Osseointegration, defined as "a direct connection between living bone and a load-carrying endosseous implant at the light microscopic level," is essential for the long-term success of dental implants (1). This direct, rigid fixation of implants to the jawbone has become a widely accepted treatment for edentulism. However, the duration of osseointegration and the timing of prosthetic loading are not standardized and typically range from 0 to 6 months (2). Researchers are actively exploring strategies to reduce this period by modifying implant surface properties and utilizing bioactive molecules that enhance osteoblastic differentiation and accelerate peri-implant bone healing (3).

Growth factors are bioactive proteins that regulate wound healing and bone regeneration. Platelet-derived preparations, such as platelet-rich fibrin (PRF) and concentrated growth factor (CGF), contain multiple growth factors, including bone morphogenetic proteins (BMPs), platelet-derived growth factor (PDGF), insulin-like growth factor (IGF), vascular endothelial growth factor (VEGF), and transforming growth factor-beta (TGF-β1 and TGF-β2), which facilitate angiogenesis, chemotaxis, and osteogenesis (4–6). These growth factors promote cellular migration, extracellular matrix synthesis, and osteoblastic activity, potentially enhancing peri-implant healing and osseointegration (7).

Various autologous platelet concentrates have been used to enhance bone regeneration, including platelet-rich plasma (PRP), PRF, and CGF (8). PRF has been extensively studied for its efficacy in tissue engineering, demonstrating promising results in regenerative dentistry (9,10). CGF, introduced by Sohn et al. in 2009, has been reported to exhibit superior regenerative potential due to its denser fibrin matrix and higher concentration of growth factors (11).

Leukocyte-Platelet Rich Fibrin (L-PRF) is a second-generation platelet concentrate containing leukocytes, growth factors, proteins, and cytokines. Unlike PRP, L-PRF does not require biochemical modifications with anticoagulants or bovine thrombin, making it a more biocompatible alternative (12,13). L-PRF releases key growth factors in a slow, sustained manner for up to 28 days, supporting early wound healing and osseointegration (14,15). When applied to titanium implant surfaces, L-PRF forms a fibrin layer that enhances platelet adhesion and growth factor release, promoting bone formation (6).

CGF differs from PRF primarily in its production method, which involves specific centrifugation protocols without any additives. This results in a fibrin matrix with superior adhesive strength, tensile properties, and growth factor content (7). CGF contains platelets, leukocytes, and CD34+ stem cells, which contribute to its regenerative potential and anti-inflammatory effects, reducing the risk of infection (8). Furthermore, CGF acts as a biological scaffold supporting cytokine attachment and cellular migration, which is crucial for osteogenesis and tissue healing (9).

Study Design and Setting

This study was conducted in the Department of Periodontology and Oral Implantology at RUHS College of Dental Sciences, Jaipur, India, from January 2020 to December 2021. Patients reporting to the department for implant placement were evaluated and recruited based on pre-defined eligibility criteria.

Sample Size and Study Groups

A total of 30 surgical sites were included in the study, which were randomly divided into three groups. Group I (Control Group) consisted of sites where no bioactive material was applied before implant placement. Group II (PRF Group) included sites where platelet-rich fibrin (PRF) was applied at the osteotomy site before implant placement, while Group III (CGF Group) consisted of sites where concentrated growth factor (CGF) was placed at the osteotomy site before implant placement.

Patient Selection Criteria

The inclusion criteria required participants to be between 16 to 65 years old, free of systemic conditions affecting bone healing, and with sufficient bone thickness and height to support implant placement. They were required to have a normal maxillo-mandibular relationship, adequate inter-arch space, and be physically and psychologically fit for implant surgery. The exclusion criteria eliminated patients with systemic conditions such as cardiac diseases, hepatic disorders, diabetes, and thyroid or parathyroid abnormalities. Patients undergoing long-term antibiotic, steroid, or hormonal therapy, pregnant or lactating women, smokers, and individuals with hematologic disorders preventing PRF and CGF fabrication were excluded. Those with previous implant placement or augmentation in the same surgical site were also excluded from the study.

Materials and Equipment

The Dentium Superline and Implantium systems were used for implant placement, with implant lengths varying from 8 mm to 16 mm and diameters of 3.5 mm (Narrow Platform - NP), 4.3 mm (Regular Platform - RP), and 5.0 mm (Wide Platform - WP). The implants were selected based on three-dimensional bone availability to optimize biomechanical load distribution and long-term crestal bone preservation. The surgical armamentarium included standard surgical instruments such as mouth mirrors, probes, tweezers, periosteal elevators, curettes, surgical scissors, and a Dentium Surgical Implant Drill Kit with a physiodispenser unit and handpiece. The study used sterile test tubes, a REMI centrifugation machine, non-resorbable black silk sutures, 2% lignocaine with epinephrine (1:100,000), sterile normal saline, and cotton gauze for PRF and CGF fabrication. Cone Beam Computed Tomography (CBCT) was used for assessing bone density and marginal bone levels.

Fabrication of Platelet Concentrates

PRF was prepared following Choukroun’s protocol. A 10 mL blood sample was drawn from the patient without anticoagulants and immediately centrifuged at 3,000 rpm for 10 minutes. This resulted in three layers: the top layer of acellular platelet-poor plasma (PPP), the middle layer of PRF clot, and the bottom layer of red blood cells (RBCs). The PRF clot was collected and placed at the osteotomy site before implant placement. CGF was prepared using a specific centrifugation protocol. Approximately 9 mL of venous blood was collected in sterile Vacuette tubes without anticoagulants and centrifuged in a stepwise manner with varying speeds, leading to the formation of four distinct layers: the top serum layer, an intermediate fibrin buffy coat, a liquid phase rich in growth factors, and the bottom RBC layer. The CGF fibrin matrix was extracted and placed at the implant osteotomy site.

Surgical Procedure

Preoperative preparation included Phase I therapy, consisting of scaling, root planing, and oral hygiene instruction. Patients rinsed with 0.2% chlorhexidine mouthwash before surgery, and local anesthesia was administered using 2% lignocaine with epinephrine (1:100,000). A crestal incision was made, and a full-thickness mucoperiosteal flap was raised. Osteotomy was performed according to the manufacturer’s protocol with sequential drilling under copious saline irrigation. In Group I (Control), implants were placed without PRF or CGF application, while in Group II (PRF Group), PRF was placed at the osteotomy site before implant placement, and in Group III (CGF Group), CGF was placed at the osteotomy site before implant placement. The implants were placed 1 mm subcrestally, ensuring primary stability with a torque of more than 25 Ncm. Cover screws were placed, and the surgical site was sutured using 3-0 black silk sutures.

Postoperative Care

Patients were prescribed postoperative medications, including amoxicillin 500 mg thrice daily for 5 days, ibuprofen 400 mg thrice daily for pain control, and chlorhexidine mouthwash (0.12%) twice daily for 2 weeks. They were advised to avoid brushing at the surgical site and to maintain oral hygiene. Sutures were removed after 10 days, and follow-up visits were scheduled at 1 month.

Outcome Assessment

Clinical parameters were evaluated, including the Plaque Index (PI) using the Silness & Loe (1964) criteria, Gingival Index (GI) using the Loe & Silness (1963) criteria, peri-implant probing depth (PD) measured at four sites per implant, and Wound Healing Index (WHI) evaluated at 1 week post-surgery. Implant stability was assessed using the Implant Stability Quotient (ISQ) through Resonance Frequency Analysis (RFA) at baseline and 1 month. Radiographic assessments included bone density measurements using CBCT grayscale values recorded at baseline and 1 month, as well as marginal bone loss (MBL), which was measured from the implant collar to the alveolar crest on CBCT images.

Statistical Analysis

Descriptive statistics, including mean, standard deviation, and percentages, were used for data analysis. Inter-group comparisons were conducted using the t-test and ANOVA, while intra-group comparisons were performed using paired t-tests and repeated measures ANOVA. A p-value of less than 0.05 was considered statistically significant.

The present study evaluated the effect of Concentrated Growth Factors (CGF) and Platelet-Rich Fibrin (PRF) on implant stability and osseointegration using clinical and radiographic parameters. The data was statistically analyzed, and the results are presented as follows:

1. Bone Density Analysis (Table 1)

Bone density was assessed at baseline and 1 month postoperatively for all groups. At baseline, no statistically significant difference in bone density was observed among the groups (p > 0.05). However, after 1 month, there was a statistically significant increase in bone density across all groups (p < 0.01).

• Group I (Control): Bone density increased from 675.85 ± 62.49 at baseline to 687.99 ± 65.65 after 1 month, with a mean change of 12.20 ± 2.77.
• Group II (PRF Group): Bone density increased from 690.32 ± 63.33 at baseline to 727.05 ± 62.72 after 1 month, with a mean change of 36.67 ± 5.20.
• Group III (CGF Group): Bone density increased from 649.68 ± 46.62 at baseline to 701.11 ± 33.21 after 1 month, with a mean change of 51.43 ± 10.43.

The CGF group showed the highest increase in bone density, which was statistically significant compared to the PRF and control groups (p < 0.01).

2. Marginal Bone Loss (Table 2)

Marginal bone level was measured at baseline and 1 month postoperatively to assess the extent of peri-implant bone resorption.

• Group I (Control): Marginal bone level reduced from 0.72 ± 0.10 mm at baseline to -0.37 ± 0.10 mm after 1 month, showing a bone loss of 1.09 ± 0.09 mm.
• Group II (PRF Group): Marginal bone level reduced from 0.59 ± 0.11 mm at baseline to -0.31 ± 0.06 mm after 1 month, showing a bone loss of 0.90 ± 0.10 mm.
• Group III (CGF Group): Marginal bone level reduced from 0.67 ± 0.09 mm at baseline to -0.22 ± 0.08 mm after 1 month, showing a bone loss of 0.90 ± 0.05 mm.

A statistically highly significant difference (p < 0.01) was observed in marginal bone loss, with Group III (CGF) demonstrating the least bone loss compared to Groups I and II.

3. Implant Stability (Table 3)

Implant Stability Quotient (ISQ) values were recorded at baseline, 1 week, and 1 month using Resonance Frequency Analysis (RFA).

• At Baseline:
• Group I: 20.24 ± 1.36
• Group II: 23.98 ± 1.23
• Group III: 24.11 ± 2.54
• Statistically significant differences were observed (p < 0.05).
• At 1 Week:
• Group I: 39.46 ± 5.20
• Group II: 45.81 ± 6.74
• Group III: 50.06 ± 5.29
• A highly significant increase in ISQ values was observed, particularly in Group III (CGF), p < 0.01.
• At 1 Month:
• Group I: 55.31 ± 5.25
• Group II: 59.05 ± 5.29
• Group III: 61.62 ± 2.27
• A statistically significant increase in implant stability was observed in all groups, with CGF showing the highest stability (p < 0.01) .

1. Bone Density (BD)

The baseline bone density was comparable across the groups, with no statistically significant difference (p > 0.05). However, after one month, a significant increase in bone density was observed in both CGF and PRF groups. The mean change in bone density was highest in Group III (CGF) at 51.43 ± 10.43, followed by Group II (PRF) at 36.67 ± 5.20, while the control group exhibited only a minor increase of 12.20 ± 2.77. The difference was statistically highly significant (p = 0.000) (Table 1).

2. Marginal Bone Loss (MBL)

The control group demonstrated the highest marginal bone loss at 1.09 ± 0.09 mm, followed by the PRF group at 0.90 ± 0.10 mm, while the CGF group had the least bone loss at 0.90 ± 0.05 mm. These differences were statistically significant (p < 0.01), indicating that CGF application resulted in better peri-implant bone preservation (Table 2).

3. Implant Stability (ISQ)

Implant Stability Quotient (ISQ) values showed a significant increase across all groups over one month. The baseline ISQ was highest in Group III (CGF) at 24.11 ± 2.54, followed by Group II (PRF) at 23.98 ± 1.23, and the lowest in the control group (20.24 ± 1.36). After one month, ISQ values increased significantly, with the CGF group reaching 61.62 ± 2.27, the PRF group 59.05 ± 5.29, and the control group 55.31 ± 5.25. These findings suggest that CGF enhances implant stability more effectively than PRF and the control (p < 0.05) (Table 3).

Intergroup Comparison of Bone Density (Table 1)

Intergroup Comparison of Marginal Bone Loss (Table 2)

Intergroup Comparison of Implant Stability (Table 3)

The application of CGF demonstrated superior outcomes in improving bone density, reducing marginal bone loss, and enhancing implant stability in the early phase of osseointegration compared to PRF. These findings highlight the potential of CGF as a promising biomaterial in implant dentistry

Dental implants have revolutionized the rehabilitation of edentulous patients, providing both functional and aesthetic benefits. However, the success of implant therapy is highly dependent on the process of osseointegration, which ensures direct bone-to-implant contact (1). Several strategies have been employed to accelerate osseointegration, including surface modifications, bioactive coatings, and the use of platelet concentrates such as Platelet-Rich Fibrin (PRF) and Concentrated Growth Factors (CGF) (2). The present study aimed to compare the efficacy of PRF and CGF in enhancing osseointegration by evaluating implant stability, bone density, and marginal bone loss.

The results of the study indicate that CGF exhibited superior performance in terms of implant stability and peri-implant bone formation. Implant Stability Quotient (ISQ) values were significantly higher in the CGF group compared to the PRF and control groups at all follow-up intervals. This is consistent with previous studies that have demonstrated the ability of CGF to enhance osteoblastic differentiation and bone regeneration due to its enriched concentration of growth factors, leukocytes, and fibrin matrix (3,4).

Marginal bone loss (MBL) is a critical parameter for assessing the long-term success of dental implants (5). In the present study, MBL was significantly lower in the CGF group compared to the PRF and control groups, indicating better preservation of peri-implant bone. This aligns with research suggesting that CGF promotes early angiogenesis and osteoconduction, thereby reducing the rate of bone resorption (6,7). The fibrin-rich matrix of CGF provides a stable scaffold that facilitates cellular migration, adhesion, and differentiation, contributing to reduced marginal bone loss (8).

Bone density measurements from CBCT scans further support the osteoinductive properties of CGF. A statistically significant increase in bone density was observed in the CGF group compared to PRF and control groups at one month postoperatively. This finding corresponds with studies by Sohn et al. (2009), who demonstrated that CGF enhances bone mineralization more effectively than PRF due to its higher concentration of growth factors such as TGF-β1, PDGF, and VEGF (9). These growth factors play a pivotal role in stimulating osteogenesis, promoting angiogenesis, and regulating inflammatory responses, all of which contribute to improved bone density (10,11).

The wound healing index (WHI) scores were also more favorable in the CGF group, demonstrating its potential in soft tissue healing. The improved healing response observed with CGF can be attributed to its higher fibrin network density and the sustained release of growth factors over a prolonged period, as reported in earlier studies (12). The antimicrobial and anti-inflammatory properties of CGF may further contribute to enhanced wound healing and reduced postoperative complications (13).

Although PRF has been widely used in regenerative procedures, its effect on osseointegration appears to be less pronounced compared to CGF. PRF has been reported to provide a short-term burst release of growth factors, while CGF ensures a more sustained release, which is crucial for long-term bone regeneration (14). Additionally, CGF has been shown to have a higher tensile strength and viscosity, which may further enhance its regenerative capacity (15).

Clinical Implications and Limitations

The findings of this study suggest that CGF is a promising biomaterial for accelerating osseointegration and improving implant stability. Its superior ability to preserve peri-implant bone, enhance bone density, and promote soft tissue healing makes it a viable alternative to PRF in implant therapy. However, the study is limited by its short follow-up period of one month. Longer-term studies are needed to assess the impact of CGF on implant survival rates and long-term bone remodeling.

Additionally, the study was limited to a small sample size, which may affect the generalizability of the results. Future studies should incorporate larger sample sizes and extended follow-up periods to validate these findings. Furthermore, while CBCT provides valuable insights into bone density changes, histological analysis would provide a more comprehensive understanding of bone-to-implant contact and cellular interactions.

The results of the present study indicate that CGF is more effective than PRF in enhancing early osseointegration, improving implant stability, and reducing marginal bone loss. These findings support the potential of CGF as a superior autologous biomaterial in implant dentistry. However, further research with long-term follow-up and larger sample sizes is necessary to confirm its clinical efficacy.

1. Hoppert M. Microscopic techniques in biotechnology. Weinheim (Germany): Wiley-VCH; 2003.
2. Drummond PD. Triggers of motion sickness in migraine sufferers. Headache. 2005;45(6):653-6.
3. Meltzer PS, Kallioniemi A, Trent JM. Chromosome alterations in human solid tumors. In: Vogelstein B, Kinzler KW, editors. The genetic basis of human cancer. New York: McGraw-Hill; 2002. p. 93-113.
4. Storey KB, editor. Functional metabolism: regulation and adaptation. Hoboken (NJ): J. Wiley & Sons; 2004.
5. Halpern SD, Ubel PA, Caplan AL. Solid-organ transplantation in HIV-infected patients. N Engl J Med. 2002;347(7):284-7.
6. Geck MJ, Yoo S, Wang JC. Assessment of cervical ligamentous injury in trauma patients using MRI. J Spinal Disord. 2001;14(5):371-7.
7. Gillespie NC, Lewis RJ, Pearn JH, Bourke ATC, Holmes MJ, Bourke JB, et al. Ciguatera in Australia: occurrence, clinical features, pathophysiology and management. Med J Aust. 1986;145:584-90.
8. Wilkinson IB, Raine T, Wiles K, Goodhart A, Hall C, O’Neill H. Oxford handbook of clinical medicine. 10th ed. Oxford: Oxford University Press; 2017.
9. Davies B, Jameson P. Advanced economics. Oxford: Oxford University Press; 2013.
10. Johnson FH, Singh J. Introduction to biochemistry. 3rd ed. New York: McGraw-Hill; 2015.
11. Smithers DW. An introduction to the study of experimental medicine. London: Oxford University Press; 1989.
12. Brown GW, Harris TO. Social origins of depression: a study of psychiatric disorder in women. London: Tavistock Publications; 1978.
13. Greenhalgh T. How to read a paper: the basics of evidence-based medicine. 5th ed. London: BMJ Publishing Group; 2014.
14. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson JL, et al., editors. Harrison's principles of internal medicine. 17th ed. New York: McGraw-Hill; 2008.
15. World Health Organization. World health statistics 2020 [Internet]. Geneva: WHO; 2020 [cited 2025 Feb 12]. Available from: https://www.who.int/data/gho/publications/world-health-statistics