Serum ACP And CRP Response To Periodontal Therapy

Acid phosphatase, C-reactive protein, chronic periodontitis, scaling and root planing, biomarkers, periodontal therapy

1
Raghvendra Saini,
1
PhD Scholar, Medical Biochemistry,
Biochemistry, National Institute of
Medical Sciences and Research, Nims
University Rajasthan, Jaipur,
Pin code- 303121, India,
Email idraghvendrasaini74@gmail.com ,
Orcid id- 0009-0002-9040-5265
2*

Dr Sushma BJ,
Professor & HOD, Medical
Biochemistry, Biochemistry, National
Institute of Medical Sciences and
Research, Nims University Rajasthan,
Jaipur, Pin code- 303121, India,
Email id- bjsushma2020@gmail.com,
Orcid id- 0009-0003-9017-9517
2*

3

Dr. Neetha Bhargava
Professor & HOD, MDS Periodontal,
Periodontist, NIMS Dental College,
Nims University Rajasthan, Jaipur,
Pin code- 303121,
Email id- veekshya@gmail.com,
Orcid id- 0000-0002-2322-9823
3

*Corresponding authorDr Sushma BJ,
Email id- bjsushma2020@gmail.com

Received: 11.11.2024
Accepted: 02.05.2025

European Journal of Prosthodontics and Restorative Dentistry (2026) 34 (2), 13–18

Serum ACP And CRP Response
To Periodontal Therapy
------------------------------------------------------Abstract
Background: Chronic periodontitis is characterized by hyperplastic tissue damage
and inflammation. The inflammatory cells C-reactive protein (CRP) is a systemic
acute phase proteins and acid phosphatase (ACP) is a local osteoclastic enzyme.
Their relative response of non-invasive treatment for periodontal disease is under
researched.
Objective: To evaluate serum levels of ACP and CRP in long-term periodontal
disease patients compared to healthy controls, assess their changes after root
planning and scaling (SRP), and examine their correlation. Methods: In this
prospective study, 86 chronic periodontitis patients (probing depth ≥5mm at ≥30%
sites) and 86 periodontally healthy controls were enrolled. Serum ACP (pnitrophenyl phosphate method) and CRP (latex-enhanced turbidimetric
immunoassay) were measured at baseline for all participants. Periodontitis patients
underwent full-mouth SRP, with biomarker re-assessment at 1 week and 1-month
post-therapy. Results: Baseline ACP (14.23±3.36 vs. 2.61±1.01 U/L, p<0.001) and
CRP (16.34±3.76 vs. 2.03±0.95 mg/L, p<0.001) were significantly higher in
periodontitis patients versus controls. Following SRP, both markers showed
progressive reduction (Repeated Measures ANOVA, p<0.001): ACP decreased to
10.75±2.73 U/L at 1 week and 7.14±1.72 U/L at 1 month; CRP decreased to
10.50±2.63 mg/L and 5.87±1.45 mg/L, respectively. No important correlation
existed between baseline ACP and CRP levels (r=0.192, p=0.077).
Conclusion: non-invasive treatment for periodontal disease effectively reduces
both local tissue-destructive (ACP) and systemic inflammatory (CRP) biomarkers.
Their independent behavior suggests they represent distinct pathological pathways
in periodontitis, supporting comprehensive biomarker assessment for monitoring
disease activity and therapeutic response.

Chronic periodontitis is a widespread inflammatory disorder of the toothsupporting apparatus, which is the gradual demolition of periodontal tissues such as the alveolar bone [1]. In addition to its oral form, periodontitis has been identified as a cause of systemic inflammation, and this has implications on different systemic diseases [2]. Circuitry is involved in the pathogenesis of the interaction between pathogenic biofilm and host immune-inflammatory responses [3]. This systemic type of inflammation that is commonly quantitated by sensitive biomarkers such as high-sensitivity CRP (hs-CRP) is a central agent in the pathogenesis of diseases such as atherosclerosis, and this type of biomarker is a cardiovascular risk predictor tool [4]. This interaction liberates a number of mediators and enzymes which are possible biomarkers of disease activity. One of them, C-reactive protein (CRP), which is produced by hepatocytes as an acutephase protein, has been widely investigated as a systemic inflammatory surrogate protein produced in periodontitis [5,6]. Notably, high levels of CRP (especially the high-sensitivity version, hs-CRP) in the body are also identified as a predictor of future cardiovascular morbidity in other chronic inflammatory conditions, including type 2 diabetes, which highlights its clinical significance [7] Its levels are also associated with the severity of the disease and drop after treatment for periodontal, which connects oral inflammation to the body state [8]. Unlike systemic markers, local tissue infiltrating enzymes would give an insight on periodontal breakdown on site of disease. ACP is a lysosomal enzyme that is highly present in osteoclasts, neutrophils, and macrophages, which is significant in the breakdown of bones and tissues [9,10]. Periodontitis has been associated with high levels of ACP in the gingiv crevularia fluid and serum which indicates a higher

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