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Peptide Therapy in Musculoskeletal Medicine

Injectable and regenerative peptide therapies in orthopaedics and sports medicine — what the evidence shows for tendon, cartilage and bone healing, and where the hype outpaces the data.

55 citationsUpdated Oct 2026
Illustration: Peptide Therapy in Musculoskeletal Medicine

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Overview

Peptide therapeutics in orthopaedics have evolved from naturally occurring agents like bone morphogenetic proteins to rationally engineered synthetics [3]. While growth factors play a critical role in the biologic processes that drive tendon healing [6], injectable peptides for sports medicine remain largely experimental [10]. It is critical that orthopaedic and sports medicine providers understand the current lack of evidence to support the clinical use of injectable peptides [1]. Because of the lack of robust efficacy and safety data, peptide supplements should not currently be recommended as a replacement or adjunct for existing orthopaedic standard of care [4].

Specific growth factors show promise in preclinical and early clinical contexts. Platelet-derived growth factor has promise for healing ligaments but must be administered in appropriate doses soon after injury [8], and recombinant human platelet-derived growth factor-BB (rhPDGF-BB) treatment is an effective therapy that may be an option for clinical applications to treat tendinopathy [9]. Insulin-like growth factor-I (IGF-I) supports the potential use of intralesional IGF-I for treatment of debilitating tendon injuries [11], although tissue levels of IGF-I protein decreased approximately 40% compared to normal tendon in the first 2 weeks after lesion induction [29]. Regarding bone morphogenetic proteins, only BMP-2 and BMP-7 can be recommended based on level I studies [12]. The use of BMP currently has two FDA-approved indications: treatment of open tibial fractures treated with intramedullary fixation and treatment of tibia long bone non-union [54]. Conversely, vascular endothelial growth factor (VEGF) is not recommended for enhancement of bone formation during distraction osteogenesis [22].

Other peptides influence musculoskeletal pathophysiology and repair mechanisms. Osteogenic growth peptide treatment resulted in a stronger expression of transforming growth factor-β, both locally and systemically, in rat fracture healing specimens [14]. Transforming growth factor-β1 regulated the expression of the type-II collagen gene in periosteum-derived cells as early as 12 hours after administration [21], whereas bone morphogenetic proteins 3 or 4 did not regulate the expression of the type-II collagen gene in periosteum-derived cells in the same manner as transforming growth factor-β1 [21]. Parathyroid hormone-related peptide may be involved in the pathophysiology of osteoarthritis [5], and a myofibroblast–mast cell–neuropeptide axis of fibrosis exists in the joint capsules in post-traumatic contractures [13]. Local delivery of specific neuropeptides could reverse the functional deficits of neuropathic ligaments in only 2 weeks in a rat model [17]. Chondrocyte-binding peptides identified by phage display may be coupled to therapeutic molecules to provide targeted treatment for cartilage disorders [2]. Loss of function in musculoskeletal tissues initiates from either a failure of the cells that produce and maintain the extracellular matrix (ECM) or as a consequence of material failure of the ECM itself [42]. Advances in the identification of candidate therapeutic cell populations and the development of new biomaterials have occurred over the last three decades to address degenerative processes in musculoskeletal tissues [42]. Therapeutic cell populations and biomaterials can be applied alone or in combination to promote healing that alters the trajectory of disease or potentially replace an entire tissue when damage has progressed to later stages [42]. It is no longer acceptable to treat various athletic conditions with medications without accounting for the effects on performance, the medical-legal implications, and the identification of exercise-induced conditions [33].

How It Works

Current Clinical Status and Safety

Orthopaedic and sports medicine providers must recognize the current lack of evidence supporting the clinical use of injectable peptide therapies [1]. Due to a lack of robust efficacy and safety data, peptide supplements should not currently be recommended as a replacement or adjunct for existing orthopaedic standard of care [4]. Reviews of therapeutic peptides in orthopaedics emphasize safety, efficacy, and future directions for responsible integration into musculoskeletal care [7].

Mechanisms in Tendon and Ligament Healing

Intralesional insulin-like growth factor-I (IGF-I) supports the potential use for treatment of debilitating tendon injuries [11]. Local delivery of specific neuropeptides could reverse the functional deficits of neuropathic ligaments in only 2 weeks [17]. Tissue responses to growth factors in tendons and ligaments may vary at different anatomic sites [18]. The pentapeptide KTTKS promotes the expressions of type I collagen and transforming growth factor-β of tendon cells [23]. This pentapeptide has potential clinical use to improve the process of tendon healing [23]. Interventions developed to improve healing of flexor tendons and tendon sheaths must address differences in the regulation of matrix molecules and growth factors between these tissues [39]. The IGFBP response of flexor tendons to injury and healing provides information necessary for the design of protocols that may enhance tendon healing through manipulation of IGF-I ligand and binding protein levels [41].

Mechanisms in Cartilage and Osteoarthritis

Effective mechanisms of growth factor delivery for articular cartilage repair may differ for different growth factors [15]. Additional in vivo studies are needed to evaluate the potential of growth factors as stimulators in cartilage repair [16]. Transduction with interleukin-1 receptor antagonist (IL-1Ra) decreased the synovial expression of IL-1α, IL-1β, and matrix metalloproteinases, indicating a mechanism for prevention of matrix degradation [24]. Insulin-like growth factor-I (IGF-I) can be successfully introduced to synovial structures by adenoviral vectors and results in effective IGF-I ligand synthesis without untoward synovial morphologic effects [35]. Cartilage fragments from osteoarthritic knees promote chondrogenic differentiation of mesenchymal stem cells without exogenous growth factor induction [36]. The actions of insulin-like growth factor binding proteins (IGFBPs) 2 and 3 in articular cartilage extend beyond the classic modulation of IGF receptor action [37]. Transforming growth factor-β (TGF-β) exerts at least some of its actions in articular cartilage via cross-talk mechanisms involving the IGF-BP-2 system [38].

Mechanisms in Bone Healing and Fracture Repair

Osteogenic growth peptide has local and systemic effects on fracture healing in rats [14]. Specimens treated with osteogenic growth peptide had a stronger expression of transforming growth factor-β, both locally and systemically [14]. Topical application of nerve growth factor increases the effectiveness and rate of repair of bone, suggesting it may play an important role in the healing processes of fractured bone [19]. Local growth factor application enhances healing in the early phase without alteration of the normal healing process [34]. Mesenchymal stem cell expression of stromal cell-derived factor-1β (SDF-1b) provides potent synergistic effects supporting BMSC-mediated bone formation and appears a suitable candidate for optimization of bone augmentation in translational protocols [40].

General Principles and Fibrosis

Regenerative medicine holds great promise for orthopaedic surgery by developing novel therapies that replace, repair, or promote tissue regeneration [20]. A myofibroblast–mast cell–neuropeptide axis of fibrosis in the joint capsules is identified as a mechanistic component of post-traumatic contractures and potential prophylactic or therapeutic interventions [13]. Epigenetic regulators are critical for normal skeletogenesis and are viable candidate drug targets for short-term local pharmacological strategies to mitigate musculoskeletal tissue degeneration [25]. Only BMP-2 and BMP-7 can be recommended based on level I studies for carrier systems and application of growth factors in orthopaedics [12]. The expression of the type-II collagen gene in periosteum-derived cells is regulated by transforming growth factor-β1, an effect observed as early as 12 hours after administration, but not observed in response to bone morphogenetic proteins 3 or 4 [21].

What the Evidence Shows

Current Clinical Status and Recommendations

Orthopaedic and sports medicine providers must understand the current lack of evidence to support the clinical use of injectable peptides, despite their potential therapeutic and regenerative capabilities [1]. The authors do not recommend the use of BPC-157 for sports performance and recovery because there are no randomized controlled trials investigating its use in human subjects, and the science is lacking to determine overall effectiveness, safety profile, and clinical indications [47].

Bone Healing and Osteogenesis

Local application of recombinant human fibroblast growth factor-2 (rhFGF-2) dose dependently increased the percentage of patients with radiographic bone union and decreased the average time needed for such union in a prospective trial on patients with osteotomy [31]. Topical application of nerve growth factor increases the effectiveness and rate of repair of bone in rats, suggesting it may play an important role in the healing processes of fractured bone [19]. Specimens treated with osteogenic growth peptide had a stronger expression of transforming growth factor-β, both locally and systemically, in a rat fracture model [14]. Vascular endothelial growth factor (VEGF) is not recommended for enhancement of bone formation during distraction osteogenesis in rabbits [22]. The osteoinductive ability of 3 mg P24 was similar to that of 1 mg rhBMP-2 in the repair of rat cranial bone defects [50]. Improved healing imparted by the addition of a BMP binding peptide (BBP) may result in lesser amounts of rhBMP-7 needed to achieve union in a rodent femoral defect model [46]. Treatment with scaffold alone improved defect stability at 16 weeks compared to nontreatment but did not achieve bone union or restoration of mechanical function in critically sized bone defects [45]. 100 ng of peptide per 0.2 mL of injectable demineralized bone matrix (DBM) gel generated the most optimal results for enhancing DBM mineralization [48].

Tendon and Ligament Healing

Platelet-derived growth factor (PDGF) has promise for healing ligaments but must be administered in appropriate doses soon after injury, as indicated by rat medial collateral ligament studies [8]. Data suggest that recombinant human platelet-derived growth factor-BB (rhPDGF-BB) treatment is an effective therapy and may be an option for clinical applications to treat tendinopathy [9]. Injections of rhPDGF-BB increased maximum load-to-failure (3 and 10 mg) and stiffness (10 mg) relative to controls and commonly used treatments in a rat Achilles tendon collagenase model [27]. Insulin-like growth factor-I (IGF-I) improves cellular and molecular aspects of healing in a collagenase-induced model of flexor tendinitis, supporting its potential use for debilitating tendon injuries [11]. Tissue responses to growth factors in tendons and ligaments may vary at different anatomic sites, as patellar tendon and anterior cruciate ligament have different mitogenic responses to PDGF and transforming growth factor β [18]. The pentapeptide KTTKS promotes the expressions of type I collagen and transforming growth factor-β of tendon cells, implicating its potential clinical use to improve tendon healing [23].

Cartilage and Osteoarthritis

Additional in vivo studies are needed to evaluate the potential of growth factors as stimulators in cartilage repair, based on bovine chondrocyte responsiveness in medium with different serum concentrations [16]. Transduction with interleukin-1 receptor antagonist (IL-1Ra) decreased the synovial expression of IL-1α, IL-1β, and matrix metalloproteinases, indicating a mechanism for prevention of matrix degradation in an osteoarthritic culture model [24]. Recombinant fibroblast growth factor-18 (sprifermin) enhances microfracture-induced cartilage healing, with the highest treatment benefit detected following 100 μg sprifermin treatment [26]. Therapeutic strategies for microfracture augmentation, such as trypsin pretreatment and growth factor-functionalized self-assembling peptide hydrogel scaffold, can be cost-effective ways to improve cartilage healing outcomes in an equine model [32]. Suppression of nerve growth factor (NGF) may result in varied effects depending on different stages of the osteoarthritic disease process, as NGF receptors in equine synovial membranes vary with disease severity [55]. Patients in control and advanced osteoarthritis groups demonstrated little elevation in myeloperoxidase (MPO) levels, and chlorinated peptides were undetectable [43].

Nerve Healing

The use of nerve growth factor and ciliary neurotrophic factor in combination may enhance regeneration in the peripheral nervous system, as supported by axonal regeneration data in an end-to-side model [56].

Glucagon-Like Peptide-1 (GLP-1) Agonists

While efficacious, GLP-1 agonists may not produce sufficient weight loss to achieve body mass index cutoffs for total joint arthroplasty depending on individual patient factors, including starting bodyweight [28]. After adjusting for metabolic confounds, the postulated skeletal benefit of GLP-1 receptor agonists did not translate to meaningful risk reductions in upper extremity fragility fracture in a population with type 2 diabetes [44].

Biomarkers and Other Findings

Patients with osteolysis had significantly elevated levels of collagen crosslinked N-telopeptide compared with the implant control group [49]. Transforming growth factor-β1 regulates the expression of the type-II collagen gene in periosteum-derived cells, an effect observed as early as 12 hours after administration but not observed in response to bone morphogenetic proteins 3 or 4 [21]. Most social media posts extrapolate from preclinical or anecdotal data, marketing peptides as panaceas for health, performance, and aesthetics, as evidenced by poor DISCERN scores [30].

Practical Considerations

General Clinical Status and Safety

Orthopaedic and sports medicine providers must understand the current lack of evidence to support the clinical use of peptide therapies [1]. Due to the lack of robust efficacy and safety data, peptide supplements should not currently be recommended as a replacement or adjunct for existing orthopaedic standard of care [4]. The integration of therapeutic peptides into musculoskeletal care requires an emphasis on safety, efficacy, and future directions [7]. Regenerative medicine in orthopaedic surgery holds promise for developing novel therapies that replace, repair, or promote tissue regeneration [20]. Treating athletic conditions with medications requires accounting for effects on performance, medical-legal implications, and the identification of exercise-induced conditions [33].

Tendon and Ligament Applications

Injections of rhPDGF-BB increased maximum load-to-failure at 3 and 10 mg doses and stiffness at the 10 mg dose relative to controls and commonly used treatments [27]. Insulin-like growth factor-I (IGF-I) supports the potential use of intralesional IGF-I for the treatment of debilitating tendon injuries [11]. Mesenchymal stem cells (MSCs) and insulin-like growth factor-I gene-enhanced mesenchymal stem cells (AdIGF-MSCs) provide a benefit for the treatment of tendinitis [51].

Cartilage and Osteoarthritis Applications

Chondrocyte-binding peptides may be coupled to therapeutic molecules to provide targeted treatment for cartilage disorders [2]. Recombinant fibroblast growth factor-18 (sprifermin) showed the highest treatment benefit following 100 μg treatment in enhancing microfracture-induced cartilage healing [26]. Therapeutic strategies for microfracture augmentation, such as those using growth factor-functionalized self-assembling peptide hydrogel scaffolds, can be cost-effective ways to improve cartilage healing outcomes [32]. Growth factor treatment of chondrocyte cell cultures for cell therapy purposes can be regarded as safe in terms of telomere biology [52].

Bone Healing and Fracture Management

Nerve growth factor administration suggests it may play an important role in the healing processes of fractured bone [19]. Recombinant human fibroblast growth factor-2 (rhFGF-2) dose dependently increased the percentage of patients with radiographic bone union and decreased the average time needed for such union [31].

Other Mechanistic and Systemic Considerations

A myofibroblast–mast cell–neuropeptide axis of fibrosis in joint capsules in post-traumatic contractures identifies potential prophylactic or therapeutic interventions [13]. Glucagon-like Peptide-1 (GLP-1) agonists may not produce sufficient weight loss to achieve body mass index cutoffs for total joint arthroplasty depending on individual patient factors, including starting bodyweight [28]. Social media posts regarding peptides in musculoskeletal health often extrapolate from preclinical or anecdotal data, marketing peptides as panaceas for health, performance, and aesthetics [30].

Key Evidence

  • [L5] While peptide therapy may possess significant therapeutic and regenerative potential, it is critical that orthopaedic and sports medicine providers understand the current lack of evidence to support the clinical use of these peptides. [1] (10.1177/03635465251357593)
  • [Paper] We anticipate that such peptides may be coupled to therapeutic molecules to provide targeted treatment for cartilage disorders. [2] (10.1002/jor.22325)
  • [Paper] Peptide therapeutics in orthopaedics have evolved from naturally occurring agents like bone morphogenetic proteins to rationally engineered synthetics. [3] (10.2106/jbjs.26.00785)
  • [L5] Because of the lack of robust efficacy and safety data, peptide supplements should not currently be recommended as a replacement or adjunct for existing orthopaedic standard of care. [4] (10.1177/03635465261464420)
  • [L4] Our results suggest that parathyroid hormone-related peptide may be involved in the pathophysiology of osteoarthritis. [5] (10.1002/jor.1100150204)
  • [Paper] It has become clear that growth factors play a critical role in the biologic processes that drive tendons to heal. [6] (10.1197/j.jht.2005.01.012)
  • [L4] This review integrates current mechanistic insights with orthopaedic relevance, emphasizing safety, efficacy, and future directions for responsible integration into musculoskeletal care. [7] (10.5435/jaaosglobal-d-25-00236)
  • [Paper] These results indicate that platelet-derived growth factor has promise for healing ligaments but that it must be administered in appropriate doses soon after injury. [8] (10.1002/jor.1100140509)
  • [Paper] Data suggest that rhPDGF-BB treatment is an effective therapy and may be an option for clinical applications to treat tendinopathy. [9] (10.1002/jor.22222)
  • [L5] Injectable peptides for sports medicine remain largely experimental. [10] (10.2106/jbjs.rvw.26.00027)
  • [Paper] These data support the potential use of intralesional IGF-I for treatment of debilitating tendon injuries. [11] (10.1016/s0736-0266(02)00009-8)
  • [Paper] Today only BMP-2 and BMP-7 can be recommended based on level I studies. [12] (10.1016/s0020-1383(08)70014-7)
  • [L5] These observations identify putative mechanistic components of a myofibroblast–mast cell–neuropeptide axis of fibrosis in the joint capsules in post-traumatic contractures and potential prophylactic or therapeutic interventions. [13] (10.1002/jor.22676)
  • [Paper] The specimens treated with osteogenic growth peptide had a stronger expression of transforming growth factor-β, both locally and systemically. [14] (10.1002/jor.1100180119)
  • [L3] These data indicate that effective mechanisms of growth factor delivery for articular cartilage repair may differ for different growth factors. [15] (10.1002/jor.22444)
  • [Paper] Additional in vivo studies are needed to evaluate the potential of these growth factors as stimulators in cartilage repair. [16] (10.1002/jor.1100180111)
  • [Paper] Local delivery of specific neuropeptides could reverse the functional deficits of these neuropathic ligaments in only 2 weeks. [17] (10.1002/jor.20335)
  • [Paper] Although growth factors have the potential to modulate soft-tissue repair, tissue responses in tendons and ligaments may vary at different anatomic sites. [18] (10.1002/jor.1100140407)
  • [Paper] The resultant increases in effectiveness and rate of repair of bone with administration of nerve growth factor suggest that it may play an important role in the healing processes of fractured bone. [19] (10.1002/jor.1100150212)
  • [L5] Regenerative medicine holds great promise for orthopaedic surgery by developing novel therapies that replace, repair, or promote tissue regeneration. [20] (10.1002/jor.20432)
  • [Paper] This effect was observed as early as 12 hours after administration of transforming growth factor-β1 but was not observed in response to bone morphogenetic proteins 3 or 4. [21] (10.1002/jor.1100150321)
  • [Paper] VEGF is not recommended for enhancement of bone formation in this setting. [22] (10.1016/s0736-0266(02)00159-6)
  • [Paper] These findings strongly implicated the potential clinical use of pentapeptide KTTKS to improve the process of tendon healing in the future. [23] (10.1002/jor.20455)
  • [Paper] Transduction with IL-1Ra decreased the synovial expression of IL-1α and IL-1β and matrix metalloproteinases, indicating a mechanism for prevention of matrix degradation. [24] (10.1016/j.orthres.2004.06.020)
  • [Paper] The combined body of molecular and genetic studies focusing on epigenetic regulators indicates that these proteins are critical for normal skeletogenesis and viable candidate drug targets for short-term local pharmacological strategies to mitigate musculoskeletal tissue degeneration. [25] (10.1002/jor.24305)
  • [Paper] We detected the highest treatment benefit following 100 μg sprifermin treatment. [26] (10.1002/jor.25063)
  • [L3] Injections of rhPDGF-BB increased maximum load-to-failure (3 and 10 m g) and stiffness (10 m g) relative to controls and commonly used treatments. [27] (10.1002/jor.22483)
  • [Paper] While efficacious, GLP-1 agonists may not produce sufficient weight loss to achieve body mass index cutoffs for total joint arthroplasty depending on individual patient factors, including starting bodyweight. [28] (10.2106/jbjs.rvw.23.00167)
  • [Paper] In the first 2 weeks after lesion induction, tissue levels of IGF-I protein actually decreased approximately 40% compared to normal tendon. [29] (10.1016/j.orthres.2004.05.007)
  • [Paper] Most posts extrapolate from preclinical or anecdotal data, marketing peptides as panaceas for health, performance, and aesthetics, as evidenced by the poor DISCERN scores. [30] (10.1177/2325967126s00290)
  • [L2] The rhFGF-2 dose dependently increased the percentage of patients with radiographic bone union, and decreased the average time needed for such union. [31] (10.1002/jor.20315)
  • [L5] Therapeutic strategies for microfracture augmentation, such as those presented in this study, can be cost-effective ways to improve cartilage healing outcomes. [32] (10.1177/03635465211021798)
  • [Paper] It is no longer acceptable to treat various athletic conditions with medications without accounting for the effects on performance, the medical-legal implications, and the identification of exercise-induced conditions. [33] (10.1016/s0278-5919(05)70076-4)
  • [Paper] In conclusion, local growth factor application enhances the healing in the early phase without alteration of the normal healing process. [34] (10.1016/j.orthres.2003.09.009)
  • [Paper] These data indicate that IGF-I can be successfully introduced to synovial structures by adenoviral vectors and results in effective IGF-I ligand synthesis without untoward synovial morphologic effects. [35] (10.1016/s0736-0266(00)00077-2)
  • [L5] The findings support the hypothesis that cartilage fragments from osteoarthritic knee promote chondrogenic differentiation without exogenous growth factor induction. [36] (10.1002/jor.21541)
  • [Paper] This suggests the hypothesis that the actions of these IGFBPs in articular cartilage extend beyond the classic modulation of IGF receptor action. [37] (10.1002/jor.20660)
  • [Paper] These data help to support the postulate that TGF-β exerts at least some of its actions in articular cartilage via cross-talk mechanisms involving the IGF-BP-2 system. [38] (10.1016/s0736-0266(02)00154-7)
  • [Paper] These findings indicate that interventions developed to improve healing of these tissues will have to address these differences, because they will likely affect the outcomes. [39] (10.1016/j.jhsa.2006.06.011)
  • [Paper] SDF-1b provides potent synergistic effects supporting BMSC-mediated bone formation and appears a suitable candidate for optimization of bone augmentation in translational protocols. [40] (10.1002/jor.22749)
  • [Paper] The results of this study document the IGFBP response of flexor tendons to injury and healing, which provides information necessary for the design of protocols that may enhance tendon healing through manipulation of IGF-I ligand and binding protein levels. [41] (10.1002/jor.20000)
  • [L4] Patients in the control and advanced OA groups demonstrated little elevation in MPO levels and Cl-peptides were undetectable. [43] (10.1002/jor.20400)
  • [L3] After adjusting for metabolic confounds, we found that the postulated skeletal benefit of GLP 1RAs did not translate to meaningful risk reductions in this population. [44] (10.1016/j.injury.2026.113456)
  • [Paper] Treatment with scaffold alone improved defect stability at 16 weeks compared to nontreatment, but did not achieve bone union or restoration of mechanical function. [45] (10.1002/jor.20372)
  • [Paper] Improved healing imparted by the addition of BBP may result in lesser amounts of rhBMP-7 needed to achieve union in the clinical setting. [46] (10.1002/jor.21252)
  • [L5] The authors do not recommend the use of BPC-157 for sports performance and recovery because there are no randomized controlled trials investigating its use in human subjects, and the science is clearly lacking to determine the overall effectiveness, safety profile, and clinical indications for sports enhancement in athletes. [47] (10.1016/j.arthro.2024.09.005)
  • [Paper] In these studies, 100 ng of peptide per 0.2 mL of injectable DBM gel generated the most optimal results. [48] (10.1002/jor.20215)
  • [L4] The patients with osteolysis had significantly elevated levels of N-telopeptide compared with the implant control group. [49] (10.1002/jor.1100180110)
  • [Paper] The osteoinductive ability of 3 mg P24 was similar to that of 1 mg rhBMP-2. [50] (10.1002/jor.21439)
  • [Paper] These findings indicate a benefit to the use of MSCs and AdIGF-MSCs for the treatment of tendinitis. [51] (10.1002/jor.20887)
  • [Paper] Growth factor treatment of chondrocyte cell cultures for cell therapy purposes can be regarded as safe in terms of telomere biology. [52] (10.1002/jor.21007)
  • [Paper] The use of BMP currently has two FDA-approved indications: treatment of open tibial fractures treated with intramedullary fixation and treatment of tibia long bone non-union. [54] (10.1016/s0020-1383(13)70008-1)
  • [Paper] Suppression of NGF may result in varied effects depending on different stages of the osteoarthritic disease process. [55] (10.1002/jor.25382)
  • [Paper] These data support the conclusion that the use of nerve growth factor and ciliary neurotrophic factor in combination may enhance regeneration in the peripheral nervous system. [56] (10.1053/jhsu.2001.24148)

See Also

  • Osteoarthritis

References

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[2] Identification of chondrocyte‐binding peptides by phage display. Journal of Orthopaedic Research. 2013. DOI: 10.1002/jor.22325

[3] Peptide Therapeutics in Orthopaedics. Journal of Bone and Joint Surgery. 2026. DOI: 10.2106/jbjs.26.00785

[4] Peptide Supplements and Their Therapeutic Applications in Sports Medicine. The American Journal of Sports Medicine. 2026. DOI: 10.1177/03635465261464420

[5] Expression of parathyroid hormone‐related peptide in human osteoarthritis. Journal of Orthopaedic Research. 1997. DOI: 10.1002/jor.1100150204

[6] The Use of Growth Factors on Tendon Injuries. Journal of Hand Therapy. 2005. DOI: 10.1197/j.jht.2005.01.012

[7] Therapeutic Peptides in Orthopaedics: Applications, Challenges, and Future Directions. JAAOS: Global Research and Reviews. 2026. DOI: 10.5435/jaaosglobal-d-25-00236

[8] Influence of dosage and timing of application of platelet‐derived growth factor on early healing of the rat medial collateral ligament. Journal of Orthopaedic Research. 1996. DOI: 10.1002/jor.1100140509

[9] Dose–response effect of an intra‐tendon application of recombinant human platelet‐derived growth factor‐BB (rhPDGF‐BB) in a rat Achilles tendinopathy model. Journal of Orthopaedic Research. 2012. DOI: 10.1002/jor.22222

[10] Injectable Peptides in Sports Medicine: A Structured Narrative Review of Evidence, Safety, and Antidoping Implications. JBJS Reviews. 2026. DOI: 10.2106/jbjs.rvw.26.00027

[11] Insulin‐like growth factor‐I improves cellular and molecular aspects of healing in a collagenase‐induced model of flexor tendinitis. Journal of Orthopaedic Research. 2002. DOI: 10.1016/s0736-0266(02)00009-8

[12] Carrier systems and application of growth factors in orthopaedics. Injury. 2008. DOI: 10.1016/s0020-1383(08)70014-7

[13] A myofibroblast-mast cell-neuropeptide axis of fibrosis in post-traumatic joint contractures: An in vitro analysis of mechanistic components. Journal of Orthopaedic Research. 2014. DOI: 10.1002/jor.22676

[14] Osteogenic growth peptide normally stimulated by blood loss and marrow ablation has local and systemic effects on fracture healing in rats. Journal of Orthopaedic Research. 2000. DOI: 10.1002/jor.1100180119

[15] Endogenous versus exogenous growth factor regulation of articular chondrocytes. Journal of Orthopaedic Research. 2013. DOI: 10.1002/jor.22444

[16] Responsiveness of bovine chondrocytes to growth factors in medium with different serum concentrations. Journal of Orthopaedic Research. 2000. DOI: 10.1002/jor.1100180111

[17] Adjuvant neuropeptides can improve neuropathic ligament healing in a rat model. Journal of Orthopaedic Research. 2007. DOI: 10.1002/jor.20335

[18] Patellar tendon and anterior cruciate ligament have different mitogenic responses to platelet‐derived growth factor and transforming growth factor β. Journal of Orthopaedic Research. 1996. DOI: 10.1002/jor.1100140407

[19] Topical application of nerve growth factor improves fracture healing in rats. Journal of Orthopaedic Research. 1997. DOI: 10.1002/jor.1100150212

[20] Regenerative medicine in orthopaedic surgery. Journal of Orthopaedic Research. 2007. DOI: 10.1002/jor.20432

[21] Regulation of the expression of the type‐II collagen gene in periosteum‐derived cells by three members of the transforming growth factor–β superfamily. Journal of Orthopaedic Research. 1997. DOI: 10.1002/jor.1100150321

[22] Effects of locally applied vascular endothelial growth factor (VEGF) and VEGF‐inhibitor to the rabbit tibia during distraction osteogenesis. Journal of Orthopaedic Research. 2003. DOI: 10.1016/s0736-0266(02)00159-6

[23] The pentapeptide KTTKS promoting the expressions of type I collagen and transforming growth factor‐β of tendon cells. Journal of Orthopaedic Research. 2007. DOI: 10.1002/jor.20455

[24] Dual transduction of insulin‐like growth factor‐I and interleukin‐l receptor antagonist protein controls cartilage degradation in an osteoarthritic culture model. Journal of Orthopaedic Research. 2005. DOI: 10.1016/j.orthres.2004.06.020

[25] Epigenetics as a New Frontier in Orthopedic Regenerative Medicine and Oncology. Journal of Orthopaedic Research. 2019. DOI: 10.1002/jor.24305

[26] Recombinant fibroblast growth factor‐18 (sprifermin) enhances microfracture‐induced cartilage healing. Journal of Orthopaedic Research. 2021. DOI: 10.1002/jor.25063

[27] Comparison of the effect of intra‐tendon applications of recombinant human platelet‐derived growth factor‐BB, platelet‐rich plasma, steroids in a rat achilles tendon collagenase model. Journal of Orthopaedic Research. 2013. DOI: 10.1002/jor.22483

[28] Glucagon-like Peptide-1 Agonists. JBJS Reviews. 2024. DOI: 10.2106/jbjs.rvw.23.00167

[29] Temporal expression of growth factors and matrix molecules in healing tendon lesions. Journal of Orthopaedic Research. 2005. DOI: 10.1016/j.orthres.2004.05.007

[30] Paper 32. Performance & Promises: A Social Media Review of Alleged Indications, Risks and Usage of “Peptides” in Musculoskeletal Health. Orthopaedic Journal of Sports Medicine. 2026. DOI: 10.1177/2325967126s00290

[31] Local application of recombinant human fibroblast growth factor‐2 on bone repair: A dose–escalation prospective trial on patients with osteotomy. Journal of Orthopaedic Research. 2007. DOI: 10.1002/jor.20315

[32] Microfracture Augmentation With Trypsin Pretreatment and Growth Factor–Functionalized Self-assembling Peptide Hydrogel Scaffold in an Equine Model. The American Journal of Sports Medicine. 2021. DOI: 10.1177/03635465211021798

[33] PREFACE. Clinics in Sports Medicine. 1998. DOI: 10.1016/s0278-5919(05)70076-4

[34] Long‐term effects of local growth factor (IGF‐I and TGF‐β1) treatment on fracture healing. A safety study for using growth factors. Journal of Orthopaedic Research. 2004. DOI: 10.1016/j.orthres.2003.09.009

[35] Gene mediated insulin‐like growth factor‐I delivery to the synovium. Journal of Orthopaedic Research. 2001. DOI: 10.1016/s0736-0266(00)00077-2

[36] Cartilage fragments from osteoarthritic knee promote chondrogenesis of mesenchymal stem cells without exogenous growth factor induction. Journal of Orthopaedic Research. 2011. DOI: 10.1002/jor.21541

[37] Subcellular distribution of the insulin‐like growth factor (IGF) binding proteins (IGFBPs) 2 and 3 in articular chondrocytes. Journal of Orthopaedic Research. 2008. DOI: 10.1002/jor.20660

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