Clinical Trial Details
— Status: Active, not recruiting
Administrative data
| NCT number |
NCT04980768 |
| Other study ID # |
AP & Systemic Markers |
| Secondary ID |
|
| Status |
Active, not recruiting |
| Phase |
N/A
|
| First received |
|
| Last updated |
|
| Start date |
February 1, 2021 |
| Est. completion date |
November 30, 2021 |
Study information
| Verified date |
July 2021 |
| Source |
Postgraduate Institute of Dental Sciences Rohtak |
| Contact |
n/a |
| Is FDA regulated |
No |
| Health authority |
|
| Study type |
Interventional
|
Clinical Trial Summary
There is lack of evidence on resolution of signs of systemic inflammatory markers by
successful elimination of periapical inflammation by endodontic treatment. Complete blood
count (CBC) may have potential to detect various inflammatory conditions but its use for this
purpose is sparsely reported. To the best of our knowledge effect of chronic apical
periodontitis on various parameters of complete blood count has not been studied.
Description:
Prevalence of Apical periodontitis (AP) is reported in the range of 17% to 65% with higher
prevalence reported in older patients. Infection of the pulp tissue of the affected tooth is
the principal cause of apical periodontitis and it is characterised by inflammation of the
periradicular tissues. Presentation of AP varies from classical signs of inflammation (pain,
swelling, loss of function) to being completely asymptomatic with only signs of apical bone
resorption on the radiograph. Histological changes seen in AP is localized infiltration of
inflammatory cells and bone resorptions. AP can be treated by root canal treatment (RCT)
which comprises elimination of microbes and their toxic products followed by filling of the
root canal by an inert material. It also acts to limit the spread of microbial infection seen
in AP to jaw and the other parts of the body.
Apical periodontics if left untreated can cause serious complications. Infection and loss of
function caused by loss of teeth may jeopardize overall health of the patients. Chronic
infection like untreated AP may also influence development and progression of other serious
conditions. Numerous inflammatory mediators are responsible for eliciting inflammatory
reactions seen in AP for example both IL-1beta and TNF-alpha are found in periapical lesions
and IL-1beta is suggested to cause greater bone resorption in patients of AP. Role of these
mediators in AP is to cause vasodilation, increased vascular permeability and recruit other
inflammatory cells. It is also been suggested that increased inflammatory mediators seen in
AP may also enhance the systemic inflammation. Inflammation induced tissue damage may vary in
different disease, however the markers that trigger this damage are very similar. They all
act to increase the rate of the inflammatory process, cause tissue destruction and may even
be involved in development of clinical symptoms. For example, markers like hsCRP is
associated with various steps of atherogenesis and is also found elevated in AP. Studies have
reported significantly higher levels of endothelial dysfunction in patients of apical
periodontitis which were found to reduce to normal level following root canal treatment.
A recent systematic review has found significant difference in levels of CRP and IL-6 in AP
subjects than control. IL-6 plays role in initiation of autoimmune disease and chronic
inflammation and also contributes in low grade systemic inflammation. The same systematic
review and meta-analysis has found only eight interventional study that studied effect on
inflammatory marker before and after treatment. The data from these studies were also
heterogenous with wide variety of treatment reported. Only two studies are available which
has evaluated effect of endodontic treatment on levels of isolated groups of inflammatory
mediators and stress markers like reactive oxygen species and circulatory immune complex.
TNF- α is indicated to be responsible for adverse pregnancy outcome and along with CRP may
enhance the insulin resistance. Similarly, complete hemogram indices like mean platelet
volume, neutrophil-lymphocyte ratio is altered in chronic inflammatory conditions and their
estimation could be useful in evaluating overall systemic inflammatory burden of patients of
AP. To the best of our knowledge no study so far has evaluated effect of non-surgical root
canal treatment on the levels of hsCRP and complete hemogram parameters. Therefore, this
study proposes to compare these markers in patients of AP and healthy control and also before
and two years after root canal treatment.
Medical and Dental Examination Prior to treatment a detailed medical and dental history will
be recorded. Oral clinical examinations will include hard and soft tissue evaluation. Pulp
sensibility test will be carried out along with percussion and palpation of the affected
tooth. The periapical radiographic examinations will be carried out at standard exposure
parameters to detect apical bone resorption. Periodontal clinical parameters will be
evaluated at 6 sites in all teeth, including probing depths (PDs), the clinical attachment
level, and bleeding on probing at the base of the crevice, excluding third molars. The
periodontal assessment will be made with a manual periodontal probe (UNC 15; Hu-Friedy,
Chicago, IL).
Blood Samples and Laboratory Analysis Fasting blood samples will be obtained by venipuncture
of the ante-cubital vein. Blood sample will be submitted to the clinical laboratory of the
Department of Biochemistry PGIMS and Department of Oral Pathology, PGIDS, Rohtak, Haryana for
the quantitative analysis of hs-CRP and complete hemogram analysis respectively.
Technique for ELISA: Whole blood sample will be kept at 4°C overnight and centrifuged for 15
minutes at approximately 6000 rpm. Serum will be separated and stored in aliquots at -80 °C
in the until use. Serum hsCRP assay kit will be used. ELISA is a sandwich enzyme immunoassay.
A monoclonal antibody specific for these markers will be pre- coated on the microplate.
Standard and sample will be pipetted into wells and any marker present will be bound by
immobilized antibody. After washing away any unbound substances, enzyme- linked polyclonal
antibody specific for hs-CRP will be added to the wells.
After an incubation period amplifier solution will be added to the wells, and the color will
develop in proportion to the amount of hsCRP bound in the initial stage. The intensity of the
color will be measured.
Root Canal treatment Access opening will be done after rubber dam isolation and
administration of local anesthesia. debridement of the pulp chamber will be done and all
canal orifices will be identified. Negotiation of canals will be done. Working length will be
determined using root ZX apex locator and will be verified radiographically. Coronal
enlargement will be done using Gates- Glidden drills. The apical third of the root canal will
be instrumented up to size 35 for mesial and up to size 45 for distal canals. Finally, root
canals will be further instrumented with step-back technique enlargement in 1 mm increments
to 3 sizes larger than the master apical file. Irrigation will be carried out using 5 mL of a
5% NaOCl solution between files. After preparation, the root canals will be irrigated with 5
mL 17% EDTA for 3 minutes to remove smear layer, followed by 5 mL 5% NaOCl. The final
irrigation will be done with 5 mL distilled water. The root canals will be dried using paper
points and filled with laterally condensed gutta-percha (Dentsply Maillefer) and Zinc oxide
Eugenol based sealer mixed according to manufacturers' instructions. Gutta- percha will be
cut with a heated instrument and vertically condensed right at the orifice opening of the
canals. Final composite resin restoration will be done following manufacturer instruction.
Follow up Follow up and clinical and radiographic examination will be carried out at six
months. Re-assessment of hs-CRP and complete hemogram indices will also be done of all
patients at 6 months
