TELAAHJURNAL

Respon Imunologis Sistemik Pada Pasien Infeksi Gigi

"Systemic Immunologogical Responses Among Dental Infection Patients

"

Dosen Pengampu :
Dr. Hj. Nunung Herlina, S.Kp.,M.Pd

Disusun Oleh :

1. KhusnulWahyuni: 2011102411055

2. Yuris Sasrnita:
201110211143

PROGRAM STUD I S1 ILMU KEPERAWATAN

FAKUL TAS ILMU KEPERAWATAN
UNIVERSITAS MUHAMMADIYAH KALIMANTAN TIMUR
2021/2022
TELAAHJURNAL
1. DESKRIPSI UMUM
No. Item
1. Judul Jurnal
Respon Imunologis Sistemik Pada Pasien Infeksi Gigi (Systemic
Immunological
Responses Among Dental Infection
Patients)
2. Penulis Jurnal
a. Zainab Khudher Ahmad Al Mahdi
b. Fatima Malik Abood
3. Nama Jurnal / dipublikasikan oleh
Jurnal lnternasional Imunologi
4. Penelaah / reviewer jurnal
a. Khusnul Wahyuni
b. Yuris Sasmita
5. Sistematika Penulisan
IMRAD ( Introduction, Methode, Result, Analyze,
Discussion)
a. Font : 12
b. Spasi : 1.15
c. Format Penulisan : Times New Roman
d. Rataan : Justify
e. Column :3
6. Referensi Daftar Pustaka
[1] WHO, World Health Organization. 2019. Oral health. What is the burden
of oral disease?. WHO. int.
[2] Negrini T. D,; Duque C.; Hofling J. F. and Goncalves R. B. (2009).
Fundamental mechanisms of immune response to oral bacteria and the main
perspectives of a vaccine against dental caries: A brief review. Rev. odonto
ci~nc.
24 (2): 198-204.
[3] Samaranayke L. (2012). Essential microbiology for dentistry.ks 4th ed.
Elsevier
Ltd. P: 279-285.
[4] Baucells, B. J.; Mercadal Hally, M.; Alvarez Sanchez, A. T.; Figueras Aloy, J.
(2016). Asociaciones de probi~ticos para la prevenci~n de la enterocolitis
necrosante y la reducci~n de la sepsis tardia y la mortalidad neonatal en reci~n
nacidos pret~rmino de menos de 1.500g: una revision sistem~tica". Anales de
Pediatria. 85 (5): 247-255
 2. DESKRI PSI KONTEN

No Komponen Jurnal Item question to help "Telaah Jurnal"

1. Pendahuluan 1. Apa rnasalah penelitian ?
Respons imunologis sistemik di antara pasien infeksi
gigi.

2. Seberapa besar rnasalah tersebut ?

Karies gigi telah dikenal sebagai masalah
kesehatan mulut yang paling penting di dunia.
Penyakit ini multifaktorial, dipengaruhi oleh host dan
faktor lingkungan yang terjadi karena
ketidakseimbangan homeostasis antara host dan
mikrobiota, mekanisme pertahanan imun host dapat
berpengaruh pada kolonisasi bakteri dan beberapa
gangguan host dapat mempengaruhi mekanisme ini
seperti defisiensi imun umum yang berhubungan
dengan malnutrisi, kelainan bawaan atau
pengobatan.
 3. Darnpak rnasalahjika tidak diatasi?
Penelitian ini menyimpulkan bahwa bakteri yang
diisolasi dari pasien infeksi gigi lebih banyak
campuran daripada infeksi tunggal, terdapat
peningkatan yang tidak signifikan pada IgA, IL-4, dan
CDS pada pasien sedangkan IL-7 dan CD4 lebih
rendah pada kelompok pasien dibandingkan kontrol.
sementara rasio CD4\CD8 lebih rendah pada
kelompok pasien, basil ini mencerminkan fakta bahwa
antigen mukosa menginduksi toleransi sistemik
sampai batas tertentu karena bakteri ini ada di
rongga mulut pada anak usia dini Oleh karena itu
menghilangkan bakteri ini selalu merupakan cara
terbaik untuk mencegah infeksi tersebut.
4. Bagaimana kesenjangan yang terjadi ? bandingkan
antara rnasalah yang ada dengan kenyataan yang
diharapkan?
Tidak ada kesenjangan dalam penelitian. Penelitian
yang dilakukan sesuai dengan harapan atau target.

5. Berdasarkan rnasalah penelitian, apa tujuan

dan hipotesis yang ditetapkan ?
Penelitian ini akan menganalisis sifat bakteri yang
di
isolasi dari pasien infeksi
gigi.

2. Metode
a. Desain 1. Desain penelitian apa yang digunakan untuk
penelitian desain eksperirnen
Desain penelitian ini adalah deskriptif.
a. Apakah menggunakan kelompok kontrol untuk
menentukan efektifitas suatu intervensi ?
Iya, peneliti menggunakan kelompok kontrol.

b. Apakah random melakukan penelitian alokasi ?

Peneliti tidak melakukan random alokasi.

c. Jika peneliti menggunakan randomisasi, bagaimana

prosedumya, apakah yang dilakukan randomisasi
sederhana blok stratifikasi ? siapa yang melakukan
randomisasi ?
Peneliti tidak melakukan randomisasi.

d. Jika temyata pada data dasar terdapat perbedaan

karakteristik/variabel perancu pada kedua kelompok,
apakah peneliti melakukan pengendalian pada uji
statistik dengan stratifikasi atau uji multivariat ?
Peneliti tidak melakukan pengendalian uji
statistik atau uji multivariat.
 e. Untuk menjamin kualitas pengukuran, apakah peneliti
melakukan blinding saat mengukur outcome ?
blinding merupakan upaya agar sampel atau peneliti
tidak mengetahui kedalam kelompok mana sampel
dimasukkan (eksperiment atau control). Hal m1
menunjukkan upaya peneliti meningkatkan validitas
informasi
Peneliti tidak melakukan blinding saat mengukur
outcome. Desain penelitian ini desskriptif.

f. Apakah peneliti melakukan masking atau

penyamaran dalam memberikan perlakuan pada
responden (responden tidak menyadari apakah
sedang mendapatkan intervensi yang diuji
cobakan ? Peneliti tidak menggunakan
masking atau
penyamaran.

b. Populasi dan Siapa populasi target dan populasi

a. sampel terjangkau?
Penelitian ini melibatkan analisis 20 pasien dengan
rata-rata usia 57,3 dari 45 hingga 72 tahun dengan
infeksi gigi dan 5 kelompok kontrol dengan rata-rata
usia 52,2 selama tahun 2017. Sampel dikumpulkan
setelah persetujuan pasien oleh dokter gigi
spesialis
mikrobiologi.
b. Siapa sampel penelitian ? apa kriteria inklusi dan
ekslusi sampel?
Sampel penelitian ini adalah 20 pasien dengan rata•
rata usia 57,3 dari 45 hingga 72 tahun dengan infeksi
gigi dan 5 kelompok kontrol dengan rata-rata usia
52,2 selama tahun 2017. Sampel dikumpulkan setelah
persetujuan pasien oleh dokter gigi spesialis
mikrobiologi.
 c. Berapa jumlah sampel yang digunakan dalam penelitian
? metode atau rumus apa yang digunakan untuk
menentukan jumlah sampel ?
Jumlah sampel yang digunakan ialah 20 pasien
dengan rata-rata usia 57,3 dari 45 hingga 72 tahun
dengan infeksi gigi dan 5 kelompok control dengan
rata-rata usia 52,2 selama tahun 2017. Untuk
pemeriksaan bakteriologis, sampel pus yang diambil
dengan swab atau paper point ukuran 40 mm
dimasukkan ke dalam saluran akar dan poket gingiva
selama 60-an dan sampel segera dimasukkan ke
dalam thyioglycolate broth untuk kultur anaerob dan
BHIB untuk kultur aerob kemudian sampel diangkut
ke laboratorium mikrobiologi oral untuk isolasi dan
penemuan bakteri yang dipelajari.
c.Pengukuran a. Variabel apa saja yang di ukur dalam penelitian?
/pengumpulan Variabel yang diukur dalam penelitian yaitu isolat
data bakteri, respon antibodi, profil sitokin, serum CD4 &
CD8.

b. Metode apa yang digunakan untuk mengumpulkan data?

Metode penelitian ini adalah kuantitatif dengan desain
deskriptif.

c. Alat ukur apa yang digunakan untuk mengumpulkan data?

Alat pengumpulan data penelitian ini yaitu
swab atau paper point ukuran 40 mm.

d. Siapa saja yang melakukan pengukuran atau pengumpulan

data ? apakah dilakukan pelatihan khusus untuk observer
atau yang melakukan pengukuran ?
Pengukuran atau pengambilan data dilakukan
oleh
Zainab Khudher Ahmad Al Mahdi dan Fatima
Malik
Abood sebagai peneliti.
 d. Analisa data D Uji statistic apa yang digunakan untuk menguji
hipotesis atau menganalisis data ?
Uji chi-square.

□ untuk penelitianeksperimen apakah peneliti menggunakan

metode intention to treta atau on treatmen analysis ?
Tidak ada penelitian eksperimen karena penelitian
ini adalah observasional

□ Program atau software statistic apa yang digunakan

peneliti untuk menganalisi data ?
Tidak dijelaskan software statistic apa yang
digunakan penelitian ini.

3. Hasil penelitian
a. Alur penelitian a. Bagaimana alur (flow) penelitian yang menggambarkan
responden yang mengikuti penelitian sampai selesai,
drop out dan loss follow up ?

dan data base Pada penelitian ini mengambil 20 pasien dan

line melibatkan 5 kelompok control dengan rata-rata
usia
52,2 selama tahun 2017.

b. Bagaimana karakteristik responden dan baseline data ?

Pada penelitian digunakan sampel sebanyak 20
responden dengan karakteristik rata-rata usia 57,3
dari 45 hingga 72 tahun dengan infeksi gigi dan 5
kelompok kontrol dengan rata-rata usia 52,2 selama
tahun 2017,
 c. Pada penelitian eksperirnen apakah variabel perancu
(counfonding variabel) dalarn database line tersebar
seirnbang pada setiap kelornpok ? jika tidak seirnbang
apa dilakukan peneliti untuk rnernbuat penelitian bebas
dari pengaruh variabel perancu ?
Tidak terdapat variabel perancu pada penelitian ini,
karena tidak menggunakan eksperimen
melainkan penelitian observasi.

b. Hasil penelitian

a. Apa hasil utarna dari penelitian? jika peneliti

rnelakukan uji hipotesis, apakah hipotesis penelitian
terbukti (bermakna atau tidak secara statistik) ? apakah
hasil penelitian juga bermakna secara klinis ?
Dari basil penelitian ini didapatkan sebagian bakteri
yang diisolasi dari plak gigi adalah bakteri gram
positif (88,88 %) sedangkan bakteri gram negative
(11,11 %). Menunjukkan bahwa IgA serum lebih tingi
pada pasien plak gigi dibandingkan dengan kelompok
control. IL-4 lebih tinggi pada kelompok uji
dibandingkan kelompok control.

b. Untuk penelitian eksperirnen dengan variable

dependen kategorik apakah peneliti rnenjelaskan tentang
nilai kepentingan klinis dari hasil penelitian seperti
number need to treat (NTT), relative risk reduction
(RRR) atau absolute risk reduction (ARR)
Peneliti tidak menjelaskan kepentingan klinis
NTT
atau RRR atau ARR.
4. Diskusi (discuss) a. Bagaimana interpretasi peneliti terhadap hasil penelitian ?
apakah peneliti membuat interpretasi yang rasional dan
ilmiah tentang hal - hal teori terkini ? catatan : meskipun
hasil penelitian tidak sesuai dengan hipotesis, namun
suatu penelitian tetap berkualitas jika peneliti mampu
menjelaskan rasional secara ilmiah mangapa hipotesisnya
tidak terbukti ?
Data saat ini mendeteksi kemungkinan bakteri di
antara kasus infeksi gigi yang didapat dari plak gigi
dengan kedalaman poket yang berbeda. Hasil
menunjukkan bahwa sebagian besar infeksi biasanya
bersifat polimikrobial (59,25%), hasil ini sesuai dengan
penelitian lain.
Hasil kami mencatat persentase tertinggi adalah
Streptococcus viridians, bakteri ini paling melimpah di
rongga mulut spesies, salah satu yang paling penting
adalah S. mutans spesies aciduric, pengasaman
yang berlebihan dari lingkungan mulut oleh bakteri
ini secara langsung terkait dengan perkembangan
karies gigi.
Studi saat ini menunjukkan bakteri Gram negatif
anaerobik berpigmen hitam (5,3%) sebagai infeksi
tunggal. Anaerob berpigmen hitam termasuk P.
gingivalis dan P. intermedia ditemukan pada plak gigi
sebesar 0,1 % dan meningkat secara kuantitatif
selama infeksi seperti perkembangan lesi gingiva.
b. Bagaimana peneliti membandingkan hasil penelitiannya
dengan penelitian penelitian terdahulu serta teori yang
ada saat ini untuk menunjukkan adanya relevansi ?
peneliti tidak mencantumkan basil
perbandingannya
dengan penelitian-penelitian terdahulu serta teori
yang ada saat ini untuk menunjukkan adanya
relevansi

c. Bagaimana peneliti menjelaskan makna dan relevansi

hasil penelitiannya dengan perkembangan ilmu
keperawatan/ kesehatan serta terhadap pemecahan
masalah ?
Peneliti tidak mencantumkan basil perbandingan
relevansi untuk basil penelitian terlebih dahulu
dengan basil penelitian saat ini.

d. Bagaimana nilai kepentingan (importancy) hasil

penelitian?
Untuk nilai kepentingan basil penelitian itu sendiri
telah dijelaskan di dalam jurnal bahwa peneliti ingin
mengetahui sifat bakteri yang di isolasi dari pasien
infeksi gigi.
e. Bagaimana applicability hasil penelitian menurut peneliti ?
apakah hasil penelitian dapat diterapkan pada tatanan
praktik keperawatan ditinjau dari aspek fasilitas,
pembiayaan, sumber daya manusia, dan aspek legal ?
Tidak, karena penelitian ini hanya dilakukan untuk
mengetahui sifat bakteri yang di isolasi dari pasien
infeksi gigi.

f. Apakah mungkin penelitian ini direplikasi pada setting

praktik klinik lainnya ?
Penelitian ini bisa di replukasi dengan meneliti
variabel faktor isolasi bakteri infeksi gigi,
respon antibodi, profil sitokin, dan serum CD4 &
CDS.

g. Apakah peneliti menjelaskan kekuatan dan kelemahan

penelitian ? apakah kelemahan ini tidak menurunkan
validitas hasil penelitian ?
Peneliti tidak menjelaskan kekuatan dan kelemahan
penelitian.
International Journal of Immunology
2021; 9(1): 6-12
http://www.sciencepublishinggroup.com/j/i
ji doi: l 0.ll648/j.iji.20210901.12 Science Publishing Group
ISSN: 2329-l77X (Print); ISSN: 2329-1753 (Online)

Systemic Immunological Responses Among Dental

Infection Patients
Zainab Khudher Ahmad Al Mahdi, Fatima Malik
Abood
Department of Microbiology, College of Dentistry, University of Babylon, Hilla City,
Iraq

Email address:
dent.zainab.almahdi@uobabylon.edu.iq (Z. K. A. Al
Mahdi)
Corresponding
author

To cite this
article:
Zainab Khudher Ahmad Al Mahdi, Fatima Malik Abood. Systemic Immunological Responses Among Dental Infection Patients.
International
Journal ofImmunology. Vol. 9, No. l, 2021, pp. 6-12. doi
l0.11648/j.iji.20210901.12

Received: December 5, 2020; Accepted: January 12, 2021; Published: January 22,
2021

Abstract: Evaluating of some immunological responses among dental infection patients is essential in the clinical
management of oral infection. Our study considered isolation of dental infection bacteria and quantitative evaluation of
serum. IgA, IL-4, IL-7 and CD4 and CD8 molecules among dental plaque patients and control group. Oral bacteria from dental
infection patients were isolated in appropriate media and diagnosed by biochemical tests and in vitro quantitative
determination of serum IgA, IL-4, IL-7 and CD4 and CD8 molecules using ELISA technique. Single and mixed bacterial
isolates were noted, mixed infection were (59.25%), the nature of bacteria was Gram positive cocci Streptococcus viridans,
Streptococcus pyogenes and Staphylococcus aureus, and Lactocacilli spps, in addition to Gram negative rods black-
pigmented bacteria, Klebsilla pneumonia, and Esherishia coli. Serum IgA was higher in patients (368.8± 182.5) ng\ml than in
control group (319 .92±79 .26) ng\ml. Serum IL-4 was higher patients (285.33±86.12) pg/ml than in control group
(257.7±94.14) pg\ml. Serum IL-7 was higher in control group (19.59±4.14) pg/ml than in dental plaque patients (17.98±3.18)
pg /ml. Serum CD4 molecules was higher in control group (1.371±0.5242) ng/ml than in dental plaque patients
(1.326±0.1292) ng/ml. Serum CD8 molecules shows non-significant elevation in patients group 0.5825±0.02717 (ng\ml)
than in control group 0.51±0.01643 (ng\ml) P:S0.05. Mean of the CD4/CD8 ratio was higher 2.783±1.126 in control group
while it was 2.355±0.24 in dental plaque patients, however the differences were non-significant (P<0.05). The present study
conclude that the bacteria isolated from dental infection patients were mixed more than single infection, there were non-
significant elevation in IgA, IL-4, and CD8 in patients while IL-7 and CD4 was lower in patients group than in control group,
while CD4\CD8 ratio were lower in patients group, these result reflect the fact that mucosa! antigen induce systemic tolerance
to some extent since these bacteria present in oral cavity in early childhood. Therefor removing these bacteria always the best
way to prevent such infections.
Keywords: Dental Infection, Immune Response, Cytokine, Oral
Bacteria

1. Introduction immune deficiencies associated with malnutrition, inherited

or medication disorders [2].
Dental caries have familiarly been considered the most Bacteria is important agent in dental infection, the
important worldwide oral health problems [l]. The disease is nature of such infection is polymicrobial, mixed aerobic
multifactorial, affected by host and environmental factors and an
that occurs due to homeostasis imbalance between the
host and microbiota, host immune defense mechanisms may
effect in the bacterial colonization and some host
disorders can affect these mechanisims such as general
aerobic bacteria encompassed Gram positive and
Gram negative bacteria [3].
Streptococcus viridans are abundant among oral bacteria
and one member of the cluster is S. mutans, the reason
behind tooth decay in most cases. likewise S. sanguinis is
additional potential reason, when introduced into the blood,
they have the potential of initiating endocarditis,
specifically in whom with injured heart valves. They are
the most common reason of sub-acute bacterial
endocarditis [4]. Microbial biofilm composed of
Staphylococcus aureus and Streptococcus mutans
responsible for formation pathogenic
 International Journal of Immunology 2021; 9(1): 6-12 7

biofilm, chronic infection and dental caries [5]. environment was incubated in an anaerobic jar or Co2
Lactobacilli unlike most indigenous microbes. Some incubator The bacteriological study including cultural
species lactobacilli are commensal, behave as planktonic, properties, microscopic examination and biochemical tests
opportunistic colonizers that may gather and multiply solitary was done according to MacFaddin, 2000; Forbes et al., 2007
in certain restrictive niches of the host, at least within the and Al-Rawi, 2012 [18-20].
oral cavity. There is relation between the number of
lactobacillus and dental caries, lactobacilli are not 2.2. Blood Collection and
existing in adults without caries lesions or that they Storage
present lower than the detection level, the ability of Blood were collected by sterile one-use syringes, from each
lactobacilli and mutans streptococci to ferment a variety group, blood samples were centrifuged for 15 minutes at
of carbohydrates and to persist in a low pH environment is 1 000xg, the supernatant were collected and saved at -
the main hallmark of the dental caries paradigm [3, 6]. 20°C, the assay was carried out during the first month after
Streptococcus pyogenes infect the mucosa! surface and storage.
can isolated from oral cavity, the bacteria capable to adhere
the mucosa! surface and bind salivary pellicle on the surface 2.3. In Vitro Quantitative ofAntibody and
of tooth [7] and responsible for many odontogenic infection Cytokines
[8].
Regarding to anaerobic Gram negative bacteria, black In vitro quantitative determination oflgA, IL-4 and IL-7 in
pigmented bacteria, isolated from dental abscess are serum of patients group and control. group
represent expected members of the oral microbiota and using Sandwich-ELISA as in manufacture instructions
become highly damaging agent influenced by capacity to (Elabscience Biotechnology Co., Ltd).
participate in oral biofilm formation [9] Additionally, the 2.4. Serological Markers of Cell-mediated
virulence factors of dark pigmented bacteria has ability Immunity
to fight phagocytosis, destroy immunoglobulins and
increase pathogenesis when mutual with other bacterial Serum soluble CD4 and CD8 were rummage-sale as
strain [10]. Furthermore, gram-negative aerobes (K. markers for cell mediated immunity among odontogenic
pneumoniae and E. coli) present in dental abscesses as patients (Elabscience company).
gram's negative bacilli from oral lesions at normal
2.5. Statistical
frequency, also they stated K. pneumoniae and E. coli as Analysis
oral normal flora that settled oral cavity and initiated
odontogenic abscess [ 11]. Statistical analysis comprise unpaired t-test for determine
Evaluation aspect of systemic immune response the significant of the differences between the two mean
represented by serum IgA level and anti-inflammatory IL-4 groups and graphs were done using GraphPad Prism-7
cytokine as regulatory cytokine for humoral and adaptive software CA. USA.
immune responses [12, 13] reflect the adaptive immune
responses among patients suffer from dental bacterial 3. Results
infection, as well as IL-7 which is important cytokine in both
T and B cell development [14, 15] these combined with 3.1. Bacterial
estimation of cell mediated immunity by measurement of Isolates
both CD4 and CD8 molecules [16, 17].
Most bacteria insulated from dental plaque were gram
positive bacteria. (88.88%) while gram negative bacteria
2. Main Body (11.11 %). Present data displays that the nature of
2.1. Patients and Sample Collection bacterial infection mostly were mixed infection (Total=32
isolates) while single bacterial infection were (total=22
This study involved the analysis of20 patients with mean of isolates). The percentage of infection with S. viridians was
age 57.3 range from 45 to72 year with dental infection and 5 higher than other bacteria followed by S. pyogenes both in
control group with mean of age 52.2 during 2017. Samples single and mixed infection. cases. Black pigmented colony
were collected after patients agreement by dentist specialized was noted among. single isolates infection (13%) and not
in microbiology. recorded with other bacteria (Table 1, Figure 1 ).
For bacteriological examination, pus samples taken by the
swabs or paper point size 40 mm were inserted in root canal 3.2. Antibody
Response
and gingival pockets for 60s and the samples were
immediately placed into thyioglycolate broth for anaerobic Result shows that serum IgA was higher among dental
culture and BHIB for aerobic culture then transport samples plaque patients than mn control group
to the laboratory of oral microbiology for isolation and (mean±SEM=368.9±38.92 (ng. \ml) and 319.9±35.45 (ng\ml)
discovery of studied bacteria. One of the culture plates was respectively), however these differences was non significant
incubated at (t=0.5802, (P-0.05)), (table 2; figure 2-A).
37°C in the incubator under aerobic and an aerobic
3.3. Cytokine
Profile

IL-4 was higher in test group than in control group

(mean=285.3±27.23 (pg\ml) and 257.7±54.36 respectively),
the differences were non significant (t=0.479, df=ll,
P=0.6;
8 Zainab Khudher Ahmad Al Mahdi and Fatima Malik Abood: Systemic Immunological Responses Among
Dental Infection Patients

Table 2, figure 2-B. The mean of serum CD4 molecules was 1.371±0.52
IL-7 was higher in control group than in test group (n=4) (ng\ml) in control group while it was 1.326±0.1292.
(19.59±1.855. (pg\ml) and 17.99±0.6795 (pg\ml) (n=20) (ng\ml) in dental plaque patients while serum
respectively and the differences were non significant (t=0.96, soluble CDS was 0.51±0.01643. (ng\ml) (n=20) in
P=0.37; table control group and
2, figure 2-0)(P<0.05). 0.5825±0.02717 (ng\ml) n=22 in dental plaque
patients, (Table 2, figure 2-D&E).
3.4. Serum CD4 & CDS
Table 1. Type ofbacterial isolates and the percentage ofisolated as mixed and single isolates.

Type of isolates
Bacterial Isolates No. &%
Single Mixed
S. viridians 6 IO 16 (29.5%)
S.pyogenes 5 7 12 (22.22%)
S.aureus 5 6 11 (20%)
Lactobacilli spp 2 7 9 (16.6%)
Black-pigmented bacteria 3 0 3(5.3%)
K. pneumonia I 2(3.4%)
E.coli 0 I (1.3%)
Total 22 32 54 (100%)

Mean of the CD4/CD8 ratio was 2.68 in control group while it was 2.27 in dental plaque patients all results
shows non-significant differences (P<0.05).

Tble 2. Immune response (antibody; cytokines & cell mediated Immunity) ofdental dental patients among test and control groups.

Immune response parameter Test group (mean± St.d) Control group (mean± St.d)
lgA 368.9±38.92 (ng\ml) 319.9±35.45 (ng\ml)
IL-4 285.3±27.23 (pg/ml) 257.7±54.36 (pg/ml)
IL-7 17.99±0.6795 (pg/ml) 19.59±1.855 (pg/ml)
CD4 1.326±0.1292 (ng\ml) 1.371±0.52 (ng\ml)
CD8 0.5825±0.02717 (ng\ml) 0.51±0.01643 (ng\ml)

- Single infection
Mixed infection

Figure 1. The nature ofbacterial infection among dental infection patients (Mixed and single infection).
 International Journal of Imm unology 2021; 9(1): 6-12 9

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" E
Groups of study
Figure 2. Immune response parameters among dental infection patients (test group) and control group; A: lgA concentration; B: IL-4 concentration; C:
IL-7 concentration (Bar graphs represent mean ofcytokine concentration ±SDV); D: CD4 concentration and E: CD8 concentration.
10 Zainab Khudher Ahmad Al Mahdi and Fatima Malik Abood: Systemic Immunological Responses Among
Dental Infection Patients

4. Discussion quantitatively in the course of infections such as progress

of gingival lesion.
The current data were detecting the possible bacteria
P. gingivalis have virulence factors such as
among dental infection cases acquired from dental plaque
fimbriae, capsule and production of enzymes such as
of different pockets depths. Results shows that most
collagenase and trypsin-like protease. P gingivalis
infections are usually polymicrobial in nature (59.25%),
constrains neutrophil migration into the lesion [27].
these result was in agree with other studies [21].
Plaque biofilm contain a lot of biologically active
Gram positive bacteria were dominant in our study
products from gram-positive and gram-negative bacteria
(88%), the consequences revealed that 16 (29 .5) of isolate
colonize the tooth surface around the gingival margin and
revealed positive bacterial culture of S. viridians (Table 1
interproximal areas. These products include endotoxins and
& Figure 1) whereas 13 (24), 11 (20) isolates of
other bacterial toxins [28-30]. These products and the host
Streptococcus. pyogenes and Staphylococcus aureus
immunological responses products such as cytokines
respectively with medium percentage of isolates belong to
infiltrate the gingival epithelium and initiate a host
Lactobacillus spp. 9 (16.5) and low gram negative
response that lead to gingivitis. Symptoms of gingivitis can
percentage of isolates belong to black pigmented bacteria,
be notified clinically with changes in tissue color from pink
Klebsiella pneumoniae and Escherichia coli 3 (5.3%), 2
to red, swelling and bleeding upon probing [31]. Chronic
(3.4%), 1 (1.3%) respectively.
gingivitis that remains for years may bring the basis for
Our results recorded the highest percentage was
more concern for systemic health than a periodontitis
Streptococcus viridians, these bacteria are most abundant
situation that is more readily treated. As the plaque
in the oral cavity species, one is the most important is S.
biofilm continues to increase, soluble compounds penetrate
mutans the aciduric species, excessive acidification of the
the secular epithelium. This, in turn, induce the gingival
oral environment by these bacteria is directly associated
epithelium to produce mediators including prostaglandins,
with the development of dental caries [22].
cytokines as interleukin- I beta (IL-1 ), tumor necrosis
S. mutanse on teeth by PCR technique and proved present
factor alpha and enzymes such as matrix
in higher percentage among other streptococci [23].
metalloproteinases. These products influence chemotaxis
Viridance group streptococci found normally in oral
recruit neutrophils to the region and lead to increased
cavity, any breach in oral mucosal barrier resulting the
permeability of gingival vessels that induce plasma proteins
penetration of microorganisms into the bloodstream,
to migrate from the blood vessels into the tissue. As the
causing bacteremia and bacterial endocardiatis [24].
inflammatory process progresses, more mediators are
Lactobacillus spp. common oral inhabitants, but
produced, and more cell types are employed to the area
include less than 1 % of the oral flora. Dental plaque
including neutrophils, monocytes and T-cells. Chronic
biofilms, commonly in small numbers; advancing forward-
inflammation results in production more proinflammatory
facing of dental caries. As levels of salivary lactobacilli
cytokines signaling of fibroblasts in the tissues [32].
associate well with consumption of dietary carbohydrates,
Present data shows elevation in serum concentrations
they are used to distinguish the cariogenic potential of the
of IgA in patients, IgA in serum is linked positively with
diet [6].
age, sex, alcohol heavy drinking, obesity and metabolic
Gram positive aerobic/facultative anaerobic S. aureus
syndrome [33].
detected in 11 case (20%) as single and mixed infection.
Serum IgA have a pro-inflammatory immune responses,
S. aureus are associated with human infections, such as
by induction pro-inflammatory cytokines production
facial furuncle and carbuncle, loose connective tissue
such as
inflammation, and tumor post-operative wound infections
TNF, IL-19, and IL-6 and enhance phagocytosis. In the
[25]. Bacterial oral biofilm serve as a reservoir of
liver
infection for respiratory bacteria, Staphylococcus aureus,
IgA does not only mediate bacterial clearance, but that
and enteric bacteria that has been shown to colonize the teeth IgA
ofpatients self-proclaimed to hospitals or long-term care also contributes to initiation of protective immunity
facilities. These bacteria when released into saliva may by controlling the balance between immune tolerance and
then aspirated into the lower airway creating respiratory inflammation by Kupffer cells. Monomeric or dimeric
infection. Intubation is another way by which oral IgA also have Inhibitory signaling, acting an active role in
bacteria can be introduced into the respiratory system. homeostasis by suppression of inflammatory functions
Inflammatory cytokines delivered by the periodontium [34].
may possibly be mechanism through which respiratory Our result recorded elevation in IL-4 among test
disease are associated with oral health. These mediators group, however the differences were non-
present in tissues of inflamed gingiva, enter the gingival significant, the anti-inflammatory action of IL-4 is well
crevicular fluid and then the saliva. These mediators can documented both in vitro and in vivo. IL-4 attenuates the
have proinflammatory outcomes in the lower airway [26]. activation of various immunocompetent cells, including
Current study shows Gram negative anaerobic black neutrophils, monocytes, and macrophages, by limiting the
pigmented bacteria (5.3%) as single infection. production of proinflammatory cytokines and regulate the
Black pigmented an anaerobes include P gingivalis inflammation processes [35].
and P intermedia found in dental plaque in 0.1 % and Elevation level of anti-inflammatory IL-4 cytokine
increase in patients may reproduce the immune tolerance which may
be encouraged by oral administration of antigen, previous
work on rabbits displays that giving antigen in oral rout
record
 International Journal of Immunology 2021; 9(1): 6-12 11

significant lower in antibody production, 4th ed. Elsevier Ltd. P: 279-285.

proinflamatory IL-1 a in associate with rabbits those
administrated to the antigen by intramuscular rout [36].
The elevation in anti-inflamatory cytokine IL-4 in
dental infection patients combined with lowering in IL-7
concentration with in the same group comparing with
control group (Table 2, figure 2-B).
IL-7 motivates the differentiation of multipotent
(pluripotent) hematopoietic stem cells into lymphoid
progenitor cells, it furthermore stimulates propagation of
all cells in the lymphoid lineage (B cells, T cells and NK
cells). It is significant for proliferation through certain steps
of B-cell maturation, T and NK cell survival. II-7 provides
an important signal for survival of thymocyte and pre-B
cell, when IL-7 withdrawn theses cell rapidly die by
apoptosis [19].
Serum CD4 molecules was higher in control group
(2.0226
±1.71) ng/ml than in dental plaque patients (1.84±2.38)
ng/ml and serum CD8 molcules was higher (0.58±0.12) in
ng/ml dental plaque patients than in control group
(0.03±0.12) ng/ml. Mean of the CD4/CD8 ratio was 3.96 in
control group while it was 2.27 in dental plaque patients.

5.
Conclusions
Our work conclude that the nature of bacteria isolated
from dental infection patients were mixed more than
single infection. There were differences in IgA, IL-4, IL-7
however the differences were non-significant,
there were non-significant differences in soluble CD4 &
CD8 between dental plaque patients and in control group
also dental plaque cause changing in CD4/CD8 ratio. The
non-significant differences between patients and control
group may be due to that the antigens in oral cavity or
mucosa! surface induce a degree of systemic immune
tolerance since these bacteria present in early childhood
and there were boundaries between the presence of bacteria
and the immune responses against such invader, therefor
removing the bacteria is important in prevention such
infections.

Acknowledgement
s
The authors would like to acknowledge college of
dentistry/ University of Babylon for providing services
and support to appearance this study. Also, we would thank
Dr. Alaa Tariq at college of science/ Babylon University for
doing ELISA test.

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