Global Stem Cells Group has Announced an Agreement with Rokit Healthcare
Global Stem Cells Group announces an agreement with the South Korean biotechnology giant known as Rokit Healthcare to represent the company’s technology in the Latin American market.
The Global Stem Cells Group (GSCG) a world leader in Regenerative Medicine Technologies has signed an agreement with South Korean-based Rokit Healthcare, an esteemed bioprinter manufacturer that is committed to advancing the field of regenerative medicine and bettering the quality of life of people around the world.
The field of bioprinting is an extremely new one, but it shows great promise. Simply, it is the automated, computer aided deposition of bio-materials (which are cells, growth factors, and biocompatible polymers) for the manufacturing of functional human tissues or organs. Growth factors are harvested and used with a proprietary printing technology to create or regenerative damaged or diseased organs. Rokit Healthcare does this primarily through the proliferation of a machine that they dub an ‘organ regenerator’– it looks like a 3D printer, but instead of using plastics to create things, they use cells and materials that will be safe to implant within the human body.
The process of 3D bioprinting human tissues and organs is a revolutionary technology in the field of tissue engineering. One of the major challenges in regenerative medicine research and tissue engineering is mimicking the micro and macro environment of human tissues. In response to this challenge, advances in additive manufacturing have inspired scientists in Korea to develop novel bioprinting technology, for human tissues and organs
With the advancements of 3D printing and regenerative medicine working together, the potential is seemingly limitless for the spreading of bioprinting technology, a process that is known as 4D Printing– and Global Stem Cells Group, in an effort make this revolutionary technology available to patients, has forged an agreement with Rokit Healthcare to promote, and distribute the company’s technology in Latin America-
The Invivo 4D Printer is Rokit Healthcare’s flagship product, and it is one that revolutionizes the application of regenerative medicine and growth factor-based therapies. creating a solution for personalized and improved patient care. By leveraging a combination of 3D and bioprinting technologies, it can better distribute a patient’s autologous tissues and cells, making it an invaluable tool for those that are looking to improve the efficacy of their results, especially for certain dermatological conditions including scarring.
“We’re extremely excited about this new opportunity and look forward to working with Rokit,” Says Benito Novas, CEO of the Global Stem Cells Group, “The Invivo 4D Printer is in a position to turn the practice of regenerative medicine onto its head, and we are planning on creating a training center in Cancun, Mexico exclusively to showcase and instruct other physicians in this cutting-edge technology,”
About Global Stem Cells Group
Global Stem Cells Group (GSCG) is a worldwide network that combines seven major medical corporations, each focused on furthering scientific and technological advancements to lead cutting-edge stem cell development, treatments, and training. The united efforts of GSCG’s affiliate companies provide medical practitioners with a one-stop hub for regenerative medicine solutions that adhere to the highest medical standards.
About ROKIT :
ROKIT Healthcare is a global healthcare company that is committed to providing an effective and autologous organ regeneration platform. In order to undertake this daunting task, the company uses proprietary biofabrication technologies that show promise in treating several types of diseases in the field of regenerative medicine. Through the proliferation of 4D bioprinting technology, autologous stem cell technologies, ROKIT Healthcare believes that supplying an avenue for organ regeneration will drastically change the way that everyday people trust and manage their own body.
- Published in News
Conventional and novel stem cell based therapies for androgenic alopecia
Dodanim Talavera-Adame,1 Daniella Newman,2 Nathan Newman1
1American Advanced Medical Corp. (Private Practice), Beverly Hills, CA,
2Western University of Health Sciences, Pomona, CA, USA
Abstract
The prevalence of androgenic alopecia (AGA) increases with age and it affects both men and women. Patients diagnosed with AGA may experience decreased quality of life, depression, and feel self-conscious. There are a variety of therapeutic options ranging from prescription drugs to non-prescription medications. Currently, AGA involves an annual global market revenue of US$4 billion and a growth rate of 1.8%, indicating a growing consumer market. Although natural and synthetic ingredients can promote hair growth and, therefore, be useful to treat AGA, some of them have important adverse effects and unknown mechanisms of action that limit their use and benefits. Biologic factors that include signaling from stem cells, dermal papilla cells, and platelet-rich plasma are some of the current therapeutic agents being studied for hair restoration with milder side effects. However, most of the mechanisms exerted by these factors in hair restoration are still being researched. In this review, we analyze the therapeutic agents that have been used for AGA and emphasize the potential of new therapies based on advances in stem cell technologies and regenerative medicine.
Introduction
The prevalence of androgenic alopecia (AGA) increases with age, and is estimated to affect about 80% of Caucasian men.1 Female AGA, also known as female pattern hair loss, affects 32% of women in the ninth decade of life.2 The consumer market for products that promote hair growth has been increasing dramatically.3 These products promote hair regeneration based on the knowledge about the hair follicle (HF) cycle.4,5 However, in most cases, the mechanisms of action of these products are not well characterized and the results are variable or with undesirable side effects.6 At present, only two treatments for AGA have been approved by the US Food and Drug Administration (FDA): Minoxidil and Finasteride.7–10Although these medications have proved to be effective in some cases, their use is limited by their side effects.11,12 With the emergence of stem cells (SCs), many mechanisms that lead to tissue regeneration have been discovered.13 Hair regeneration has become one of the targets for SC technologies to restore the hair in AGA.14 Several SC factors such as peptides exert essential signals to promote hair regrowth.15,16 Some of these signals stimulate differentiation of SCs to keratinocytes which are important for HF growth.17 Other signals can stimulate dermal papilla cells (DPCs) that promote SC proliferation in the HF.18,19 In this review, we describe HF characteristics and discuss different therapies used currently for AGA and possible novel agents for hair regeneration. These therapies include FDA-approved medications, non-prescription physical or chemical agents, natural ingredients, small molecules, biologic factors, and signals derived from SCs.
HF and SC niche
The HF undergoes biologic changes from an actively growing stage (anagen) to a quiescent stage (telogen) with an intermediate remodeling stage (catagen).4 HFSCs are located in the bulge region of the follicle and they interact with mesenchymal SCs (MSCs) located in the dermal papilla (DP).18 These signal exchanges promote activation of some cellular pathways that are essential for DPC growth, function, and survival, such as the activation of Wnt signaling pathway.19–21 Other signals, such as those from endothelial cells (ECs) located at the DP, are also essential for HF maintenance.22 EC dysfunction that impairs adequate blood supply may limits or inhibits hair growth.22 For instance, Minoxidil, a synthetic agent, is able to promote hair growth by increasing blood flow and the production of prostaglandin E2 (PGE2).7 It has been shown that proteins that belong to the transforming growth factor (TGF) superfamily, such as bone morphogenetic proteins (BMPs), also exert signals to maintain the capacity of DPCs to induce HF growing in vivo and in vitro.23 These BMPs may be released by several cells that compose the follicle, including ECs.24–26 ECs may provide signals for BMP receptor activation in DPCs similar to those signals that promote survival of MSCs in human embryoid bodies composed of multipotent cells.24,25 DPCs have been derived from pluripotent SCs in an attempt to study their potential for hair regeneration in vitro and in vivo.27 Together, dermal blood vessels and DPCs orchestrate a suitable microenvironment for the growth and survival of HFSCs.28,29 Interestingly, the expression of Forkhead box C1 regulates the quiescence of HFSCs located in the bulge region (Figure 1).30 HFSCs are quiescent during mid-anagen and maintain this stage until the next hair cycle.29,30 However, during early anagen stage, these cells undergo a short proliferative phase in which they self-renew and produce new hair.30 Therefore, the bulge region constitutes a SC niche that makes multiple signals toward quiescence or proliferation stages.30–34 It is known that fibroblasts and adipocyte signals are able to inhibit the proliferation of HFSCs.34 Additionally, BMP6 and fibroblast growth factor 18 (FGF18) from bulge cells exert inhibitory effects on HFSC proliferation.34 Dihydrotestosterone (DHT) also inhibits HF growth.35 Agents that reduce DHT, such as Finasteride, promote hair regrowth by inhibiting Type II 5a-reductase.8,14,36 In contrast to these inhibitory effects, DPCs located at the base of the HF provide activation signals (Figure 1).18,34 The crosstalk between DPCs and HFSCs leads to inhibition of inhibitory effects with the resultant cell proliferation toward hair regeneration (anagen).30,31,37 With the self-renewal of HFSCs, the outer root sheath (ORS) forms, and signals from DPCs to the bulge cells diminish in a way that the bulge cells start again with their quiescent stage.4,34As mentioned earlier, Forkhead box C1 transcription factor has an important role in maintaining the threshold for HFSC activation.30 The knockdown of these factors in bulge cells reduces the cells’ threshold for proliferation, and the anagen cycle starts more frequently due to promotion of HFSC proliferation in shorter periods of time.30
Laser therapy
Light amplification by stimulated emission of radiation (LASER) generates electromagnetic radiation which is uniform in polarization, phase, and wavelength.45 Low-level laser therapy (LLLT), also called “cold laser” therapy, since it utilizes lower power densities than those needed to produce heating of tissue. Transdermal LLLT has been used for therapeutic purposes via photobiomodulation.46,47 Several clinical conditions, such as rheumatoid arthritis, mucositis, pain, and other inflammatory diseases, have been treated with these laser devices.48–50 LLLT promotes cell proliferation by stimulating cellular production of adenosine triphosphate and creating a shift in overall cell redox potential toward greater intracellular oxidation.51 The redox state of the cell regulates activation of signaling pathways that ultimately promotes high transcription factor activity and gene expression of factors associated with the cell cycle.52 Physical agents such as lasers have been also used to prevent hair loss in a wavelength range in the red and near infrared (600–1,070 nm).5,47,51,53 Laser therapy emits light that penetrates the scalp and promotes hair growth by increasing the blood flow.54 This increase gives rise to EC proliferation and migration due to upregulation of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase.55,56 In addition, the laser energy itself stimulates metabolism in catagen or telogen follicles, resulting in the production of anagen hair.53,54A specific effect of LLLT has been demonstrated to promote proliferation of HFSCs, forcing the hair to start the anagen phase.57
Biologic agents that promote hair growth and their mechanisms of action
SC signaling
Recently, it has been found that SCs release factors that can promote hair growth.16 These factors and their mechanisms of action have been summarized in Table 3. These factors, known as “secretomes”, are able to promote skin regeneration, wound healing, and immunologic modulation, among other effects.58,59 Some of these factors, such as epidermal growth factor (EGF), basic fibroblast growth factor, hepatocyte growth factor (HGF) and HGF activator, VEGF, insulin-like growth factor (IGF), TGF-ß, and platelet-derived growth factor (PDGF), are able to provide signals that promote hair growth.15,60–64 As mentioned before, DPCs provide signals to HFSCs located in the bulge that proliferate and migrate either to the DP or to the epidermis to repopulate the basal layer (Figure 1).32,65 Enhancement in growth factor expression (except for EGF) has been reported when the adipose SCs are cultured in hypoxic conditions.15 Also, SCs increase their self-renewal capacity under these conditions.66–68 Low oxygen concentrations (1%–5%) increase the level of expression of SC factors that include VEGF, basic fibroblast growth factor, IGF binding protein 1 (IGFBP-1), IGF binding protein 2 (IGFBP-2), macrophage colony-stimulating factor (M-CSF), M-CSF receptor (M-CSFR), and PDGF receptor ß (PDGFR-ß).15,69,70 While these groups of factors promote HF growth in intact skin, another group of factors, such as M-CSF, M-CSFR, and interleukin-6, are involved in wound-induced hair neogenesis.71 HGF and HGF activator stimulate DPCs to promote proliferation of epithelial follicular cells.61 Epidermal growth factor promotes cellular migration via the activation of Wnt/ß-catenin signaling.60 VEGF promotes hair growth and increases the follicle size mainly by perifollicular angiogenesis.72 Blocking VEGF activity by neutralizing antibodies reduced the size and growth of the HF.72 PDGF and its receptor (PDGFR-a) are essential for follicular development by promoting upregulation of genes involved in HF differentiation and regulating the anagen phase in HFs.64,73 They are also expressed in neonatal skin cells that surround the HF.73 Monoclonal antibodies to PDGFR-a (APA5) produced failure in hair germ induction, supporting that PDGFR-a and its ligand have an essential role in hair differentiation and development.73 IGF-1 promotes proliferation, survival, and migration of HF cells.69,74 In addition, IGF binding proteins (IGFBPs) also promote hair growth and hair cell survival by regulating IGF-1 effects and its interaction with extracellular matrix proteins in the HF.70 Higher levels of IGF-1 and IGFBPs in beard DPCs suggest that IGF-1 levels are associated with androgens.74 Furthermore, DPCs from non-balding scalps showed significantly higher levels of IGF-1 and IGFBP-6, in contrast to DPCs from balding scalps.74
Table 3
Stem cell factors and small molecules that promote hair growth and their mechanisms of action
| Factor | Mechanism of action |
|---|---|
| HGF and HGF activator61 | Factor secreted by DPC that promotes proliferation of epithelial follicular cells |
| EGF60 | Promotes growth and migration of follicle ORS cells by activation of Wnt/ß-catenin signaling |
| bFGF62 | Promotes the development of hair follicle |
| IL-693 | Involved in WIHN through STAT3 activation |
| VEGF72 | Promotes perifollicular angiogenesis |
| TGF-ß63 | Stimulates the signaling pathways that regulate hair cycle |
| IGF-169 | Promotes proliferation, survival, and migration of hair follicle cells |
| IGFBP-1 to -670 | Regulates IGF-1 effects and its interaction with extracellular matrix proteins at the hair follicle level |
| BMP23 | Maintains DPC phenotype which is crucial for stimulation of hair follicle stem cell |
| BMPR1a23 | Maintains the proper identity of DPCs that is essential for specific DPC function |
| M-CSF71 | Involved in wound-induced hair regrowth |
| M-CSFR71 | Involved in wound-induced hair regrowth |
| PDGF and PDGFR-ß/-a64 | Upregulates the genes involved in hair follicle differentiation. Induction and regulation of anagen phase. PDGF and its receptors are essential for follicular development |
| Wnt3a97 | Involved in hair follicle development through ß-catenin signaling |
| PGE279,80 | Stimulates anagen phase in hair follicles |
| PGF2a and analogs79,80 | Promotes transition from telogen to anagen phase of the hair cycle |
| BIO98 | GSK-3 inhibitor |
| PGE2 or inhibition of PGD2 or PGD2 receptor D2/GPR4477 | Promotes follicle regeneration |
| Iron and l-lysine95 | Under investigation |
Abbreviations: bFGF, basic fibroblast growth factor; BIO, (2’Z,3’E)-6-bromoindirubin-3′-oxime; BMP, bone morphogenetic protein; DPCs, dermal papilla cells; EGF, epidermal growth factor; GSK-3, glycogen synthase kinase-3; HGF, hepatocyte growth factor; IGF-1, insulin-like growth factor 1; IGFBP-1, insulin-like growth factor-binding protein 1; IL-6, interleukin-6; M-CSF, microphage colony-stimulating factor; M-CSFR, microphage colony-stimulating factor receptor; ORS, outer root sheath; PDGF, platelet-derived growth factor; PDGFR-a, platelet-derived growth factor receptor alpha; PDGFR-ß, platelet-derived growth factor receptor beta; PGD2, prostaglandin D2; PGE2, prostaglandin E2; TGF-ß1, transforming growth factor ß1; VEGF, vascular endothelial growth factor; WIHN, wound-induced hair neogenesis; Wnt3a, wingless-type MMTV integration site family, member 3A.
Small molecules
Small molecules with low molecular weight (<900 Da) and the size of 10-9 m are organic compounds that are able to regulate some biologic processes.75 Some small molecules have been tested for their role in hair growth.76 Synthetic, non-peptidyl small molecules that act as agonists of the hedgehog pathway have the ability to promote follicular cycling in adult mouse skin.76 PGE2 and prostaglandin D2 (PGD2) have also been associated with the hair cycle (Table 3).77 PGD2 is elevated in the scalp of balding men and inhibits hair lengthening via GPR44 receptor.78 Also, it is known that PGE2 and PGF2a promote hair growth, while PGD2 inhibits this process.77,79 Prostaglandin analogs of PGF2a have been used originally to decrease ocular pressure in glaucoma with parallel effects in the growth of eyelashes, which suggests a specific effect in HF activation.80 PGD2 receptors are located in the upper and lower ORS region and in the DP, suggesting that these prostaglandins play an important role in hair cycle.81 Molecules such as quercetin are able to inhibit PGD2 and, in this way, promote hair growth.82–84 Antagonists of PGD2 receptor (formally named chemoattractant receptor-homologous expressed in Th2 cells) such as setipiprant have been used to treat allergic diseases such as asthma, but they also have beneficial effects in AGA.85–87 Another small molecule l-ascorbic acid 2-phosphate promotes proliferation of ORS keratinocytes through the secretion of IGF-1 from DPCs via phosphatidylinositol 3-kinase.88 Recently, it has been described that small-molecule inhibitors of Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway promote hair regrowth in humans.89 Janus kinase inhibitors are currently approved by the FDA for the treatment of some specific diseases such as psoriasis and other autoimmune-mediated diseases.90–94 Also, another group of small molecules such as iron and the amino acid l-Lysine are essential for hair growth (Table 3).95
Cellular therapy
The multipotent SCs in the bulge region of the HF receive signals from DPCs in order to proliferate and survive.27,28,65,84,96 It has been shown that Wnt/ß-catenin signaling is essential for the growth and maintenance of DPCs.19,97 These cells can be isolated and cultured in vitro with media supplemented with 10% fetal bovine serum and FGF-2.37,98 However, they lose versican expression that correlates with decrease in follicle-inducing activity in culture.98 Versican is the most abundant component of HF extracellular matrix.99 Inhibition of glycogen synthase kinase-3 by (2’Z,3’E)-6-bromoindirubin-3′-oxime (BIO) promotes hair growth in mouse vibrissa follicles in culture by activation of Wnt signaling.98 Therefore, the increase of Wnt signaling in DPCs apparently is one of the main factors that promote hair growth.19 DPCs have been also generated from human embryonic SCs that induced HF formation after murine transplantation.27
Platelet-rich plasma
Platelets are anucleate cells generated by fragmentation of megakaryocytes in the bone marrow.100 These cells are actively involved in the hemostatic process after releasing biologically active molecules (cytokines).100–102 Because of the platelets’ higher capacity to produce and release these factors, autologous platelet-rich plasma (PRP) has been used to treat chronic wounds.103 Therefore, PRP can be used as autologous therapy for regenerative purposes, for example, chondrogenic differentiation, wound healing, fat grafting, AGA, alopecia areata, facial scars, and dermal volume augmentation.101,104–108 PRP contains human platelets in a small volume that is five to seven times higher than in normal blood and it has been proven to be beneficial to treat AGA.10,105,109–111 The factors released by these platelets after their activation, such as PDGFs (PDGFaa, PDGFbb, PDGFab), TGF-ß1, TGF-ß2, EGF, VEGF, and FGF, promote proliferation of DPCs and, therefore, may be beneficial for AGA treatment.109,112–114 Clinical experiments indicate that patients with AGA treated with autologous PRP show improved hair count and thickness.109
In search of novel therapies
In this paper, we reviewed and discussed the use of therapeutic agents for hair regeneration and the knowledge to promote the development of new therapies for AGA based on the advances in regenerative medicine. The HF is a complex structure that grows when adequate signaling is provided to the HFSCs. These cells are located in the follicle bulge and receive signals from MSCs located in the dermis that are called DPCs. The secretory phenotype of DPCs is determined by local and circulatory signals or hormones. Recent discoveries have demonstrated that SCs in culture are able to activate DPCs and HFSCs and, in this way, promote hair growth. The study of these cellular signals can provide the necessary knowledge for developing more effective therapeutic agents for the treatment of AGA with minimal side effects. Therefore, advancements in the field of regenerative medicine may generate novel therapeutic alternatives. However, further research and clinical studies are needed to evaluate their efficacy.
Disclosure
The authors report no conflicts of interest in this work.
References
|
Blumeyer A, Tosti A, Messenger A, et al; European Dermatology Forum (EDF). Evidence-based (S3) guideline for the treatment of androgenetic alopecia in women and in men. J Dtsch Dermatol Ges. 2011;9(Suppl 6):S1–S57. |
||
|
Ramos PM, Miot HA. Female pattern hair loss : a clinical and pathophysiological review. An Bras Dermatol. 2015;90(4):529–543. |
||
|
Otberg N, Finner AM, Shapiro J. Androgenetic alopecia. Endocrinolo Metab Clin North Am. 2007;36(2):379–398. |
||
|
Plikus MV, Chuong CM. Complex hair cycle domain patterns and regenerative hair waves in living rodents. J Invest Dermatol. 2008;128(5):1071–1080. |
||
|
McElwee KJ, Shapiro JS. Promising therapies for treating and/or preventing androgenic alopecia. Skin Therapy Lett. 2012;17(6):1–4. |
||
|
Perez-Mora N, Velasco C, Bermüdez F. Oral finasteride presents with sexual-unrelated withdrawal in long-term treated androgenic alopecia in men. Skinmed. 2015;13(3):179–183. |
||
|
Gupta AK, Charrette A. Topical minoxidil: systematic review and meta-analysis of its efficacy in androgenetic alopecia. Skinmed. 2015;13(3):185–189. |
||
|
Shapiro J, Kaufman KD. Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss). J Investig Dermatol Symp Proc. 2003;8(1):20–23. |
||
|
Rossi A, Anzalone A, Fortuna MC, et al. Multi-therapies in androgenetic alopecia: review and clinical experiences. Dermatol Ther. 2016;29(6):424–432. |
||
|
Varothai S, Bergfeld WF. Androgenetic alopecia: an evidence-based treatment update. Am J Clin Dermatol. 2014;15(3):217–230. |
||
|
Rossi A, Cantisani C, Melis L, Iorio A, Scali E, Calvieri S. Minoxidil use in dermatology, side effects and recent patents. Recent Pat Inflamm Allergy Drug Discov. 2012;6(2):130–136. |
||
|
Motofei IG, Rowland DL, Georgescu SR, Mircea T, Baleanu BC, Paunica S. Are hand preference and sexual orientation possible predicting factors for finasteride adverse effects in male androgenic alopecia? Exp Dermatol. 2016;25(7):557–558. |
||
|
Reijo Pera RA, Gleeson JG. Stems cells and regeneration: special review issue. Hum Mol Gen. 2008;17(R1):R1–R2. |
||
|
Jain R, De-Eknamkul W. Potential targets in the discovery of new hair growth promoters for androgenic alopecia. Expert Opin Ther Targets. 2014;18(7):787–806. |
||
|
Park BS, Kim WS, Choi JS, et al. Hair growth stimulated by conditioned medium of adipose-derived stem cells is enhanced by hypoxia : evidence of increased growth factor secretion. Biomed Res. 2010;31(1):27–34. |
||
|
Fukuoka H, Suga H. Hair regeneration treatment using adipose-derived stem cell conditioned medium :follow-up with trichograms. Eplasty. 2015;15:65–72. |
||
|
Du Y, Roh DS, Funderburgh ML, et al. Adipose-derived stem cells differentiate to keratocytes in vitro. Mol Vis. 2010;16:2680–2689. |
||
|
Zhang P, Kling RE, Ravuri SK, et al. A review of adipocyte lineage cells and dermal papilla cells in hair follicle regeneration. J Tissue Eng. 2014;5:2041731414556850. |
||
|
Tsai SY, Sennett R, Rezza A, et al. Wnt/ß-catenin signaling in dermal condensates is required for hair follicle formation. Dev Biol. 2014;385(2):179–188. |
||
|
Choi YS, Zhang Y, Xu M, et al. Distinct functions for Wnt/ß-catenin in hair follicle stem cell proliferation and survival and interfollicular epidermal homeostasis. Cell Stem Cell. 2013;13(6):720–733. |
||
|
Rao TP, Kuhl M. An updated overview on Wnt signaling pathways a prelude for more. Circ Res. 2010;106(12):1798–1806. |
||
|
Yano K, Brown LF, Detmar M. Control of hair growth and follicle size by VEGF-mediated angiogenesis. J Clin Invest. 2001;107(4):409–417. |
||
|
Rendl M, Polak L, Fuchs E. BMP signaling in dermal papilla cells is required for their hair follicle-inductive properties. Genes Dev. 2008;22(4):543–557. |
||
|
Talavera-Adame D, Gupta A, Kurtovic S, Chaiboonma KL, Arumugaswami V, Dafoe DC. Bone morphogenetic protein-2/-4 upregulation promoted by endothelial cells in coculture enhances mouse embryoid body differentiation. Stem Cells Dev. 2013;22(24):3252–3260. |
||
|
Talavera-Adame D, Wu G, He Y, et al. Endothelial Cells in Co-culture Enhance Embryonic Stem Cell Differentiation to Pancreatic Progenitors and Insulin-Producing Cells through BMP Signaling. Stem Cell Rev. 2011;7(3):532–543. |
||
|
Talavera-Adame D, Ng TT, Gupta A, Kurtovic S, Wu GD, Dafoe DC. Characterization of microvascular endothelial cells isolated from the dermis of adult mouse tails. Microvascular Res. 2011;82(2):97–104. |
||
|
Gnedeva K, Vorotelyak E, Cimadamore F, et al. Derivation of hair-inducing cell from human pluripotent stem cells. PLoS One. 2015;10(1):1–14. |
||
|
Lavker RM, Sun T, Oshima H, et al. Hair follicle stem cells. J Investig Dermatol Symp Proc. 2003;8(1):28–38. |
||
|
Bernard B. Advances in understanding hair growth. F1000Res. 2016;5:1–8. |
||
|
Lay K, Kume T, Fuchs E. FOXC1 maintains the hair follicle stem cell niche and governs stem cell quiescence to preserve long-term tissue-regenerating potential. Proc Natl Acad Sci U S A. 2016;113(1): E1506–E1515. |
||
|
Leirós GJ, Attorresi AI, Balañá ME. Hair follicle stem cell differentiation is inhibited through cross-talk between Wnt/ß-catenin and androgen signalling in dermal papilla cells from patients with androgenetic alopecia. Br J Dermatol. 2012;166(5):1035–1042. |
||
|
Chacon-Martinez CA, Klose M, Niemann C, Glauche I, Wickström SA. Hair follicle stem cells= cultures reveal self-organizing plasticity of stem cells and their progeny. EMBO J. 2017;36(2):151–164. |
||
|
Soler AP, Gilliard G, Megosh LC, O’Brien TG. Modulation of murine hair follicle function by alterations in ornithine decarboxylase activity. J Invest Dermatol. 1996;106(5):1108–1113. |
||
|
Hsu YC, Pasolli HA, Fuchs E. Dynamics between stem cells, nich and progeny in the hair follicle. Cell. 2011;144(1):92–105. |
||
|
Kang JI, Kim SC, Kim MK, et al. Effects of dihydrotestosterone on rat dermal papilla cells in vitro. Eur J Pharmacol. 2015;757:74–83. |
||
|
Yamana K, Labrie F, Luu-The V. Human type 3 5a-reductase is expressed in peripheral tissues at higher levels than types 1 and 2 and its activity is potently inhibited by finasteride and dutasteride. Horm Mol Biol Clin Investig. 2010;2(3):293–299. |
||
|
Osada A, Iwabuchi T, Kishimoto J, Hamazaki TS, Okochi H. Long-term culture of mouse vibrissal dermal papilla cells and de novo hair follicle induction. Tissue Eng. 2007;13(5):975–982. |
||
|
Choi GS, Kim JH, Oh SY, et al. Safety and tolerability of the dual 5-alpha reductase inhibitor dutasteride in the treatment of androgenetic alopecia. Ann Dermatol. 2016;28(4):444–450. |
||
|
Carson C 3rd, Rittmaster R. The role of dihydrotestosterone in benign prostatic hyperplasia. Urology. 2003;61(4 Suppl 1):2–7. |
||
|
Kamimura A, Takahashi T. Procyanidin B-2, extracted from apples, promotes hair growth: a laboratory study. Br J Dermatol. 2002;146(1):41–51. |
||
|
Kamimura A, Takahashi T. Procyanidin B-3, isolated from barley and identified as a hair-growth stimulant, has the potential to counteract inhibitory regulation by TGF-beta1. Exp Dermatol. 2002;11(6):532–541. |
||
|
Ulbricht C, Basch E, Bent S, et al. Evidence-based systematic review of saw palmetto by the Natural Standard Research Collaboration. J Soc Integr Oncol. 2006;4(4):170–186. |
||
|
Rondanelli M, Perna S, Peroni G, Guido D. A bibliometric study of scientific literature in Scopus on botanicals for treatment of androgenetic alopecia. J Cosmet Dermatol. 2015;15(2):120–130. |
||
|
Blume-Peytavi U, Kunte C, Krisp A, Garcia Bartels N, Ellwanger U, Hoffmann R. [Comparison of the efficacy and safety of topical minoxidil and topical alfatradiol in the treatment of androgenetic alopecia in women.] J Dtsch Dermatol Ges. 2007;5(5):391–395. German. |
||
|
Farivar S, Malekshahabi T, Shiari R. Biological effects of low level laser therapy. J Lasers Med Sci. 2014;5(2):58–62. |
||
|
Maiman TH. Biomedical lasers evolve toward clinical applications. Hosp Manage. 1966;101(4):39–41. |
||
|
Cung H, Dai T, Sharma SK, et al. The nuts and bolts of low-level laser (light) therapy. Ann Biomed Eng. 2013;40(2):516–533. |
||
|
Bjordal JM, Couppé C, Chow RT, Tunér J, Ljunggren EA. A systematic review of low level laser therapy with location-specific doses for pain from chronic joint disorders. The Aust J Physiother. 2003;49(2):107–116. |
||
|
Brosseau L, Welch V, Wells G, et al. Low level laser therapy (classes I, II and III) in the treatment of rheumatoid arthritis. Cochrane Database Syst Rev. 2005;19(2):CD002049. |
||
|
Cauwels RGEC, Martens LC. Low level laser therapy in oral mucositis: a pilot study. Eur Arch Paediatr Dent. 2011;12(2):118–123. |
||
|
Schindl A, Schindl M, Pernerstorfer-Schön H, Schindl L. Low-intensity laser therapy: a review. J Investig Med. 2000;48(5):312–326. |
||
|
Liu H, Colavitti R, Rovira II, Finkel T. Redox-dependent transcriptional regulation. Cir Res. 2005;97(10):967–974. |
||
|
Gupta AK, Lyons DCA, Abramovits W. Low-level laser/light therapy for androgenetic alopecia. Skinmed. 2014;12(3):145–147. |
||
|
Jimenez JJ, Wikramanayake TC, Bergfeld W, et al. Efficacy and safety of a low-level laser device in the treatment of male and female pattern hair loss: a multicenter, randomized, sham device-controlled, double-blind study. Am J Clin Dermat. 2014;15(2):115–127. |
||
|
Chen CH, Hung HS, Hsu SH. Low-energy laser irradiation increases endothelial cell proliferation, migration, and eNOS gene expression possibly via PI3K signal pathway. Lasers Surg Med. 2008;40(1):46–54. |
||
|
Tuby H, Maltz L, Oron U. Modulations of VEGF and iNOS in the rat heart by low level laser therapy are associated with cardioprotection and enhanced angiogenesis. Lasers Surg Med. 2006;38(7):682–688. |
||
|
Avci P, Gupta GK, Clark J, Wikonkal N, Hamblin MR. Low-level laser (light) therapy (LLLT) for treatment of hair loss. Laser Surg Med. 2015;46(2):144–151. |
||
|
Rodrigues C, de Assis AM, Moura DJ, et al. New therapy of skin repair combining adipose-derived mesenchymal stem cells with sodium carboxymethylcellulose scaffold in a pre-clinical rat model. PloS One. 2014;9(5):e96241. |
||
|
Gimble JM, Katz AJ, Bunnell BA. Adipose-derived stem cells for regenerative medicine. Cir Res. 2007;100(9):1249–1260. |
||
|
Zhang H, Nan W, Wang S, et al. Epidermal growth factor promotes proliferation and migration of follicular outer root sheath cells via Wnt/ß-catenin signaling. Cell Physiol Biochem. 2016;39(1):360–370. |
||
|
Lee YR, Yamazaki M, Mitsui S, Tsuboi R, Ogawa H. Hepatocyte growth factor (HGF) activator expressed in hair follicles is involved in in vitro HGF-dependent hair follicle elongation. J Dermatol Sci. 2001;25(2):156–163. |
||
|
du Cros DL. Fibroblast growth factor influences the development and cycling of murine hair follicles. Dev Biol. 1993;156(2):444–453. |
||
|
Niimori D, Kawano R, Felemban A, et al. Tsukushi controls the hair cycle by regulating TGF-ß1 signaling. Dev Biol. 2012;372(1):81–87. |
||
|
Tomita Y, Akiyama M, Shimizu H. PDGF isoforms induce and maintain anagen phase of murine hair follicles. J Dermatol Sci. 2006;43(2):105–115. |
||
|
Ohyama M, Terunuma A, Tock CL, et al. Characterization and isolation of stem cell – enriched human hair follicle bulge cells. J Clin Invest. 2006;116(1):249–260. |
||
|
Grayson WL, Zhao F, Bunnell B, Ma T. Hypoxia enhances proliferation and tissue formation of human mesenchymal stem cells. Biochem Biophys Res Commun. 2007;358(3):948–953. |
||
|
Potier E, Ferreira E, Andriamanalijaona R, et al. Hypoxia affects mesenchymal stromal cell osteogenic differentiation and angiogenic factor expression. Bone. 2007;40(4):1078–1087. |
||
|
Ren H, Cao Y, Zhao Q, et al. Proliferation and differentiation of bone marrow stromal cells under hypoxic conditions. Biochem Biophys Res Commun. 2006;347(1):12–21. |
||
|
Su HY, Hickford JG, Bickerstaffe R, Palmer BR. Insulin-like growth factor 1 and hair growth. Dermatol Online J. 1999;5(2):1. |
||
|
Batch JA, Mercuri FA, Werther GA. Identification and localization of insulin-like growth factor-binding protein (IGFBP) messenger RNAs in human hair follicle dermal papilla. J Invest Dermatol. 1996;106(3):471–475. |
||
|
Osaka N, Takahashi T, Murakami S, et al. ASK1-dependent recruitment and activation of macrophages induce hair growth in skin wounds. J Cell Biol. 2007;176(7):903–909. |
||
|
Yano K, Brown LF, Detmar M. Control of hair growth and follicle size by VEGF-mediated angiogenesis. J Clin Invest. 2001;107(4):409–417. |
||
|
Takakura N, Yoshida H, Kunisada T, Nishikawa S, Nishikawa SI. Involvement of platelet-derived growth factor receptor-a in hair canal formation. J Invest Dermatol. 1996;107(5):770–777. |
||
|
Panchaprateep R, Asawanonda P. Insulin-like growth factor-1: roles in androgenetic alopecia. Exp Dermatol. 2014;23(3):216–218. |
||
|
Castoreno AB, Eggert US. Small molecule probes of cellular pathways and networks. ACS Chem Biol. 2011;6(1):86–94. |
||
|
Paladini RD, Saleh J, Qian C, Xu GX, Rubin LL. Modulation of hair growth with small molecule agonists of the hedgehog signaling pathway. J Iinvest Dermatol. 2005;125(4):638–646. |
||
|
Nieves A, Garza LA. Does prostaglandin D2 hold the cure to male pattern baldness? Exp Dematol. 2014;(29):224–227. |
||
|
Nelson AM, Loy DE, Lawson JA, Katseff AS, Fitzgerald GA, Garza LA. Prostaglandin D2 inhibits wound-induced hair follicle neogenesis through the receptor Gpr44. J Invest Dermatol. 2013;133(4):881–889. |
||
|
Sasaki S, Hozumi Y, Kondo S. Influence of prostaglandin F2alpha and its analogues on hair regrowth and follicular melanogenesis in a murine model. Exp Dermatol. 2005;14(5):323–328. |
||
|
Choi YM, Diehl J, Levins PC. Promising alternative clinical uses of prostaglandin F2a analogs: beyond the eyelashes. J Am Acad Dermatol. 2015;72(4):712–716. |
||
|
Colombe L, Michelet JF, Bernard BA. Prostanoid receptors in anagen human hair follicles. Exp Dermatol. 2008;17(1):63–72. |
||
|
Zhang Q, Major MB, Takanashi S, et al. Small-molecule synergist of the Wnt/beta-catenin signaling pathway. Proc Natl Acad Sci U S A. 2007;104(18):7444–7448. |
||
|
Fong P, Tong HH, Ng KH, Lao CK, Chong CI, Chao CM. In silicoprediction of prostaglandin D2 synthase inhibitors from herbal constituents for the treatment of hair loss. J Ethnopharmacol. 2015;175:470–480. |
||
|
Weng Z, Zhang B, Asadi S, et al. Quercetin is more effective than cromolyn in blocking human mast cell cytokine release and inhibits contact dermatitis and photosensitivity in humans. PloS One. 2012;7(3):e33805. |
||
|
Norman P. Update on the status of DP2 receptor antagonists; from proof of concept through clinical failures to promising new drugs. Expert Opin Investig Drugs. 2014;23(1):55–66. |
||
|
Pettipher R. The roles of the prostaglandin D(2) receptors DP(1) and CRTH2 in promoting allergic responses. Br J Pharmacol. 2008;153(Suppl 1):S191–S199. |
||
|
Garza LA, Liu Y, Yang Z, et al. Prostaglandin D2 inhibits hair growth and is elevated in bald scalp of men with androgenetic alopecia. Sci Transl Med. 2012;4(126):126ra34. |
||
|
Kwack MH, Shin SH, Kim SR, et al. I-Ascorbic acid 2-phosphate promotes elongation of hair shafts via the secretion of insulin-like growth factor-1 from dermal papilla cells through phosphatidylinositol 3-kinase. Br J Dermatol. 2009;160(6):1157–1162. |
||
|
Harel S, Higgins CA, Cerise JE, et al. Pharmacologic inhibition of JAK-STAT signaling promotes hair growth. Sci Adv. 2015;1(9):e1500973. |
||
|
Quintás-cardama A, Vaddi K, Liu P, et al. INCB018424 : therapeutic implications for the treatment of myeloproliferative neoplasms Preclinical characterization of the selective JAK1 / 2 inhibitor INCB018424 : therapeutic implications for the treatment of myeloproliferative neoplasms. Blood. 2014;115(15):3109–3117. |
||
|
Geyer HL, Mesa RA. Therapy for myeloproliferative neoplasms: when, which agent, and how? Hematology Am Soc Hematol Educ Program. 2014;2014(1):277–286. |
||
|
Ghoreschi K, Jesson MI, Li X, et al. Modulation of innate and adaptive immune responses by tofacitinib (CP-690,550). J Immunol. 2012;186(7):4234–4243. |
||
|
Kontzias A, Laurence A, Gadina M, O’Shea JJ. Kinase inhibitors in the treatment of immune-mediated disease. F1000 Med Rep. 2012;4:5. |
||
|
Bao L, Zhang H, Chan LS. The involvement of the JAK-STAT signaling pathway in chronic inflammatory skin disease atopic dermatitis. JAKSTAT. 2013;2(3):1–8. |
||
|
Rushton DH. Nutritional factors and hair loss. Clin Exp Dermatol. 2002;27(5):396–404. |
||
|
Oshima H, Rochat A, Kedzia C, Kobayashi K, Barrandon Y. Morphogenesis and renewal of hair follicles from adult multipotent stem cells. Cell. 2001;104(2):233–245. |
||
|
Huelsken J, Vogel R, Erdmann B, Cotsarelis G, Birchmeier W. beta-Catenin controls hair follicle morphogenesis and stem cell differentiation in the skin. Cell. 2001;105(4):533–545. |
||
|
Yamauchi K, Kurosaka A. Inhibition of glycogen synthase kinase-3 enhances the expression of alkaline phosphatase and insulin-like growth factor-1 in human primary dermal papilla cell culture and maintains mouse hair bulbs in organ culture. Arch Dermatol Res. 2009;301(5):357–365. |
||
|
Sotoodehnejadnematalahi F, Burke B. Structure, function and regulation of versican: the most abundant type of proteoglycan in the extracellular matrix. Acta Med Iran. 2013;51(11):740–750. |
||
|
Xu XR, Zhang D, Oswald BE, et al. Platelets are versatile cells: new discoveries in hemostasis, thrombosis, immune responses, tumor metastasis and beyond. Crit Rev Clin Lab Sci. 2016;53(6):409–430. |
||
|
Lacci KM, Dardik A. Platelet-rich plasma: support for its use in wound healing. Yale J Biol Med. 2010;83(1):1–9. |
||
|
Mussano F, Genova T, Munaron L, Petrillo S, Erovigni F, Carossa S. Cytokine, chemokine, and growth factor profile of platelet-rich plasma. Platelets. 2016;27(5):467–471. |
||
|
Martinez-Zapata MJ, Martí-Carvajal AJ, Solà I, et al. Autologous platelet-rich plasma for treating chronic wounds. Cochrane Database Syst Rev. 2016;(5):CD006899. |
||
|
Modarressi A. Platlet Rich Plasma (PRP) improves fat grafting outcomes. World J Plast Surg. 2013;2(1):6–13. |
||
|
Gentile P, Garcovich S, Bielli A, Scioli MG, Orlandi A, Cervelli V. The Effect of platelet-rich plasma in hair regrowth: a randomized placebo-controlled trial. Stem Cells Transl Med. 2015;4(11):1317–1323. |
||
|
Lynch MD, Bashir S. Applications of platelet-rich plasma in dermatology: a critical appraisal of the literature. J Dermatolog Treat. 2016;27(3):285–289. |
||
|
Trink A, Sorbellini E, Bezzola P, et al. A randomized, double-blind, placebo- and active-controlled, half-head study to evaluate the effects of platelet-rich plasma on alopecia areata. Br J Dermatol. 2013;169(3):690–694. |
||
|
Oh Y, Kim BJ, Kim MN. Depressed facial scars successfully treated with autologous platelet-rich plasma and light-emitting diode phototherapy at 830 nm. Ann Dermatol. 2014;26(3):417–418. |
||
|
Singhal P, Agarwal S, Dhot PS, Sayal SK. Efficacy of platelet-rich plasma in treatment of androgenic alopecia. Asian J Transfus Sci. 2015;9(2):159–162. |
||
|
Valente Duarte de Sousa IC, Tosti A. New investigational drugs for androgenetic alopecia. Expert Opin Investig Drugs. 2013;22(5):573–589. |
||
|
Alves R, Grimalt R. Randomized placebo-controlled, double-blind, half-head study to assess the efficacy of platelet-rich plasma on the treatment of androgenetic alopecia. Dermatol Surg. 2016;42(4):491–497. |
||
|
Cho JW, Kim SA, Lee KS. Platelet-rich plasma induces increased expression of G1 cell cycle regulators, type I collagen, and matrix metalloproteinase-1 in human skin fibroblasts. Int J Mol Med. 2012;29(1):32–36. |
||
|
Mehta V. Platelet-rich plasma: a review of the science and possible clinical applications. Orthopedics. 2010;33(2):111. |
||
|
Leo MS, Kumar AS, Kirit R, Konathan R, Sivamani RK. Systematic review of the use of platelet-rich plasma in aesthetic dermatology. J Cosmet Dermatol. 2015;14(4):315–323. |
- Published in Blog
What’s all the fuss about Regenerative Medicine?
In popular media, the term Regenerative Medicine, or Stem Cell Therapy, are becoming buzz words. This is because the field of medicine and healthcare is expanding and advancing every day, and many new treatments for otherwise common ailments are being discovered. These conditions range from burns, joint pain, strain, and pretty much every other common ailment out there.
Many patients have given up hope with trying to find traditional medicines that work. This is why many people are flocking to try Regenerative Medicine. This is also something that many people who are into holistic healing are trying, as it is simply the body working to heal itself.
Regenerative Medicine works as it takes a sample of your own blood, bone marrow, and other tissues, and then it goes through a process in which to take out a certain material known as Platelet-Rich Plasma. This PRP is then applied to the infected area, so that your body’s own platelets can work to heal your body back to full health, without having to worry about any invasive surgeries.
A good question to ask is why our body does this do this itself. Well, this is because research has shown that by isolating them, they activate, and as a result when injected back into the body start to work harder to fix the issues, such as in a joint, or helping to relieve pain. Many patients who try it say they have gotten good results from the treatment.
Many doctors predict that this therapy will help physicians provide a more non-intrusive treatment that has fewer side effects, and can be big within the coming years. Many compare it to the invention of penicillin with how important it is. It is even growing in popularity with many physicians using training courses to help their patients, leaving many of them happier and healthier.
- Published in Blog
7 PRP Treatments That Are Popular Right Now
The time it takes to draw a patient’s blood, add a little citrate, and use a centrifugal machine with a PRP kit is only 15-20 minutes. This is the amount of time needed to create Platelet-Rich Plasma, or PRP. This can then be used for many purposes, using speeding up a patients recovery.
PRP is by far the best healing agent that has growth factors and platelets to help with the healing process, which is also completely free and natural to obtain.
What are The Advantages Of Using PRP Correctly?
It is easy to create PRP simpy by placing blood in a centrifuge, but it can have very little, if any, platelets, and would otherwise be useless. However, with the right equipment, you can make PRP with up to 7x the amount of platelets. This can be amplified by using fat tissue and collagen fibers to create a PRP matrix.
7 Popular PRP Treatments
- Facial Treatments
Many skin centers are thriving due to being one of the first to adopt PRP therapies. With the lack of side effects or down time, it became incredibly popular. These treatments include wrinkle reduction, skin rejuvenation, dark circle and bag erasure, rosacea treatment, and even lip augmentation.
One popular and generic treatment option includes combining PRP and a treatment known as microneedling. When this is applied, it’s effects are similar to Botox, or facelifts, for far less cost and side effects.
- Hair Loss
PRP growth factors can be beneficial when it comes to reversing non-genetic early stage hair loss. Despite there being a huge market for this, almost no practitioners actually utilize it. Many clients have seen promise after hair thinning, and many have seen beard regrowth over time.
- Arthritis and Cartilage
Arthritis treatments alone cost patients 6.4 billion dollars in 2013 for the US alone, with projections of up to 9 billion by the end of the decade. However, unlike the other treatments, PRP is seen as the only treatment that can not just reduce symptoms, but also regrow the cartilage. One of the most popular examples would be treatments for Temporomandibulaar Joint Osteoarthritis.
- Anti-aging Properties
When it comes to the anti-aging market, there are a endless number of treatments and procures available. Yet, none of them even stand close to the effectiveness of PRP therapy. PRP combined with Microneedling can ve highly effective for strech marks, acne scars, breast augmentation, and even skin conditions like Lichen Sclerosus.
- Pain Relief and Musculoskeletal Healing
There are a ton of treatments in this category, with many of them being incredibly more effective than leading treatments. These include healing Rotator Cuffs, Tennis Elbow, Achilles Tendonitis, Patellar Tendonitis, Back Pain, Hip and Pelvic problems, Degenerative Disc Disease, Golfer’s Elbow, Labaral Tear, Brusitis, neck pain, avascular Necrosis, and even pain related to nerve regeneration.
Almost all of these treatment, as opposed to those in other categories on this list, also use ultrasound guidance when injecting the PRP directly into the affected tissue. This can allow patients to see fantastic results in as little as 2 weeks.
- Fertility
Ovarian Rejuvination is where PRP is injected directly into a woman’s ovaries. This is meant to help reverse menopause and help lower fertility issues. This treatment can even be used for sexual regeneration. Although similar, this treatment is not the same as other treatments where PRO is injected into the vagina, and is supposed to treat looseness, dryness, low sex drive, and incontinence.
- COPD (Chronic Obstructive Pulmonary Disease)
Allergies, asthma, and COPD are among the growing list of things that PRP is being used as a treatment for. For this to work, the PRP is mixed with a saline solution, and then, using a nebulizer, is inhaled, and helps to regenerate the lung tissue.
Although it can take up to 2 months for patients to see the effects, many are seeing improvements. Almost 1 million people suffer from COPD a year, so anything that can help treat the condition is beneficial.
The Future
PRP has been trending rather well in the recent years, and seems to be here for the long term. Not only it is a fully natural remedy, but it is one that works better than most or all traditional treatments. Many like it due to the fact that there are few side effects, it only takes a short amount of time, and there is no recovery period.
PRP has been adopted by thousands of clinics and practices throughout the US and the world. The demand for these treatments have been increasing almost faster than practices are choosing to provide them. Many patients are even willing to travel long distances just to receive these treatments.
So are you providing PRP treatments yet?
- Published in Blog
Stem Cell Platelet-Rich Plasma: The Best Regenerative Therapy?
To understand why stem cell platelet-rich plasma or co-transplantation of Adipose-derived mesenchymal stem cells and PRP, is such a remarkable idea in regenerative medicine, let’s spend a little time looking at the mechanics of PRP.
Platelet-Rich Plasma’s Role As Repairmen
The one thing that makes Platelet-Rich Plasma a hero in several fields (if not all) of medicine is the fact that the diverse growth factors in it are able to stimulate stem cell proliferation and cell differentiation (the factors that determine effective tissue regeneration and healing) on any part of the body.
These growth factors are abundant in the blood and act as the natural repairmen of tissues.
In the perfect scenario, there’s plenty of blood flow to every part of the body and these “repairmen” are always on-call to address any healing needs that may arise. However, if the injured area has a poor blood supply — especially areas that are constantly move like tendons, ligaments and joints — demand for these repairmen can outgrow supply. Meaning, healing (or regeneration of tissues) is put on hold till further repairmen are available.
The train of Platelet-Rich Plasma then arrives with enough of these repairmen to warrant resumption of healing.
There’s another part of this picture we haven’t talked about so far: stem cells.
As far as Platelet-Rich Plasma and it’s growth factors are concerned, they are mere repairmen. They can’t do the work by themselves. They need the basic raw materials to work with. And that raw material here is the stem cells.
Stem cells are the ones actually being regenerated to form new tissues for healing.
Stem Cells As The Raw Materials For PRP
Stem cells are the only raw materials that PRP works with for regeneration. These are like the fundamental building blocks of all other cells. These cells can be can be guided into becoming specialized cells under the right conditions.
In addition, they can also divide themselves to form new stem cells or new specialized cells.
So for Platelet-Rich Plasma to work well, it needs to be applied to an area with lots of stem cells like the heart, liver, blood vessels etc. Incidentally Platelet-Rich Plasma’s healing properties were first discovered by cardiac surgeons who played with concentrated blood for faster healing of heart after surgery and it showed tremendous promise because stem cells are abundant in heart tissues.
But what if healing is needed in an area where there are not much stem cells?
With the new developments in stem cell technology that can be solved too. Because now we can supply the stem cells to areas where there are less like the joints, ligaments and tendons. For this, scientists usually use “mesenchymal stem cell” or MSCs. These are cells isolated from stroma and can differentiate to form adipocytes, cartilage, bone, tendons, muscle, and skin.
The most easiest way is to harvest it from adipose tissue or fat that we call Adipose-derived mesenchymal stem cells or ADSC.
Stem Cell Platelet-Rich Plasma
Supplying Both PRP And Stem Cells For Regeneration
In regions with hypoxia (poor blood supply) like joints, meniscus tissue, rotator cuff, spinal discs etc the supply of platelets (and therefore growth factors) as well as the stem cells are limited. So what if we supplied both the stem cells and Platelet-Rich Plasma for triggering the regeneration process?
That’s the question these Japanese scientists answered in their research. Here’s another group of scientists who took on the same challenge.
They used Adipose-derived mesenchymal stem cells (ADSC) which is known for their ease of isolation and extensive differentiation potential. These researchers noted that these stem cells often can’t survive in areas of local hypoxia, oxidative stress and inflammation – thereby making them ineffective. However, when Platelet-Rich Plasma (or thrombin-activated PRP) is added to ADSC, it kept them alive for prolonged periods and the growth factors in the Platelet-Rich Plasma triggered cell differentiation and proliferation more easily.
Why This Exact Combination Is The Future
Done this way, both Adipose-derived mesenchymal stem cells (ADSC) and Platelet-Rich Plasma are raw materials for healing that’s already available in plenty in almost every one (there are exceptions of course). That means, for complete healing to take place this combination treatment, still in it’s very primitive stage of development, may have the potential to replace expensive synthetic drugs that carry complex unexplained side effects. The procedure takes our body’s natural healing agents — stem cells from body fat and PRP from blood — and then inject it inside knee or other joints (or other areas where they are insufficient) for regeneration.
Isn’t that like the most wonderful thing ever?
Whether it’s cartilage cell, or a bone cell, or a collagen cell for ligaments and tendons that needs to be healed, all you need is a same-day procedure by a local, but specialized doctor, using the natural ingredients of the body.
I believe this special combo is a huge win for Platelet-Rich Plasma.
The Challenges For Growing Adoption Of This Treatment
We know Platelet-Rich Plasma has safe, yet high-speed recovery potential with it’s multiple growth factors. And it is effective in regenerative healing of cartilage injuries – the most toughest injuries to heal – as well as Osteoarthritis. However the challenges are Platelet Quality. We need to somehow ensure the Platelet-Rich Plasma quality is uniform. Currently it varies from two to several fold above baseline concentration based on donor’s physical condition.
Next we need to identify the exact PRP growth factors that promote ADSC proliferation. Scientists believe growth factors such as basic fibroblast growth factor (bFGF), epidermal growth factor, and platelet-derived growth factor stimulate stem cell proliferation while some growth factors under certain conditions are known to inhibit the process.
The percentage of PRP matters too. 5 percent, 10 percent, 15 percent and 20 percent Platelet-Rich Plasma in ADSC are tested by scientists.
The Only Treatment In Modern Medicine For Cartilage Regeneration
The bottom line is that Stem Cell Platelet-Rich Plasma or ADSC + PRP procedure is the only treatment in modern medicine that has showed cartilage regeneration. So it’s too important to ignore. And it could one of greatest advances that science has brought to the millions of people suffering from serious pain in their joints, knee and spine as well people suffering from all kinds of tendon diseases and injuries.
- Published in Blog
How Foot and Ankle Surgeons Can Benefit From PRP
Since it is a new science, many people are skeptical about Platelet-Rich Plasma, otherwise known as PRP. There are some studies out there that state that PRP work no better than a similarly administered placebo, but there are many other studies and doctors that claim that PRP works and works well. This also works well at a much lower cost and less side effects, than traditional medicine.
One branch where the skepticism is loud and clear is podiatry, which deals with feet and ankles. Trying to combat this skepticism can help many surgeons to lower complication rates, improve patient satisfaction, and have better outcomes. For instance, here is a list of cases where PRP has been effective for the feet and ankles.
- Plantar Fasciitis
PRP has become rather common as a treatment for Plantar Fasciitis, with many studies to prove the efficacy of this treatment. For instance, Dr. Daanial Kassicieh or Sarasota Neurology claims that PRP is one of the most effective treatments for this condition, and that PRP is actually fully cure it. Many of his patients have avoided surgery just by utilizing PRP therapy.
This is done with no down time, no rehabilitation, and no side effects. This woud explain why plantar fasciitis is the 5th popular medical condition treated by PRP. This can be explained by over 3 million people that are diagnosed with this and no other treatment really works for it, besides, in fact, PRP.
- Archilles Tendonitis
This is another condition that can be fairly hard to treat, and gets worse over time unless healed. Many surgical approaches are often trickey and generally do not end up with good results. Because of this, the main treatment option is simply to give patients corticosteroids to reduce the pain, but really nothing else to treat the symptoms.
However, there have been many studies done that have shown that PRP is a lot more effective, including that from the European Foot and Ankle Society. This means that PRP is safer and more effective alternative than any other treatments available.
- Diabetic Foot Ulcers
Diabetic foot ulcers can be troublesome, especially when they do not heal or heal properly. Over 2.5 million Americans with diabetes who suffer from these ulcers. About 11% of these cases may need amputation of their affected limb. However, some studies have noted that just one injection of PRP and a topical solution bi-weekly started to heal the ulcers in just 8 weeks. Topical PRP also has been shown to work better than anti-septic creams as well.
- Regenerating Bones
Bone regeneration is most commonly needed in food and ankle area. Although mechanical stabilization works best, the utilization of PRP has been surprising. PRP helps with healing bones and soft tissue at the damage site. According to a recent systematic review of 64 articles, the conclusion was to include more PRP therapy into the healing of foot and ankle bones.
The science behind this is solid, for bone or tissue to form, three things are needed in the area:
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- A scaffold for the growth to take place
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- Biological stimulants to signal proteins
- Stem cells that provide bone building potential
All three of these are crucial for bone formation.. PRP can provide at least two of these, so there is no reason to ignore it when it comes to bone regeneration.
- Ankle Sprains
This is an incredibly common condition, and can be effectively treated by using PRP therapy. In one randomized controlled trial, researchers studied the effects of PRP injections on athletes with ankle sprains. This study showed that not only did PRP reduce the healing time by 20 days, but that they also experienced much less pain. This can reduce the recovery period from 6 weeks, for just about 2 or 3 weeks.
Immobilization is Vital
When it comes to foot and ankle related injuries, one thing that really cannot be avoided in rest and rehabilitation. This is true regardless of whether PRP is administered. Because of this, many of the studies that shows PRP to be ineffective often don’t use rest and rehabilitation, and that alone can be an issue.
PRP is in no way a magic pill. All foot injuries need rest and rehabilitation in order to properly heal. With these two combined, it can drastically reduce healing times.
How can Foot and Ankle Surgeons Benefit?
Using PRP in foot and ankle injuries is not going anywhere, so utilizing it would be the best way to go. Test it out with your patients, and try using platelet-rich plasma therapy instead of simply prescribing pills or doing costly surgeries. Your patients will thank you in the end.
- Published in Blog
Stem Cell Research Goes Crimson: International Leader in Stem Cell Research Named New Dean of Harvard Medical School
George Q. Daley, MD, PhD, Harvard Medical School’s newly appointed dean, led dozens of international colleagues in developing ethical guidelines for stem cell research. On March 9, 2009, President Barack H. Obama issued Executive Order 13505: Removing Barriers to Responsible Scientific Research involving Human Stem Cells, stating that the Secretary of Health and Human Services, through the Director of the National Institute of Health (NIH), may support and conduct responsible, scientifically worthy human stem cell research, including human embryonic stem cell (hESC) research, to the extent permitted by law. Internal NIH policies and procedures, consistent with Executive Order 13505 and these Guidelines, govern the conduct of intramural NIH stem cell research.
A prominent stem cell researcher has been named the new dean of Harvard Medical School, the university announced August 9th
George Q. Daley, MD, PhD, who led dozens of international colleagues to unite around ethical guidelines for stem cell research, is
taking on a new challenge—unifying the powerful hospitals that train Harvard’s medical students.
Daley will assume the position effective Jan. 1, 2017, succeeding Jeffrey Flier, MD, who stepped down July 31st. Barbara McNeil, MD, the founding head of the Department of Health Care Policy at Harvard Medical School, is filling the position in the interim.
The internationally recognized leader in stem cell science and cancer biology and a longtime member of the Harvard Medical School (HMS) faculty whose work includes the fields of basic science and clinical medicine, Daley was the driving force behind creating international guidelines around first, human embryonic stem cell research, and then the clinical application of stem cells, according to Nancy Witty, CEO of the International Society for Stem Cell Research (ISSCR).
Daley, who cofounded the organization, counseled two dozen scientists through the sensitive ethical discussions involved in establishing stem cell research guidelines, utilized additional input from 60 groups around the world to construct the guidelines which were first published by the National Institute of Health in 2009.
“That’s a very difficult task,” Witty said. “It takes a tremendous amount of diplomacy.” 
Daley is working to adapt insights in stem cell research to improved therapies for genetic and malignant diseases. Important research contributions from his laboratory at Harvard-affiliated Boston Children’s Hospital include the development of customized stem cells to treat genetic immune deficiency in a mouse model (in collaboration with Rudolf Jaenisch, a Professor of Biology at MIT); the differentiation of germ cells from embryonic stem cells (cited as a “Top Ten Breakthrough” by Science magazine in 2003), and the generation of disease-specific pluripotent stem cells by direct reprogramming of human fibroblasts (cited in the “Breakthrough of the Year” issue of Science magazine in 2008).
As a graduate student working with Nobel laureate Dr. David Baltimore, Daley demonstrated that the BCR/ABL oncogene induces chronic myeloid leukemia (CML) in a mouse model, which validated BCR/ABL as a target for drug blockade and encouraged the development of imatinib (GleevecTM; Novartis), a revolutionary magic-bullet chemotherapy that induces remissions in virtually every CML patient. Dr. Daley’s recent studies have clarified mechanisms of Gleevec resistance and informed novel combination chemotherapeutic regimens.
Daley has spent his entire career in Cambridge and Boston, earning a medical degree from Harvard and a PhD in biology from MIT. As Dean of Harvard Med School, Daley’s achievements in stem cell research is expected to shine a distinguished light on the stem cell industry.
Although the position of dean of Harvard Med may be one of the most prominent roles in medicine, the position is not as powerful it might seem: Harvard Med does not directly oversee any hospitals. Instead it relies on 15 affiliated hospitals and clinical sites, which have historically operated as separate, competitive bailiwicks, to train its students and postdoctoral fellows, and support its researchers. Only 151 of the nearly 12,000 people who call themselves Harvard Medical faculty actually work directly for Harvard in its 10 basic science departments.
Daley sees his new position as a congregator who “builds bridges among the institutions” —heavyweight research institutions such as Brigham and Women’s, Massachusetts General, and Boston Children’s hospitals. Persuasiveness, rather than power, is all that Daley says is needed to achieve an alliance.
Daley’s predecessor, Flier, says he spent a full 30 percent to 40 percent of his time as dean trying to build relationships with and coordinate Harvard’s affiliated hospitals and clinics, a challenge Daley says he’s up to. He has a head start in building those relationships through the many positions he has held around Boston’s biomedical community, including chief resident at Mass. General
“My vision is one of increasing connectivity across the community,” Daley says.
Currently a professor of biological chemistry and molecular pharmacology at Harvard Medical School and director of the stem cell transplantation program at Boston Children’s and Dana-Farber Cancer Institute, Daley sees areas of common interest, such as immuno-oncology, which harnesses the body’s own immune system against cancer cells, where the hospitals can work more closely together.
Described by colleagues as a natural leader, Daley recently led an effort to coordinate big-name scientists across several institutions on a collaborative grant to compare two types of stem cells—just one example of how he earned a reputation; he knows how to get different groups talking together in a constructive way.
He also says he wants Harvard Medical’s faculty, students, and staff to reflect the global community the school intends to serve, and that he promotes diversity in hiring for his 30-person lab.
Daley has a keen interest in sickle-cell anemia, which affects people of African descent, including African Americans, and he believes the federal government should invest in a moonshot effort to cure the disease.
Daley plans to continue teaching molecular medicine at Harvard Med after assuming his position as dean. He also plans to spend one day per week in his lab researching blood stem cells.
“It’s important for a dean to remain relevant by continuing to publish papers,” Daley says. “Plus, I just love science.”
Among his priorities is raising money. Despite its worldwide reputation, and its relative influence when it comes to landing federal grants, Harvard Med has seen annual deficits of between $31 million and $45 million for three consecutive years. Suggestions are being made for Harvard to rename its medical school in return for a billion-dollar donation. Daley only says that the idea would be worth considering down the road.
With opportunities for federal grants in decline, Daley says he sees an opportunity to bring in money from corporate partnerships.
For the stem cell research and medical community, Daley’s appointment as dean of Harvard Med is a fitting step toward validating regenerative medicine’s place as an authoritative leader in the future of medicine—one that’s been a long time coming.
Learn more about Dr. Daley here.
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Insulin-producing Stem Cells Grown in the Lab Mark a New Era in Stem Cell Therapies for Diabetes
A new discovery by researchers on how to activate lab-grown beta cells to mature into functioning cells that produce and release insulin in response to glucose take a significant step toward a cell therapy treatment for diabetes.
Difficulties in manipulating beta cells derived from human stem cells to mature beyond the precursor stage into fully functioning insulin releasers has been an on-going challenge for researchers..
However, researchers from the Salk Institute for Biological Studies and a team of researchers have achieved this goal with lab-grown beta cells by activating a protein called estrogen-related receptor γ (ERRγ). Their study findings were recently published in the journal Cell Metabolism.
Self-renewing capacity of human pluripotent stem cells (hPSCs)
Ronald Evans, senior author of the study, titled, “ERRγ Is required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells,”
says the self-renewing capacity of human pluripotent stem cells (hPSCs) and their ability to differentiate into most cell types—from neurons to skin cells, to muscles cells and insulin-producing pancreatic beta cells—has inspired many research teams to find ways to make glucose-responsive beta cells in the lab.
Evans and his research team discovered the answer to the insulin-releasing cell conundrum, and summed it up thusly:
“In a dish, with this one switch, it’s possible to produce a functional human beta cell that’s responding almost as well as the natural thing.”
Evans, a molecular biologist at the Salk Institute, says that to create the different types of cells in the lab, researchers coax the pluripotent stem cells (hPSCs) down the various branching paths that fetal cells normally travel in order to differentiate into the various cell types. However, he explains there are many developmental points in this process, and in the case of lab-grown pancreatic beta cells, research kept getting stuck at an early stage.
Adult beta cells have more ERRγ protein for a very energy-intensive process
In order to determine what might trigger the next step in getting the cells to mature, the researchers compared transcriptomes of adult and fetal beta cells. The transcriptome contains, among other things, the full catalog of molecules that switch genes on and off in the genome, which led them to discover that the nuclear receptor protein ERRγ was more abundant in adult beta cells. The team was already familiar with the protein’s role in muscle cells and had studied its ability to enhance endurance running.
Evans says that in muscles, protein promotes greater growth of mitochondria—the power generators inside cells that accelerate the burning of sugars and fats to make energy.
“It was a little bit of a surprise to see that beta cells produce a high level of this regulator,” Evans says. “But beta cells have to release massive amounts of insulin quickly to control sugar levels. It’s a very energy-intensive process.”
The research team then decided to run some tests to look more closely at what role ERRγ might play in insulin-producing beta cells.
A new era in creating functional, insulin-producing beta cells
After they genetically engineering a deficiency of ERRy in mice, the researchers found the animals’ beta cells did not produce insulin in response to spikes in blood sugar.
Next they tried to get beta cells made from hPSCs to produce more ERRγ, and it worked! The cells in culture began to respond to glucose and release insulin.
Finally, the team transplanted the lab-grown insulin-producing beta cells into diabetic mice and found that from day one, the cells produced insulin in response to glucose spikes in the animals’ blood.
Evans and the research team were justifiably excited by the results. It appears that just switching on the ERRγ protein is sufficient to get the lab-grown beta cells to mature and produce insulin in response to glucose – both in cultures and in live animals.
Speculating on the implications of their findings, Evans suggests that when a fetus is developing, because it gets a steady supply of glucose from the mother, it does not need to produce insulin to regulate its blood sugar, so the switch is inactive. But, when the baby is born and takes its first breath and takes in oxygen, this activates the switch.
Previous lab attempts to produce beta cells got stuck at the fetal stage. The Salk Institute researchers discovered how to take it to the adult stage, using the same protein that is switched on in nature.
“I believe this work transitions us to a new era in creating functional beta cells at will,” Evans says.
He and his research team now plan to examine how the switch might work in more complex models of diabetes treatments.
The Salk Institute study proceeds another study Medical News Today in which researchers generated mini-stomachs that produce insulin when transplanted into mice.
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Regenerating and Restoring Brain Cells in the Aged With Donor Neural Stem Cells
The human brain, as it turns out, is far more malleable than we once thought. Even adult brains. But they are subject to age-related diseases and disorders, such as dementia and diminished cognitive function.
There is hope that medical science may be able to replace brain cells and restore memory in aging patients thanks to new discoveries in neural stem cell techniques. Researchers at the Texas A&M Health Science Center College of Medicine recently published new findings in the journal Stem Cells Translational Medicine that suggests a new technique for preparing donor neural stem cells and grafting them into an aged brain can regenerate tissue that has succumbed to structural, chemical, and functional changes, as well as a host of neurocognitive changes that can be attributed to aging.
The study, titled “Grafted Subventricular Zone Neural Stem Cells Display Robust Engraftment and Similar Differentiation Properties and Form New Neurogenic Niches in the Young and Aged Hippocampus,” was led by Ashok K. Shetty, Ph.D., a professor in the Department of Molecular and Cellular Medicine. associate director of the Institute for Regenerative Medicine, and research career scientist at the Central Texas Veterans Health Care System.
Shetty and his team at Texas A&M focus on the aged hippocampus, which plays an important role in making new memories and connecting them to emotions. They took healthy donor neural stem cells and implanted them into the hippocampus of an animal model, essentially enabling them to regenerate tissue.
The hippocampus in the aging brain
“We chose the hippocampu
s because it’s so important in learning, memory and mood function,” Shetty said. “We’re interested in understanding aging in the brain, especially in the hippocampus, which seems particularly vulnerable to age-related changes.”
The volume of this part of the brain seems to decrease during the aging process, and this decrease may be related to age-related decline in neurogenesis (production of new neurons) and the memory deficits some people experience as they grow older.
The aged hippocampus also exhibits signs of age-related degenerative changes in the brain, such chronic low-grade inflammation and increased reactive oxygen species.
Bharathi Hattiangady, assistant professor at the Texas A&M College of Medicine and co-first author of the study said his team was excited to discover that the aged hippocampus can accept grafted neural stem cells as well as the young hippocampus does, a discovery that has significant implications for treating age-related neurodegenerative disorders.
“It’s interesting that even neural stem cell niches can be formed in the aged hippocampus,” Hattiangady says.
Shetty’s previous research focused on the benefits of resveratrol (an antioxidant that is famously found in red wine and the skin of red grapes, as well as in peanuts and some berries) to the hippocampus. Although the results indicated important benefits for preventing memory loss in aging brains, his newest work demonstrates a way to affect the function of the hippocampus more directly.
Neural stem cell grafting
In this new study, the team found that the neural stem cells engrafted well onto the hippocampus in the young animal models (which was expected) as well as the older ones that would be, in human terms, about 70 years old. Not only did these implanted cells survive, they divided several times to make new cells.
“They had at least three divisions after transplantation,” Shetty said. “So the total yield of graft-derived neurons and glia (a type of brain cell that supports neurons) were much higher than the number of implanted cells, and we found that in both the young and aged hippocampus, without much difference between the two.”
In both old and young brains, a small percentage of the grafted cells retained their stemness feature—an essential characteristic of a stem cell that distinguishes it from ordinary cells—and continuously produced new neurons. This is called creating a new ‘niche’ of neural stem cells, and these niches seemed to be functioning well. They were still producing new neurons at least three months after implantation, and these neurons are capable of migrating to different parts of the brain.
Past efforts to rejuvenate brains using fetal neurons in this way weren’t nearly as successful. Immature cells, such as neural stem cells, seem to do a better job because they can tolerate the hypoxia (lack of oxygen) and trauma of the brain grafting procedure better than post-mitotic or relatively mature neurons. When researchers tried in the past to implant these partially differentiated cells into the aged hippocampus, they didn’t do nearly as well. The research team used a new technique of preparing the donor neural stem cells, which Shetty says is why this result has never been seen before.
Brain marrow
The researchers used donor cells from the sub-ventricular zone of the brain, an area called the “brain marrow,” because it is analogous to bone marrow in that it holds a number of neural stem cells that persist throughout life. These neural stem cells continuously produce new neurons that migrate to the olfactory system. They also respond to injury signals in conditions such as stroke and traumatic brain injury and replace some of the lost cerebral cortical neurons.
Induced pluripotent cells from skin
Even a small stem cell sample is good enough to expand in culture, so the procedure isn’t terribly invasive. However, in the future, a single skin cell might suffice, as similar neural stem cells can be obtained in large numbers from skin. In fact, it is well known in medical science that a number of cells in the body—including skin cells—can be modified in such a way to create induced pluripotent stem cells.
With these cells, scientists can do any number of things, such as making neural stem cells that will make both more of themselves, and make new neurons. It’s not necessary to get the cells from the brain, just take a skin biopsy and push them into neural stem cells, according to Shetty.
Although the way the grafted cells thrived is promising, there is still a good deal of work to be done to determine if the extra grey matter actually improves cognition.
“Next, we want to test what impact, if any, the implanted cells have on behavior and determine if implanting neural stem cells can actually reverse age-related learning and memory deficits,” Shetty said. “That’s an area that we’d like to study in the future.
“I’m always interested in ways to rejuvenate the aged brain to promote successful aging, which we see when elderly persons exhibit normal cognitive function and the ability to make memories.”
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Stem Cell-stimulating Fillings Help Regenerate Teeth Damaged by Disease, Decay
Researchers from Harvard University and the University of Nottingham have developed a new filling that stimulates stem cells in dental pulp to regenerate and even regrow teeth damaged by disease and decay. According to Newsweek Magazine, the discovery earned a prize from the Royal Society of Chemistry after judges described it as a “new paradigm for dental treatments.”
The treatment is believed to potentially eliminate the need for root canals.
Filling materials stimulate stem cells to encourage dentin growth
The filling works by stimulating the body’s natural store of stem cells to encourage the growth of dentin—the bony material that makes up the majority of the tooth—allowing patients to effectively regrow teeth that are damaged through dental disease. The filling’s synthetic biomaterials are used similarly to dental fillings, placed in direct contact with pulp tissue in the damaged tooth. This stimulates the tissue’s native stem cell population to repair and regenerate pulp tissue and the surrounding dentin.
The discovery is a significant step forward from current methods to treat cavities, which involve drilling out decay and putting in a filling made of gold; porcelain; silver amalgam (which consists of mercury mixed with silver, tin, zinc, and copper); or tooth-colored plastic or composite resin. When these fillings fail to halt the tooth’s decay, a root canal is needed to remove the pulp of the tooth, damaging it even further.
Alternative to traditional fillings in teeth
Researchers hope to develop the technique with industry partners in order to make it available for dental patients as an alternative to traditional fillings. Marie Curie research fellow Adam Celiz says that existing dental fillings are toxic to cells and are therefore incompatible with pulp tissue inside the tooth.
“In cases of dental pulp disease and injury, a root canal is typically performed to remove the infected tissues,” Celiz says.
The promise of using therapeutic biomaterials to bring stem cell medicine to restorative dentistry could significantly impact millions of dental patients each year. In fact, the approach is so promising it won second prize in the materials category of the Royal Society of Chemistry’s Emerging Technology Competition for 2016.
Competition entries were judged on the degree of innovation of the technology, its potential impact, and the quality of the science behind it. Increasing innovation in the chemical sciences is a key element of the Royal Society of Chemistry’s industry strategy.
Effective and practical approach to regenerating teeth
The stem cell stimulating filling promises to change the future of dentistry, according to David Mooney, Pinkas Family Professor of Bioengineering at the John Paulson School of Engineering and Applied Sciences at Harvard and the Wyss Institute for Biologically Inspired Engineering.
“’These materials may provide an effective and practical approach to allow a patient to regenerate components of their own teeth,’ Pinkas says.
Stem cells can induce regenerative, self-healing qualities in any tissue found in the body and can, as a result, provide unlimited potential for medical applications. Current studies are underway worldwide to learn how stem cells may be used to prevent or cure diseases and injuries such as Parkinson’s disease, type 1 diabetes, heart disease, spinal cord injury, muscular dystrophy, Alzheimer’s disease, strokes, burns, osteoarthritis, vision and hearing loss, and more. Stem cells may also be used to replace or repair tissue damaged by disease or injury.
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