Platelet-rich plasma (PRP) refers to plasma with a platelet concentration higher than that found in whole blood. It is classified into four types based on its leukocyte and fibrin content: leukocyte-rich or -poor, and fibrin-rich or -poor.1 Initially used by haematologists in the 1970s as platelet transfusions for thrombocytopenia, PRP gained traction in the 1980s in maxillofacial surgery and sports medicine due to its potential anti-inflammatory effects.2 Since then, its applications have extended to regenerative medicine and pain management because of its abundance of growth factors and cytokines.3 Despite its widespread use in degenerative and pain conditions—such as osteoarthritis, low back pain, and tendinitis—evidence for PRP efficacy in humans remains limited and controversial.4 5 Understanding of PRP practice and efficacy among anaesthetists is particularly scarce. This study aimed to characterise current PRP practice patterns at a university-affiliated private pain clinic in Hong Kong, focusing on case mix and treatment outcomes in patients with chronic musculoskeletal pain.

This study included patients aged 18 years or older who attended the Peter Hung Pain Specialist Clinic and received PRP injection therapy for chronic pain between January 2023 and December 2024. Patients were excluded if they were younger than 18 years, had been diagnosed with cancer-related pain, or did not proceed with PRP therapy after pain assessment.

Leukocyte-rich PRP was prepared by collecting autologous blood and subjecting it to two centrifugation cycles using sterile technique and an Eppendorf Centrifuge 5702 (Eppendorf SE, Hamburg, Germany). Whole blood was first centrifuged at 3800 rpm for 2 minutes to sediment red blood cells and form a buffy coat-rich plasma layer, without excessive platelet loss into the erythrocyte fraction. The plasma/buffy coat fraction was then transferred and centrifuged again at 3800 rpm for 5 minutes, applying the same centrifugal force in longer duration to this less viscous, cell-reduced plasma to achieve further platelet sedimentation and centration while minimising platelet damage or premature activation. The same force with longer duration is considered having the same effect as higher force with shorter duration by the manufacturer. Each PRP injection session targeted all painful regions deemed suitable by the same attending pain specialist under monitored anaesthesia care or general anaesthesia.

Data were extracted from the pain clinic and hospital databases, including patient age, sex, sites and types of chronic pain, duration of pain prior to PRP therapy, use of pain medications, history of surgical or interventional procedures for pain, and the indications, locations, and dosage for each PRP treatment. Standard pain assessment for patients undergoing PRP therapy included evaluation of overall and site-specific pain improvement at follow-up visits. In this study, pain improvement at the first follow-up after PRP therapy was specifically assessed and categorised as ‘no improvement’, ‘mildly improved’, ‘moderately improved’, or ‘much improved’. Additional outcomes included the proportion of patients able to discontinue oral analgesics and identification of factors associated with a favourable pain relief response to PRP therapy.

Results are presented as numbers (with percentages) and medians (with interquartile ranges [IQRs] and ranges). Categorical variables before and after PRP therapy were compared using the McNemar test. One-way analysis of variance was used to assess the association between the duration of chronic pain prior to PRP therapy and the likelihood of reporting ‘much improved’ pain at the first follow-up. Logistic regression analysis was conducted to determine whether specific pain pathologies or anatomical regions were associated with better responses to PRP therapy. All statistical tests were two-tailed and performed using SPSS (Windows version 29.0; IBM Corp, Armonk [NY], United States). A P value <0.05 was considered statistically significant.

A total of 248 patients aged 20 to 97 years who received at least one session of PRP therapy during the study period were included. Of these, 61.3% were women. The duration of pain prior to PRP therapy varied widely, ranging from 1 month to over 20 years, with a median of 15 months. More than 70.2% of patients (n=174) were taking two or more analgesics before PRP therapy. Fourteen patients (5.6%) had previously received ketamine infusions for pain; two of these had undergone interventional procedures such as radiofrequency thermocoagulation of the trigeminal ganglion, ultrasound- and X-ray–guided radiofrequency with injection to the left glossopharyngeal nerve, and X-ray–guided steroid injection at the L4/5 level of the lumbar spine. Ninety patients (36.3%) reported pain in more than one anatomical region. Baseline characteristics, including analgesic use, are summarised in Table 1.

Platelet-rich plasma therapy was administered to 404 anatomical sites across the 248 patients. The median volume of PRP injected during the first session was 17.0 mL (mean=18.3, IQR=10.0-20.5; range, 2-50). Twenty-six patients (10.5%) required more than one PRP session, with a median interval of 4.0 months (mean=4.0, IQR=2.8-5.0; range, 1-15). Seven patients (2.8%) received three sessions during the 2-year study period.

The median time to first follow-up after PRP therapy was 4.0 weeks (mean=4.5, IQR=4.0-4.5; range, 1-20). Thirty patients (12.1%) did not return for follow-up. Among the remaining 218 patients, over 60% reported their pain as either ‘moderately improved’ or ‘much improved’. The distribution of pain relief levels is shown in Table 2. Among all factors assessed, only the duration of chronic pain prior to PRP therapy was significantly associated with the likelihood of reporting ‘much improved’ pain at first follow-up. Specifically, longer pain duration was inversely associated with improvement (odds ratio=0.91 per 6-month increment in pain duration prior to PRP therapy, 95% confidence interval=0.85-0.98; P=0.008) [Table 3]. Patients with chronic pain lasting less than 2 years appeared to respond best to PRP therapy (Fig). The volume of PRP injected was not significantly associated with reporting ‘much improved’ pain.

The median time to second follow-up was 9.0 weeks (mean=9.7, IQR=8.0-11.0; range, 2-32). Over the 12-month period after PRP therapy, a substantial number of patients were able to discontinue oral analgesics (Table 4).

In this descriptive study, over 60% of patients reported moderate to significant improvement in pain symptoms after their first PRP treatment session. Among the 26 patients who received a second session, only one reported no improvement, suggesting a favourable response to repeated treatment. This improvement was accompanied by a substantial reduction in the use of oral analgesics. Given the known adverse effects associated with polypharmacy—particularly involving antidepressants, gabapentinoids, and opioids—this reduction may contribute to improved quality of life of patients.

Our cohort included patients with a wide range of chronic pain conditions affecting various anatomical sites. Intriguingly, there was no apparent correlation between the number of pain sites and the degree of pain relief, suggesting that PRP may have broad applicability across multiple pain syndromes. However, due to the heterogeneity of pain presentations and the presence of multiple pain regions in many patients, we were unable to determine whether PRP was more effective for specific types or anatomical regions of pain. This highlights the need for future randomised controlled trials involving more homogeneous patient populations to confirm the long-term impact of PRP on quality of life according to pain pathology.

Although PRP therapy is considered a form of regenerative therapy,3 its mechanisms of action are not yet fully understood.5 Platelets contain granules that release a variety of bioactive substances, including growth factors, antimicrobial proteins, metalloproteases, coagulation factors, and membrane glycoproteins that influence the synthesis of interleukins and chemokines. Other bioactive molecules, including neurotransmitters such as serotonin, dopamine, adenosine diphosphate, adenosine triphosphate, and histamine, may also play roles in tissue modulation and regeneration.4 Some research suggests that leukocyte-rich PRP has stronger anti-inflammatory effects and higher concentrations of growth factors, which may be important for conditions such as knee osteoarthritis.6 7 However, evidence as to whether leukocyte-rich PRP is superior to leukocyte-poor PRP remains inconclusive. One of the largest randomised controlled trials assessing PRP for knee osteoarthritis concluded that leukocyte-poor PRP was not significantly more effective than placebo in improving symptoms or joint structure among patients with mild to moderate knee osteoarthritis over 12 months.8 Conversely, a recent systematic review and meta-analysis found that leukocyte-poor PRP provided moderate pain relief compared with other active treatments; no significant difference was observed between leukocyte-rich PRP and other therapies.5 In the present study, all patients received leukocyte-rich PRP; therefore, we were unable to compare the efficacy of different PRP formulations.

The data showed that 13 patients with a history of cancer (either active with metastasis, in remission, or with unclear status) received PRP for pain clinically unrelated to their cancers (Table 1). Currently, there is no strong evidence regarding the safety of PRP use in patients with cancer. A recent formal consensus from the International Research Group on Platelet Injections recommended that PRP may be performed in patients with cancers in remission or with metastasis—after discussion with an oncologist—although the supporting evidence is contradictory or inconclusive and largely based on expert opinion, with very limited or absent literature.9

This study has several limitations. First, without a control group, placebo effects cannot be excluded. Second, PRP dosing was not standardised; the volume administered varied according to the number and size of pain sites, and detailed documentation of per-site dosing was unavailable. Additionally, over 10% of patients did not return for follow-up, and reasons for loss to follow-up were not documented, introducing potential selection bias. The heterogeneity of pain conditions further complicated data interpretation. Although current evidence suggests that leukocyte-rich PRP may cause greater initial flare-up than leukocyte-poor PRP for intra-articular injections,10 any initial worsening of symptoms was not captured in our study because of variability in the timing of first follow-up. Finally, pain improvement was assessed using non-standardised, subjective descriptors (‘much improved’, ‘moderately improved’, or ‘mildly improved’). These terms reflect patient satisfaction but do not permit precise quantification of pain reduction. Future studies should incorporate validated quantitative assessment tools, such as the Brief Pain Inventory, to enhance the reliability of outcome measurement.

Leukocyte-rich PRP appeared effective in improving chronic musculoskeletal pain. The majority of patients reported meaningful symptom relief, and many were able to reduce or discontinue oral analgesics—an outcome that may substantially improve quality of life, particularly given the adverse effects associated with polypharmacy involving antidepressants, gabapentinoids, and opioids. Well-designed randomised controlled trials focusing on chronic musculoskeletal pain of less than 2 years’ duration—and incorporating standardised protocols for leukocyte-rich PRP preparation, injection volume, and patient selection criteria—are needed to confirm its long-term impact on quality of life of patients.

Concept or design: MHM Chu, WS Chan, KM Ho.
Acquisition of data: WS Chan, HL Wong.
Analysis or interpretation of data: MHM Chu, KM Ho.
Drafting of the manuscript: MHM Chu, KM Ho.
Critical revision of the manuscript for important intellectual content: WS Chan, ACY Li, HMK Wong.

All authors had full access to the data, contributed to the study, approved the final version for publication, and take responsibility for its accuracy and integrity.

All authors have disclosed no conflicts of interest.

We are grateful to the staff in Peter Hung Pain Specialist Clinic and Operating Theatre of CUHK Medical Centre for their assistance in patient care and study logistics.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

This research was approved by the Clinical Research Ethics Committee of CUHK Medical Centre, Hong Kong (Ref No.: CREC-202409). A waiver of patient consent was approved by the Committee due to the retrospective and observational nature of the study. Only de-identified data were used for analysis.

1. Arnoczky SP, Delos D, Rodeo SA. What is platelet-rich plasma? Oper Tech Sports Med 2011;19:142-8. Crossref

2. Cao Y, Zhu X, Zhou R, He Y, Wu Z, Chen Y. A narrative review of the research progress and clinical application of platelet-rich plasma. Ann Palliat Med 2021;10:4823-9. Crossref

3. Arita A, Tobita M. Current status of platelet-rich plasma therapy under the act on the safety of regenerative medicine in Japan. Regen Ther 2023;23:37-43. Crossref

4. Cole BJ, Seroyer ST, Filardo G, Bajaj S, Fortier LA. Platelet-rich plasma: where are we now and where are we going? Sports Health 2010;2:203-10. Crossref

5. Wang F, Meng F, Chan TC, Wong SS. Platelet-rich plasma for treating chronic noncancer pain: a systematic review and meta-analysis of randomized controlled trials. Pain Ther 2025;14:1169-88. Crossref

6. Jayaram P, Mitchell PJ, Shybut TB, Moseley BJ, Lee B. Leukocyte-rich platelet-rich plasma is predominantly anti-inflammatory compared with leukocyte-poor platelet-rich plasma in patients with mild-moderate knee osteoarthritis: a prospective, descriptive laboratory study. Am J Sports Med 2023;51:2133-40. Crossref

7. Lin KY, Chen P, Chen AC, Chan YS, Lei KF, Chiu CH. Leukocyte-rich platelet-rich plasma has better stimulating effects on tenocyte proliferation compared with leukocyte-poor platelet-rich plasma. Orthop J Sports Med 2022;10:23259671221084706. Crossref

8. Bennell KL, Paterson KL, Metcalf BR, et al. Effect of intra-articular platelet-rich plasma vs placebo injection on pain and medial tibial cartilage volume in patients with knee osteoarthritis: the RESTORE randomized clinical trial. JAMA 2021;326:2021-30. Crossref

9. Eymard F, Louati K, Noël É, et al. Indications and contraindications to platelet-rich plasma injections in musculoskeletal diseases in case of infectious, oncological and haematological comorbidities: a 2025 formal consensus from the GRIIP (International Research Group on Platelet Injections). Knee Surg Sports Traumatol Arthrosc 2025;33:2293-306. Crossref

10. Lu J, Li H, Zhang Z, Xu R, Wang J, Jin H. Platelet-rich plasma in the pathologic processes of tendinopathy: a review of basic science studies. Front Bioeng Biotechnol 2023;11:1187974. Crossref