Radiol Oncol 2025; 59(4): 589-596. doi: 10.2478/raon-2025-0025 research article The influence of periodontal disease and periodontal treatment on colorectal cancer Ursa Potocnik Rebersak1,2, Erik Brecelj3, Rok Schara1,2 1 Center of Oral Diseases and Periodontology, Dental Clinic, University Medical Centre Ljubljana, Slovenia 2 Faculty of Medicine, University of Ljubljana, Slovenia 3 Institute of Oncology Ljubljana, Slovenia Radiol Oncol 2025; 59(4): 589-596. Received 18 February 2025 Accepted 26 March 2025 Correspondence to: Urša Potočnik Reberšak, D.M.D., Center of Oral Diseases and Periodontology, Dental Clinic, University Medical Centre Ljubljana, Hrvatski trg 6, SI-1000 Ljubljana, Slovenia, E-mail: ursa.potocnik.rebersak@kclj.si Disclosure: No potential conflicts of interest were disclosed. This is an open-access article distributed under the terms of the CC-BY license (https://creativecommons.org/licenses/by/4.0/). Background. Periodontal disease (PD) is associated with more than 50 diseases and conditions, including colorectal cancer. The study aimed to investigate if periodontal treatment influences the blood levels of C-reactive protein (CRP) in colorectal cancer patients. In addition, the aim was to isolate periodontal pathogenic bacteria Fusobacterium nu- cleatum (FN) and Porphyromonas gingivalis (PG), which are most linked to colorectal cancer (CRC), from the mucosa of the cancer-affected intestine. Patients and methods. To assess the effect of periodontal treatment on colorectal cancer, we measured the CRP levels in the blood during cancer therapy on the day of the initial examination by the oncological surgeon, two days following surgery, and at the first follow-up appointment. We compared the CRP levels between two groups: the group of subjects who underwent periodontal treatment and the patients who did not receive periodontal disease treatment. An attempt was made to isolate the periodontal pathogenic bacteria FN and PG from the mucosa of the cancerous tissue in the colon by using quantitative culture. Results. We found no statistically significant difference between the groups in the initial CRP measurements before starting cancer treatment. There was no statistically significant difference between the groups in the CRP measure- ments taken 1st and 2nd day after surgery and at the follow-up appointment. We could not isolate periodontal patho- genic bacteria FN and PG from cancer-altered intestine mucosa using the quantitative culture method. Conclusions. Our study did not find any correlation between periodontal treatment and CRC. Key words: periodontal disease; colorectal cancer; periodontal treatment; fusobacterium nucleatum; porphy- romonas gingivalis; C-reactive protein Introduction Periodontal disease (PD) is a chronic multifactorial inflammatory disease triggered by dysbiosis in the dental plaque biofilm and characterized by severe chronic inflammation, which leads to the progres- sive destruction of the tooth’s supporting tissue. PD is a significant public health problem.1,2 According to the World Health Organization, approximately 19% of the global population suf- fers from severe periodontal disease, representing more than 1 billion cases in individuals over the age of 15.3 Periodontal disease (PD) is associated with more than 50 diseases and conditions, such as cardiovas- cular diseases, Alzheimer’s disease, diabetes, rheu- matoid arthritis, aspiration pneumonia, and cancer, including colorectal cancer (CRC).4 CRC is the third most common type of cancer worldwide. In 2022, more than 1.9 million cases were diagnosed. CRC Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer590 is the second most common cause of cancer-related death, with more than 900,000 deaths annually.5 An increasing body of evidence has confirmed that, in addition to smoking, obesity, aging, and other risk factors, chronic inflammation also plays a role in the development of CRC.6 PD is one of humans’ most common chronic inflammatory diseases.7 In 2010, PD was the 6th most common health condition.8 Despite the anatomical distance between the oral cavity and the intestine, studies have shown that bacteria from the mouth can spread to the intestine, especially in the presence of PD. Periodontopathogenic bacteria, such as Fusobacterium nucleatum (FN) and Porphyromonas gingivalis (PG), can alter the composition of the local microbiome in the colorectal region, which subsequently leads to the development of gastro- intestinal diseases.9 In a study by Li et al., a systematic review of the literature and meta-analysis investigated the po- tential link between PD and CRC. They found that there is a 44% increased risk of developing CRC associated with PD. This connection could help raise awareness of the importance of maintaining periodontal health and, consequently, contribute to reducing the burden of CRC.10 The study aimed to investigate if periodontal treatment influences the blood levels of C-reactive protein (CRP) in colorectal cancer patients. In ad- dition, the aim was to isolate periodontal patho- genic bacteria Fusobacterium nucleatum (FN) and Porphyromonas gingivalis (PG), which are most linked to colorectal cancer (CRC), from the mucosa of the cancer-affected intestine. Patients and methods The study was conducted at the Center of Oral Diseases and Periodontology at the Dental Clinic, University Medical Centre Ljubljana, Slovenia, in collaboration with the Institute of Oncology Ljubljana, Slovenia, from October 2023 to September 2024. The study was approved by the Medical Ethics Committee of the Republic of Slovenia (No. 0120-486/2021/6). ClinicalTrials.gov Identifier: NCT06799182 Patients The patients included in the study were divided into two groups: the experimental group and the control group. Due to ethical concerns, patients were not randomly assigned to the control group. All patients newly diagnosed with CRC under- went an oral cavity examination and received periodontal treatment based on the examination results. Samples were taken for microbiological testing using quantitative culture for FN and PG. Inclusion criteria for the experimental group A new diagnosis of CRC, planned for surgical treatment, and consent to participate in the study. Exclusion criteria for the experimental group The exclusion criteria were patient refusal to par- ticipate in the study, age under 18, periodontal treatment in the last 12 months, antibiotic therapy 3 months before the study, edentulism, advanced cancer for which only palliative treatment was planned, prior radiation of the intestines, and chemotherapy before surgery that could alter the composition of the intestinal microbiome. Inclusion criteria for the control group Patients who had started CRC therapy before the beginning of our study in October 2023 were se- lected. The study included patients who attended a follow-up examination for CRC at the Institute of Oncology Ljubljana surgical clinic between June 2024 and September 2024, met the inclusion crite- ria, and consented to participate. Patients were re- cruited through targeted questionnaires. Inclusion criteria for the control group were: CRC primarily treated surgically, consent to participate (comple- tion of the questionnaire), blood tests for CRP as part of cancer treatment at the first examination, after surgery, and at the first follow-up, and age over 18 years. Exclusion criteria for the control group The exclusion criteria were edentulism, non-coop- eration, periodontal treatment 12 months before surgery, advanced cancer for which only palliative treatment was planned, and smokers (to match the experimental group). Oral clinical examination All patients in the experimental group underwent a comprehensive oral cavity examination, includ- ing the mucosa, dental, and periodontal tissues. Precise recordings of probing depths, gingival Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer 591 recession, and bleeding on probing at six sites around each tooth, degree of tooth mobility, and involvement of furcations in multi-rooted teeth were made. Each patient also underwent radio- graphic imaging (panoramic radiograph, with a local radiograph performed later if needed). The periodontal condition was diagnosed according to the 2017 Classification of Periodontal and Peri- implant Diseases and Conditions. Periodontal treatment All patients with diseased periodontal tissues un- derwent non-surgical treatment for periodontal disease. Treatment included the removal of su- pragingival and subgingival plaque, root scaling and planing at all sites with increased probing depth (≥ 4 mm), and bleeding on probing. Tooth extractions were performed for teeth with a hope- less prognosis. We also provided oral hygiene in- structions and demonstrated the use of tools for maintaining thorough oral hygiene. CRC diagnosis and CRP blood testing From the medical records of the participants at the Institute of Oncology Ljubljana, who were in- cluded in the study, we obtained data on the CRC diagnosis, histopathological type, disease stage, and CRP values at the first examination after sur- gery (2 consecutive measurements), and at the first follow-up examination. Microbiological testing Samples for microbiological testing were taken from both periodontal pockets and the mucosa of cancer-altered intestines. Samples from the periodontal pocket were taken from the most inflamed spot. After remov- ing supragingival plaque (if present) and relative drying of the sampling area, we inserted a paper point (0.3 mm diameter, Maillefer, Ballaigues, Switzerland) into the periodontal pocket for 30 seconds. The paper point was placed in a transport medium (RTF 1.5 ml) and delivered to the labora- tory within 2 hours. Samples of cancer-altered colon tissue were taken at the Institute of Oncology Ljubljana during CRC surgery. All tissue samples were obtained in a manner that did not jeopardize further cancer di- agnostics. After collection, the tissue samples were placed in the transport medium (RTF 1.5 ml) and delivered to the laboratory within 24 hours. Microbiological testing - quantitative culture for Fusobacterium nucleatum (FN) and Porphyromonas gingivalis (PG) Samples from periodontal pockets and the mu- cosa of cancer-altered intestines were cultured at the Laboratory for Bacteriological Diagnostics of Respiratory Infections, Institute of Microbiology and Immunology, Medical Faculty, Ljubljana, us- ing standard procedures on non-selective anaero- bic media. All samples were processed within 24 hours of collection. Before processing, the samples were stored in an RTF transport medium at room temperature. The samples were first diluted 10-fold with PBS solution (NaCl 8 g/l, KCl 2 g/l, Na3HPO4 *H2O 1.15 g/l, KH2PO4 0.2 g/l). Then, 100 µl of each dilu- tion was inoculated onto non-selective blood agar (Oxoid No. 2; Oxoid, Basingstoke, UK) supplement- ed with 5% horse blood, hemin (5 mg/l), where the bacteria were cultured in anaerobic conditions (80% N2, 10% H2, 10% CO2) at 37°C. After one week, all grown colonies were counted, and the colonies of FN and PG were identified and counted. For the identification of bacterial colonies, standard methods were used: recognition of col- ony morphology, cell morphology (Gram stain- ing), aerotolerance, catalase production, and mass spectrometry (MALDI, Biotyper, Bruker Daltonics, Germany)11. Statistical analysis Descriptive statistics in tables and graphs were used to analyze patients’ data and the results of microbiological tests. Statistical analysis was performed using IBM SPSS Statistics for Windows, Version 29.0.2.0 (IBM Corp., Armonk, NY: IBM Corp., 2023). To determine the differences in CRP levels during CRC treatment between the experimental group with additional periodontal disease therapy and the control group, we used the t-test for inde- pendent samples. A p-value of <0.05 was consid- ered statistically significant. Results Patient data Experimental group A total of ten patients were included in the ex- perimental group, all of whom met the inclusion criteria and agreed to participate in the study. The Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer592 average age of the patients was 66.6 years, with six female and four male participants. In the study, nine patients were non-smokers, and 1 was an oc- casional smoker who smoked 0-5 cigarettes daily. Table 1 presents the patient data. In the experimental group, a detailed exami- nation of the periodontal tissues was performed, and a diagnosis of periodontal disease was made according to the 2017 classification of periodontal diseases and conditions. Out of the ten patients, four had generalized periodontal disease (stage IV, grade B), five had localized periodontal disease (stage III, grade B), and one had localized perio- dontal disease (stage III, grade A). None of the pa- tients had healthy periodontal tissues. Control group Ten patients completed the questionnaires. One patient was excluded from the study due to hav- ing undergone periodontal treatment in the year before starting cancer treatment. The average age of the remaining nine participants was 65.1 years. The group consisted only of non-smokers, includ- ing five males and four females. Table 2 presents the patient data. No dental examination was performed for the control group, and the status of periodontal tissues was obtained through the questionnaires. Of the nine participants, five did not report any issues with their gums during cancer treatment, while 4 reported problems with their gums. Among them, three had been diagnosed with periodontal dis- ease and had lost one or more teeth as a result. CRP levels We found no statistically significant difference be- tween the groups in the initial CRP measurements before starting colorectal cancer (CRC) treatment (p = 0.242; 95% CI [-3.9897; 14.7385]). There was also no statistically significant difference between the groups in the CRP measurements taken 1 day after surgery for CRC (p = 0.592; 95% CI [-34.915; 59.2661]). Similarly, no statistically significant difference was observed between the groups in the second CRP measurement taken 2 days after the surgery (p = 0.485; 95% CI [-77.409; 38.3646]). Additionally, no statistically significant difference was found when comparing the control CRP meas- urements between the groups (p = 0.533; 95% CI [-7.2638; 3.9083]). TABLE 1. Patient data for the experimental group Patient Gender Age(years) Clinical diagnosis and location of the CRC Histo- pathological diagnosis TNM** classification BMI* Other systemic diseases Smoker 1 M 64 Transverse colon cancer Adenocarcinoma T3N0 28.3 High cholesterol, high blood pressure NO 2 F 60 Right colon cancer Adenocarcinoma T3N1bM0 25 No systemic diseases NO 3 F 87 Cecum cancer Adenocarcinoma T4N3bM0 27.2 Asthma, hypothyroidism NO 4 M 60 Sigmoid colon cancer Adenocarcinoma T2N0M0 30 Asthma, hypothyroidism NO 5 M 83 Ascending colon cancer Adenocarcinoma T3N1bM0 25.1 Type 2 diabetes, high blood pressure NO 6 F 70 Colon polyp Tubular adenoma with low dysplasia / 25.4 High blood pressure NO 7 M 64 Ascending colon cancer Non-Hodgkin lymphoma T3N1cM0 28 No systemic diseases NO 8 F 68 Transverse colon cancer Squamous cell carcinoma T4aN1M0 21 Rheumatoid arthritis, hypothyroidism YES 0-5/day 9 F 57 Cecum cancer Adenocarcinoma T3bN1bM0 22.5 Hypothyroidism NO 10 F 53 Sigmoidcolon cancer Adenocarcinoma pT2N0 21 No systemic diseases NO *BMI = mody mass index; **TNM classification: T0 - tumor not present, T1 - invasion into submucosa, T2 - invasion into muscularis propria, T3 - invasion into subserosa, T4 - invasion through all layers of the colon and into the visceral peritoneum or adjacent structures; N (lymph nodes): N0 - no regional lymph nodes involved, N1 - 1−3 regional lymph nodes involved, N2 - 4−6 regional lymph nodes involved, N3 - 7+ regional lymph nodes involved; M (metastasis): M0 - no distant metastases, M1 - presence of distant metastases; Ca = cancer; CRC = colorectal cancer; F = female; M = male Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer 593 Figure 1 schematically shows the movement of CRP levels in the blood during cancer therapy for the control and experimental groups. Microbiological tests performed in the experimental group Isolation of Porphyromonas gingivalis (PG) We successfully isolated the PG bacteria from peri- odontal pockets in five out of ten patients (50%). However, using the quantitative culture method, we could not isolate the bacteria from any of the colorectal cancer (CRC) tissue samples (0%). Isolation of Fusobacterium nucleatum (FN) We successfully isolated the FN bacteria from the periodontal pockets in all the patients (100%). However, using the quantitative culture method, we could not isolate the bacteria from any of the CRC tissue samples (0%). Discussion In our study, using quantitative culture, we suc- cessfully isolated FN from the periodontal pockets TABLE 2. Patient data from the control group Patient Gender Age(years) Clinical diagnosis and location of the CRC Histo- pathological diagnosis TNM** classification B*MI Other systemic diseases Smoker K1 M 72 Cecumcarcinoma Adenocarcinoma T3N1 21.4 High blood pressure, heart rhythm disorders, prostate cancer survivor, hyper lipoproteinemia NO K2 M 58 Sigmoid colon cancer Adenocarcinoma T2 26 High blood pressure, high cholesterol NO K3 M 52 Sigmoid colon cancer Adenocarcinoma T3cN1a 37.2 High cholesterol, hyperglycemia NO K4 M 86 Transverse colon cancer Adenocarcinoma T3N1 21.9 High blood pressure, enlarged prostate NO K5 F 51 Sigmoid colon cancer Adenocarcinoma T1N1a 16.67 Herniated disc NO K6 M 67 Colorectal cancer (location not specified) Adenocarcinoma T3N1a 27 No systemic diseases NO K7 F 72 Sigmoid colon cancer Adenocarcinoma T3bN0 28.4 High blood pressure, hyper-lipoproteinemia, mild heart failure, ischemic heart disease NO K8 F 60 Left colon cancer Adenocarcinoma T1N0 21.5 No systemic diseases NO K9 F 68 Sigmoid colon cancer Adenocarcinoma T2N0 27.2 High blood pressure, high cholesterol, glaucoma NO *BMI = mody mass index; **TNM classification: T0 - tumor not present, T1 - invasion into submucosa, T2 - invasion into muscularis propria, T3 - invasion into subserosa, T4 - invasion through all layers of the colon and into the visceral peritoneum or adjacent structures; N (lymph nodes): N0 - no regional lymph nodes involved, N1 - 1−3 regional lymph nodes involved, N2 - 4−6 regional lymph nodes involved, N3 - 7+ regional lymph nodes involved; M (metastasis): M0 - no distant metastases, M1 - presence of distant metastases; Ca = cancer; CRC = colorectal cancer; F = female; M = male 7,13 83,42 80,43 1,831,76 71,24 99,96 3,51 0,00 20,00 40,00 60,00 80,00 100,00 CR P m g/ L FIGURE 1. Changes in the CRP levels in the serum of the experimental (blue line) and control groups (orange line) during colorectal cancer therapy. Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer594 of all patients (ten out of ten). In contrast PG was isolated from the periodontal pockets of half the patients (five out of ten). However, in the cancer-al- tered mucosa of the colon, none of the tested peri- odontal pathogenic bacteria were isolated. Furthermore, we compared the impact of peri- odontal treatment between the experimental group, which had undergone non-surgical peri- odontal therapy before the surgical phase of CRC treatment, and the control group. Due to ethi- cal concerns, we did not conduct a randomized clinical trial. The patients in the control group were recruited through directed questionnaires. They were patients who had completed the active phase of CRC therapy and were attending follow- up appointments at the Institute of Oncology in Ljubljana. Data on CRP levels were obtained retro- spectively from their medical records. Our study did not find statistically significant differences between the groups regarding CRP measurements before and during CRC therapy. One potential mechanism linking PD and CRC is the spread of periodontal pathogens, particu- larly PG and FN, from the oral cavity to the intes- tinal mucosa. In theory, there are two pathways through which bacteria can spread from the oral cavity to the intestine. The first is the hematoge- nous route, where bacteria enter the bloodstream through lesions in the oral cavity, like that of the ulcerated epithelium of the periodontal pocket, and reach the intestinal mucosa via the blood. The second is the enteral route, where bacteria travel through the stomach to the intestine. Although the human body has defense mechanisms along this path, such as neutralization by stomach acid and a colonization barrier against foreign microorgan- isms, there are cases where these defense mecha- nisms are weakened.12 In the study by Abed et al., the researchers aimed to confirm the hypothesis that FN originates from the oral cavity and that colonization of the intestine by the bacteria is effective. They collected samples from the oral cavity and adenocarcinoma during resections. As in our study, FN was successfully isolated in all saliva samples. Additionally, FN DNA was confirmed in the adenocarcinoma sam- ples using PCR, but live FN was only successfully cultured from one sample. So, they attempted to isolate FN from adenocarcinoma samples obtained during colonoscopy, where antibiotic prophylaxis is not required. They received numerous colonies of FN from both biopsy samples and saliva sam- ples, and genomic analysis indicated a high degree of similarity between the strains isolated from the oral cavity and the adenocarcinoma of the same patient. This suggested that the strains of FN in the oral cavity might have migrated and proliferated in the colorectal cancer tissue.13 In contrast to Abed et al., our study did not iso- late any live FN from colorectal cancer tissue (zero out of nine) collected during resective surgery. Like in the study of Abed et al., all our patients had received preoperative antibiotics (cefazolin and metronidazole), which may have hindered the iso- lation of live bacteria from the cancerous tissue. We tried to mitigate the effects of antibiotic treatment and collected tissue samples during colonoscopy from one patient who had not received antibiotics preoperatively. However, FN was not isolated from this sample either. We also attempted to isolate PG from the cancerous colorectal mucosa but were un- able to detect it in the colon in any of the patients, but we were successful in isolating it from the peri- odontal pocket in 50% of patients. Other studies have used molecular methods like PCR to detect PG in colorectal cancer tissue. Kerdreux et al. used PCR to detect PG in 6.2% of colorectal cancer tissue samples14, and Wang et al. used qPCR to find PG in 10 out of 31 CRC tissue samples, with a statisti- cally significant difference in the presence of PG between cancerous and adjacent normal tissue.15 Although culture methods remain the gold standard, they have limitations, including difficul- ties in culturing certain bacteria, imprecision in counting microorganisms, and the costs involved. This has led to developing more sensitive, accurate, and cost-effective molecular methods for detecting and quantifying bacteria in biofilms. In our study, we could not isolate live PG and FN from colorec- tal cancer tissue using quantitative cultures, and this failure could be attributed to several factors. These include the perioperative administration of antibiotics, possible errors in sample collection, storage, and transport, or the absence of these bac- teria in the colorectal cancer tissue of our patients. Some studies have focused on the other mecha- nisms, inflammatory mediators, and molecules that could serve as a link between PD and system- ic diseases. Among these mediators is C-reactive protein (CRP). CRP is an acute-phase inflamma- tory mediator whose primary functions include complement activation, phagocytosis promotion, and immune response enhancement. CRP con- centration in plasma directly indicates inflamma- tion, and the liver stimulates its synthesis under the influence of IL-1 and IL-6. The normal serum concentration is below 5 mg/L, but it can increase rapidly in response to inflammation (even up to Radiol Oncol 2025; 59(4): 589-596. Potocnik Rebersak U et al. / Periodontal disease and colorectal cancer 595 1000 times), although it also decreases quickly af- terward. Increased CRP levels are commonly as- sociated with infections (including PD), inflamma- tion, injuries, pregnancy, and cancer.16 Some studies have suggested that periodontal treatment reduces CRP levels in serum. Kumar et al. investigated the impact of periodontal therapy on CRP in gingival crevicular fluid (GCF). They collected samples before treatment (6.345 ± 3.781) as well as on the 15th (2.675 ± 1.528) and 45th (0.587 ± 0.082) days after therapy. The study included pa- tients diagnosed with generalized periodontitis, probing depth ≥5 mm, radiographic bone loss, no systemic disease, and satisfactory oral hygiene. They found that CRP levels decreased by 57% on day 15 and 90% on day 45 compared to baseline measurements. This reduction was attributed to the inflammation being resolved after non-sur- gical periodontal treatment, which lowered CRP levels.17 D’Aiuto et al. also observed a reduction of 0.5 mg/L in CRP levels 6 months after periodontal therapy, concluding that non-surgical treatment of periodontal disease decreases serum mediators and markers of acute inflammatory response.18 It is also important to mention that non-surgical periodontal treatment alone could cause a tran- sient increase in CRP levels. In another study by D’Aiuto et al., they measured the transient increase in blood CRP levels following intensive periodon- tal treatment (full mouth treatment in 6 hours). Measurements were taken before the periodontal therapy and on the 1st, 3rd, 5th, 7th, and 30th days. They found a transient increase in CRP levels in the blood. A significant increase in CRP was observed on the first day after therapy and persisted from the initial measurement on days 3, 5, and 7 post- treatment. The CRP levels returned to pre-therapy concentrations only after 1 month. The conclusion was that the most intense rise in CRP occurs 2-5 hours after performing periodontal therapy. This study demonstrates that even intensive periodon- tal treatment alone leads to a transient increase in CRP levels in the blood, which takes about one month to return to pre-therapy levels. The cause of this increase is the transient bacteremia and the extent of surgical trauma.19 Graziani et al. demon- strated that this can be avoided using less inten- sive periodontal treatment approaches, such as quadrant-based therapy.20 In our study, the aver- age time from non-surgical periodontal treatment to the surgical procedure was 40.3 days, which, ac- cording to research, should not impact the increase in CRP levels after the cancer resection surgery. The results of our study did not show a statis- tically significant difference between the groups. However, when observing the movement of aver- age CRP levels throughout the therapy, we noticed a considerable increase in CRP levels in the control group on the second day after the surgical proce- dure (the difference was 19.53 from the test group) despite a lower baseline CRP level. Similarly, the final average CRP level in the test group was lower (1.83) than in the control group (3.51) despite high- er initial values. The key difference between our study and the studies mentioned above is that our patients were not systemically healthy individuals with peri- odontal disease but already had at least one severe systemic disease that influenced CRP levels. This may explain why the differences observed after periodontal therapy in a systemically healthy pop- ulation did not manifest in our study. At the time of this writing, no other studies have explored the impact of periodontal therapy on CRP levels in pa- tients undergoing CRC treatment. A limitation of our study is the small sample size and the lack of randomization in the control group. Future studies with a larger cohort of CRC patients, including a control group with healthy periodontal tissues, would help better understand periodontal therapy’s impact on CRP levels during CRC treatment. Additionally, employing molecu- lar methods for microbiological analysis would provide more accurate and sensitive detection of PG and FN in cancerous colorectal tissue. In our study, with all its limitations, we did not find any correlation between periodontal treat- ment and CRC. Acknowledgments I want to thank Dr. Jurij Bednarik, M.D., who was willing to listen to our ideas and help recruit the patients. 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