that periodontal treatment
had minimally influenced the serum adiponectin level
[9,39-42]. The present study added up this relationship,
in which serum adiponectin level was relatively
minimally influenced by the alteration of the periodontal
condition. Indeed, adiponectin is said to be an anti-
inflammatory molecule that can be impaired by resistin
[43]. Regarding TNF-α, we demonstrated that the TNF-α
level at baseline slightly positively affected periodontal
disease progression (regression coefficient of 0.39 and
0.31 for change of sites with PD ≥ 4 mm, and sites with
PD ≥ 4 mm concomitant BOP, respectively). TNF-α is a
well-recognized cytokine related to the inflammatory
process, and this molecule could be secreted by
adipocytes [44], and immune cells [45]. Some studies
have shown the positive association between serum
TNF-α and periodontitis [46,47]. Our study is in line with
these studies and contributes to the establishment of
the role of the TNF-α in inflammatory enhancement.
Regarding the number of tooth loss which had a strong
association with the reduction of the sites with PD ≥ 4
mm in 4 years, it is a common phenomenon that teeth
which had been diagnosed on the basis of periodontal
etiology/criteria, as having a poor prognosis in the elderly,
on the basis of periodontal etiology/criteria, were the
main sources of multiple, and relatively deep periodontal
pockets. Based on theoretical and clinical knowledge such
teeth would be extracted. The data of the present study
showed that approximately 5.1 – 7.8% of teeth were lost
during the 4 years in LR and HR group, respectively. This
was considered an important factor that dramatically
reduced the sites with PD ≥ 4 mm and these sites PO ≥
4 concomitant BOP, which collectively improved the
periodontal condition as shown in the study population.
Additionally, it is useful to include other age groups, the
leukocyte related parameters e.g. leukocyte count, and
genetic information to clarify the general resistin function.
Especially from a genetic point of view, although there
is no clear association, some Finnish [48] and Japanese
[49] study subjects suggested that single nucleotides
polymorphism (SNP) in the promoter region of the
resistin gene (RETN -420C>G, rs1862513) associated with
obesity and diabetes, which may be a link to the increase
of the inflammatory reaction. Based on the fact that all
participants were non-diabetic and almost classified
into normal BMI individuals, the majority of our subjects
probably might not have this SNP locus.
The present study has some limitations that should be
carefully taken into consideration when interpreting
the results. First, because of the observational nature
of our study, we could not discourage individuals
from receiving periodontal treatment, thus improving
of individual periodontal condition. This might have
in part contributed to the observed effect of the
periodontal treatment they received. Furthermore, as
aforementioned almost all participants were relatively
in a good periodontal condition from the beginning of
the study, therefore detecting the association between
severe periodontitis and the serum resistin level could
not be achieved. Finally, we had no data on the serum
resistin level as well as the other serological parameters
at the follow-up period to re-evaluate the relationship
of serum resistin level and other adipokines/cytokines,
and periodontal condition in a low inflammatory state.
Monitoring the level of adipokines/cytokines at the
end of study should be included in the future studies.
5. Conclusion
The present results provide evidence