The long-term inflammatory disease known as chronic periodontitis is brought on by the buildup of microbial plaque and maintained by a changed host immunological response, which causes the periodontal supporting tissues to gradually deteriorate. Although chronic periodontitis has always been thought of as a localised dental illness, there is mounting evidence that it is a continuous source of systemic inflammation that affects haematological parameters and circulating inflammatory mediators. Chronically inflamed periodontal tissues operate as an active reservoir of bacterial products and inflammatory cytokines that can enter the systemic circulation and cause a quantifiable acute-phase response.^[1]

Pro-inflammatory mediators such tumour necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) are released as a result of the ongoing stimulation of host immune systems by the microbial environment of periodontal pockets. These cytokines are essential for stimulating hepatocytes to produce acute-phase proteins, which causes changes in systemic inflammation.^[2] With its quick and noticeable rise in response to inflammatory stimuli, C-reactive protein (CRP) is thought to be the most sensitive and clinically significant indicator of inflammation among these proteins.

The liver primarily produces the pentameric protein CRP in response to cytokine signalling, namely IL-6. By attaching itself to microorganisms and injured cells and encouraging complement activation and opsonisation, it takes part in innate immune defence. CRP levels are minimal under physiological settings, but they can rise sharply within 24 to 72 hours during inflammatory situations.^[3] It has been demonstrated that persistent periodontal inflammation sustains high CRP levels, which are indicative of a persistent low-grade systemic inflammatory load.^[1]

Peripheral blood cellular patterns are influenced by periodontitis-related inflammation in addition to serological markers. Changes in leukocyte distribution, neutrophil predominance, lymphocyte suppression, and minute fluctuations in platelet counts can all result from cytokine-mediated modifications in haematopoiesis.^[4] These haematological alterations have been suggested as contributing factors between periodontal disease and systemic illnesses including cardiovascular disease. They are indicative of systemic immune activation. The cornerstone of managing periodontal disease is still non-surgical periodontal treatment, often known as Phase I therapy. Disrupting the microbial biofilm, lowering periodontal inflammation, and restoring periodontal health are the goals of mechanical debridement using scaling and root planing. This is demonstrated clinically by improvements in clinical attachment levels, decreases in plaque buildup, gingival inflammation, and probing pocket depth.^[1]

But periodontal instrumentation is a regulated inflammatory stimulation in and of itself. Short-term systemic inflammatory activation may arise from mechanical displacement of the subgingival biofilm, which can cause tissue damage and temporary bacteremia. Phase I periodontal treatment has been shown by several researchers to cause a transient increase in CRP levels and changes in haematological markers, which are similar to traditional acute-phase inflammatory reactions. Usually self-limiting, these alterations go away as periodontal repair advances.^[5]

It is clinically important to comprehend these fleeting systemic reactions, especially in patients who have underlying systemic risk factors. Following periodontal therapy, monitoring CRP levels and haematological parameters emphasises the importance of periodontal health in overall systemic well-being and offers important insight into the systemic impact of periodontal intervention.^[6] With a focus on temporal fluctuations in serum CRP levels and peripheral blood parameters, the current research was created to assess temporary systemic inflammatory and haematological alterations in patients with chronic periodontitis after Phase I non-surgical periodontal treatment.

AIM AND OBJECTIVES

Aim

To evaluate the effect of Phase I periodontal therapy on transient systemic inflammatory and hematological changes in chronic periodontitis patients.

Objectives

1. To assess changes in CRP, leukocyte count, and hematocrit before therapy and up to 30 days following Phase I therapy.

To clinically evaluate plaque index, clinical attachment loss, and probing pocket depth at baseline and 30 days post-therapy.

Study Design: This was a prospective observational clinical study conducted to evaluate systemic inflammatory and hematological responses following Phase I periodontal therapy. Study Setting: The study was carried out in the Department of Periodontology and Implantology, Amargadh, Bhavnagar. Study Population: A total of 40 patients diagnosed with chronic generalized periodontitis were enrolled. Participants were aged between 25 and 64 years and were systemically healthy. Inclusion Criteria • Patients diagnosed with chronic generalized periodontitis • Age between 25 and 64 years • Systemically healthy individuals • Presence of periodontal pockets and attachment loss • Exclusion Criteria • History of systemic inflammatory or metabolic diseases • Tobacco use in any form • Pregnant or lactating women • Periodontal therapy within the preceding 6 months • Use of antibiotics or anti-inflammatory drugs • Ethical Approval and Consent All participants were informed about the nature and purpose of the study. Written informed consent was obtained prior to clinical examination and sample collection. Clinical Periodontal Assessment The following parameters were recorded at baseline and on the 30th day: • Plaque Index (PI) • Gingival Index (GI) • Probing Pocket Depth (PPD) • Clinical Attachment Loss (CAL) To guarantee consistency and repeatability of probing data, acrylic stents were made. Orthopantomograms and intraoral periapical radiographs were acquired as needed. At baseline and during follow-up visits, extraoral and intraoral photos were taken. Phase I Periodontal Therapy All subjects underwent Phase I non-surgical periodontal therapy consisting of ultrasonic scaling and root planing using a piezo-ultrasonic scaler. Local anesthesia was administered where necessary. Comprehensive oral hygiene instructions were provided to all participants. Hematological and Serological Evaluation Venous blood samples were collected using sterile techniques at the following time points: • Baseline (pre-therapy) • Day 1 post-therapy • Day 7 post-therapy • Day 30 post-therapy Samples were analyzed for: • Serum C-reactive protein (CRP) • Complete blood count (CBC) • Fasting blood sugar (FBS) All laboratory analyses were performed at the central laboratory following standardized protocols. Follow-Up Schedule Patients were re-evaluated clinically and systemically at Day 1, Day 7, and Day 30 following Phase I therapy.

Table 1: Baseline Demographic and Clinical Characteristics of the Study Population (n = 40)                                           

Table 1 presents the baseline demographic and clinical profile of the study population. A total of 40 systemically healthy patients diagnosed with chronic generalized periodontitis were included. The participants ranged in age from 25 to 64 years, with a mean age of 44.6 ± 9.8 years. The study group comprised 17 males (42.5%) and 23 females (57.5%). All subjects exhibited periodontal pocketing and clinical attachment loss at baseline. None of the participants reported tobacco use or systemic illness, ensuring that systemic inflammatory changes observed during the study period were attributable to periodontal status and therapeutic intervention.

Figure 1: Gender Distribution

Table 2: Changes in Serum C-Reactive Protein (CRP) Levels Following Phase I Periodontal Therapy

*Statistically significant compared to baseline

Table 2 shows the temporal changes in serum C-reactive protein (CRP) levels following Phase I periodontal therapy. Mean baseline CRP levels were 2.12 ± 1.18 mg/L. A significant increase in CRP was observed on Day 1 post-therapy (5.76 ± 2.21 mg/L; p < 0.001), indicating an acute-phase inflammatory response. Subsequently, CRP levels decreased to 2.48 ± 0.72 mg/L on Day 7 and further declined to 1.09 ± 0.29 mg/L by Day 30. The reduction at Day 30 was statistically significant compared to baseline, reflecting resolution of systemic inflammation following periodontal healing.

Figure 2: Changes in Serum C-Reactive Protein (CRP) Levels Following Phase I Periodontal Therapy

Table 3: Total and Differential Leukocyte Count Changes After Phase I Therapy

Table 3. Total and Differential Leukocyte Count Changes After Phase I Therapy

Table 3 summarizes the changes in total and differential leukocyte counts at baseline and at subsequent follow-up intervals. The mean total leukocyte count increased from 7,420 ± 1,120 cells/mm³ at baseline to 8,160 ± 1,340 cells/mm³ on Day 1, followed by a gradual decline toward baseline values on Days 7 and 30. Neutrophil percentage showed a transient increase on Day 1 (62.4 ± 9.2%) compared to baseline (60.1 ± 8.4%), while lymphocyte percentage demonstrated a temporary reduction on Day 1 (29.1 ± 8.4%). Both neutrophil and lymphocyte values returned to near baseline levels by Day 30.

Table 4: Hematological Changes (Hemoglobin, Hematocrit, Platelets) Following Therapy

Table 4 depicts variations in hemoglobin, hematocrit, and platelet counts during the study period. Mean hemoglobin levels showed a slight reduction on Day 1 (12.6 ± 1.3 g/dL) compared to baseline (12.9 ± 1.2 g/dL), with gradual normalization by Day 30. Hematocrit values followed a similar pattern, with minimal fluctuation across time points. Platelet counts demonstrated a mild increase on Day 1, followed by a gradual decrease by Day 30. None of these changes were clinically significant, and all parameters remained within physiological limits.

Figure 4: Hematological Changes (Hemoglobin, Hematocrit, Platelets) Following Therapy

Table 5: Summary of Systemic Inflammatory Response Pattern After Phase I Therapy

Interpretation:
Phase I periodontal therapy produced a classical acute-phase inflammatory response followed by complete systemic recovery within 30 days.

Table 5 provides a summary of the systemic inflammatory and hematological response observed following Phase I periodontal therapy. An acute inflammatory response characterized by elevated CRP levels, transient neutrophilia, and lymphopenia was evident immediately after therapy. By Day 30, all evaluated parameters showed normalization or improvement beyond baseline levels, indicating resolution of the transient inflammatory response induced by periodontal instrumentation.

The present study assessed the systemic inflammatory and hematological responses following Phase I periodontal therapy in systemically healthy patients with chronic generalized periodontitis. The findings demonstrate that nonsurgical periodontal therapy induces a transient systemic inflammatory response, evidenced by a short-term rise in serum C-reactive protein (CRP) levels and reversible alterations in leukocyte counts, followed by normalization or improvement by 30 days post-therapy.

The baseline demographic parameters (Table 1) revealed that the participants had no history of tobacco use or systemic illness, and their mean age was 44.6 ± 9.8 years. The observed alterations were mostly attributable to periodontal disease and its treatment since this homogeneity reduced confounding variables that may independently affect systemic inflammatory markers. Previous periodontal research assessing systemic inflammatory effects have highlighted similar methodological techniques. Machado V et al.^[7]

The notable increase in serum CRP levels on Day 1 after Phase I treatment was one of the main findings (Table 2). A well-known indicator of systemic inflammation, CRP is a sensitive acute-phase reactant produced by the liver in reaction to pro-inflammatory cytokines, especially interleukin-6 (IL-6). Olson ME et al.^[3] The acute immunological activation brought on by periodontal tissue manipulation and temporary bacteremia linked to scaling and root planing are probably the causes of the immediate post-therapy increase in CRP. The consistency of this inflammatory response pattern is supported by reports by Machado et al. of similar transitory CRP rises after extensive periodontal treatment. Machado V et al.^[7]

After that, by Day 7, CRP levels were drastically decreased, and by Day 30, they were below baseline. This finding is consistent with the body of research showing that successful nonsurgical periodontal treatment lowers the systemic inflammatory load over time. Luthra S et al.^[8] Reduced periodontal microbial load, local inflammation resolution, and periodontal tissue integrity restoration may all contribute to the long-term drop in CRP.

Acute systemic immunological activation was also confirmed by alterations in leukocyte patterns (Table 3). On Day 1, there was a brief drop in the proportion of lymphocytes and a brief rise in the total leukocyte count and neutrophil percentage. After periodontal instrumentation, neutrophilia indicates the innate immune response's activation, which aims to regulate microbial assault and promote tissue healing.^[9] Leukocyte numbers returned to normal by Day 30, suggesting that the inflammatory response was transient and did not cause long-term systemic immunological dysregulation.

Hematological parameters, including hemoglobin, hematocrit, and platelet counts, exhibited only mild and clinically insignificant fluctuations throughout the study period (Table 4). In line with findings from other clinical trials, our results imply that Phase I periodontal treatment does not negatively impact haematological stability in systemically healthy persons. Sundaram SG et al. ^[10] Even though there was a brief rise in platelet count just after treatment, values stayed within normal physiological ranges and returned to normal on their own.

A balanced inflammatory cascade, marked by an acute-phase reaction followed by full resolution within 30 days, is highlighted by the overall systemic response pattern shown in Table 5. D'Aiuto et al., who suggested periodontal therapy as a paradigm for examining acute inflammatory responses without pharmacological or toxic stimuli, have reported similar systemic inflammatory dynamics after periodontal therapy^[11]. Given the known link between increased systemic inflammation and metabolic and cardiovascular disorders, the observed decrease in CRP levels following periodontal treatment is significant from a clinical standpoint. Zhang Y et al. ^[12] These results support periodontal therapy's function in reducing the burden of systemic inflammation. However, individuals with pre-existing systemic risk factors should be carefully considered due to the immediate post-therapy inflammatory spike.

The present study demonstrates that Phase I periodontal therapy in systemically healthy patients with chronic generalized periodontitis induces a transient systemic inflammatory response, characterized by a short-term elevation in serum C-reactive protein levels and reversible alterations in leukocyte distribution. This acute response was most pronounced within the first 24 hours following therapy and is likely attributable to periodontal tissue manipulation and temporary bacteremia associated with nonsurgical instrumentation. Importantly, the inflammatory changes observed were self-limiting, with progressive normalization of systemic inflammatory and hematological parameters by Day 30 post-therapy. A significant reduction in CRP levels below baseline values at the end of the observation period highlights the beneficial systemic impact of periodontal treatment, reflecting effective control of periodontal inflammation and restoration of host immune balance. The findings reinforce the concept that periodontal disease contributes to systemic inflammatory burden and that appropriate periodontal intervention can result in measurable systemic benefits. Clinically, these results underscore the importance of periodontal health not only for oral disease management but also for maintaining systemic inflammatory homeostasis. LIMITATIONS OF THE STUDY The current study has certain limitations that should be noted despite its clinical significance. First, the results may not be as applicable to larger populations due to the limited sample size. Second, there was no control group in the trial that did not get periodontal therapy, which would have bolstered conclusions about systemic inflammatory alterations that could only be attributed to Phase I therapy. Third, patients with systemic conditions like diabetes mellitus or cardiovascular problems, in which systemic inflammatory responses may vary, were not included in the research population since it was limited to non-smoking, systemically healthy adults. Furthermore, only a few inflammatory and haematological indicators were evaluated; a more thorough picture of systemic immune regulation would have been obtained by include cytokines like interleukin-6 or tumour necrosis factor-α. Lastly, longer-term assessments would be required to ascertain the durability of the noted systemic benefits, as the follow-up time was restricted to 30 days. To further understand the systemic consequences of periodontal treatment, greater sample sizes, longer follow-up periods, the inclusion of patients with systemic impairment, and a more comprehensive biomarker assessment are all necessary.

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