In an evaluation by Merchant,[4] the clinical implication of the

study by Hutter[2] was said to be limited because of potential

residual confounding by smoking, failure to show the association
among non or past smokers, and failure to adjust for menopausal
status in women. To do away with these drawbacks, only males
were included in this study.
Further, both past and present smokers were excluded to remove
any confounding effect of smoking.
Dalam evaluasi oleh Merchant, [4] implikasi klinis dari penelitian oleh
Hutter [2] dikatakan terbatas karena potensi sisa pembaur oleh
merokok, kegagalan untuk menunjukkan hubungan antara perokok non
atau masa lalu, dan kegagalan untuk menyesuaikan menopause Status
pada wanita. Untuk menyingkirkan kelemahan ini, hanya laki-laki
dilibatkan dalam penelitian ini. Selanjutnya, perokok baik dulu dan
sekarang dikeluarkan untuk menghilangkan efek pengganggu dari
merokok.

correlation between the degree of anemia and the severity of the

underlying disease.

Wanita :
In India, anemia is more prevalent in females because of poor nutrition,
increased menstrual losses, high incidence of tropical and intestinal infections,
and other miscellaneous factors. Iron deficiency anemia is the most common
type of anemia seen in India. Females are also prone to hormonal imbalance
during puberty, during the reproductive phase, and toward menopausal age. The
microbial flora and host immune response are altered leading to exaggerated
response of the periodontal tissues to local factors. [27] Therefore, to eliminate
bias, only male patients were included in the study. [8]
Rokok :

Smokers were also excluded from the study. Various studies [28],[29],[30] have
evaluated the PPD, CAL, PI, GI, and radiographic bone measurements of
smokers and non-smokers, and found a positive correlation between smoking
and these clinical parameters. Studies also indicate elevated concentrations of
TNF and IL-6 as a consequence of smoking. [31]

Pengobatan jangka panjang :

The change in hemoglobin and RBC values in our study is
statistically highly significant but not as high as observed in
anemia due to other inflammatory conditions like rheumatoid
arthritis[13] and multiple myeloma.[14] This might be due to the
reason that the other diseases are more severe inflammatory
conditions than periodontitis. So anemia resulting from
periodontitis is relatively mild. This also might be the reason why
few studies[3] failed to find any relation between hematocrit
indices and periodontal status.

Proinflammatory cytokines such as TNF-, IL-1, INF- and PGE2

are found in high concentrations in inflamed periodontal tissues.
The various cytokines can enter the blood circulation and affect
distant sites and organs.[1] The same inflammatory cytokines have
been found to be central in the pathogenesis of ACD.[6,7] So, it
can be concluded that periodontitis, like other chronic
inflammatory conditions, leads to ACD.
Kelemahan : However this study had a drawback of limited sample
size. Further, a relation between severity of periodontitis and
anemia was not explored in the present study. Further studies with
larger sample size are warranted.
Diskusi tidak menjelaskan secara rinci mekanisme..
Tidak menjelaskan alasan kriteria ekslusi

Waktu penelitian tidak diberitahu

Mekanisme :
According to these authors and a few studies [11],[12],[13],[14],[15],[16],[17],[18] in
the past, periodontitis patients have elevated levels of acute phase proteins,
interleukin (IL)-1, IL-6, and tumor necrosis factor (TNF). These inflammatory
mediators are shown to suppress mature erythroid progenitors [19] and inhibit in
vitro colony formation by erythroid burst-forming units and erythroid colonyforming units from normal human marrow. [20],[21],[22] Inhibition of erythropoietin,
the hormone responsible for erythropoiesis, was also seen. [23] This leads to
decrease in RBC count.
Some studies also showed a disturbance in iron regulatory system. In vitro
stimulation of fresh human hepatocytes with IL-6 showed strong induction of
hepcidin, a liver hormone which caused disturbance in iron regulatory
mechanism. [24] Hepcidin causes ferroportin internalization and degradation,
thereby decreasing iron transfer into blood plasma from the duodenum, from
macrophages involved in recycling senescent erythrocytes, and from iron-storing
hepatocytes, with the iron stores being adequate. This response restricts the iron
supply to erythropoietic precursors, and hence, a decrease in Hb count was
seen. [25]