Background: Platelet-rich plasma (PRP) is a minimally invasive treatment option to reduce pain and promote tissue healing. At the time this study was performed, there was limited published literature analyzing outcomes for patients treated with PRP for hip osteoarthritis.
Methods: Thirty-six patients aged 49-85 (66.0 ± 12.1) years with chronic hip pain who met inclusion criteria underwent image-guided intra-articular hip PRP injection. Outcomes were measured at baseline, two weeks, three months, and up to six months using the visual analog scale (VAS) for pain and the Hip Disability and Osteoarthritis Outcome Score (HOOS). The proportion of responders, as defined by a ≥50% reduction in VAS pain score, was assessed at three and six months.
Results: At two weeks, there was a significant improvement (P < 0.05) of function in two HOOS subscales: Symptoms and Activities of Daily Living. There was a significant improvement in all HOOS categories at six months. A significant improvement in VAS was observed at six months (baseline VAS = 6.9 ± 0.7 &→ 4.3 ± 1.8, 95% confidence interval = 2.0 to 3.2, P < 0.05). Sixty-seven percent (24/36) of the patients reported a ≥50% improvement in pain at three months; 58% (21/36) reported a ≥50% improvement in pain at six months. Stratification by Kellgren-Lawrence grades revealed that 86% and 82% of the KL grades 1 and 2 were responders at six months, respectively.
Conclusions: In patients with mild/moderate hip osteoarthritis, PRP may provide pain relief and functional improvement for up to six months.
Keywords: Hip Osteoarthritis; Osteoarthritis; Platelet-Rich Plasma; Regenerative Medicine.
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Stem cells are attracting attention as a key element in future medicine, satisfying the desire to live a healthier life with the possibility that they can regenerate tissue damaged or degenerated by disease or aging. Stem cells are defined as undifferentiated cells that have the ability to replicate and differentiate themselves into various tissues cells. Stem cells, commonly encountered in clinical or preclinical stages, are largely classified into embryonic, adult, and induced pluripotent stem cells. Recently, stem cell transplantation has been frequently applied to the treatment of pain as an alternative or promising approach for the treatment of severe osteoarthritis, neuropathic pain, and intractable musculoskeletal pain which do not respond to conventional medicine. The main idea of applying stem cells to neuropathic pain is based on the ability of stem cells to release neurotrophic factors, along with providing a cellular source for replacing the injured neural cells, making them ideal candidates for modulating and possibly reversing intractable neuropathic pain. Even though various differentiation capacities of stem cells are reported, there is not enough knowledge and technique to control the differentiation into desired tissues in vivo. Even though the use of stem cells is still in the very early stages of clinical use and raises complicated ethical problems, the future of stem cells therapies is very bright with the help of accumulating evidence and technology.
One of the major achievements in the development in modern medicine is the discovery of stem cells. Stem cells are attracting attention as a key element in future medicine, satisfying the desire to live a healthier life with the possibility that they can regenerate tissue damaged or degenerated by disease or aging. Development of cell therapy and regenerative medicine using stem cells is expanding the medical industry and businesses as well as increasing the understanding of the nature of the cell itself. Stem cell medicine brings a new paradigm to modern medicine which has relied heavily on medicine or surgery.
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Purpose of Review
The purpose of this review is to update the reader on the current applications of platelet-rich plasma (PRP) in the treatment of knee osteoarthritis (KOA). This review will focus on PRP’s effect on the osteoarthritic joint, how PRP compares to traditional treatments of KOA, and provide clinical feedback on the use of PRP in an orthopedic and sports medicine practice.
Recent research into the applications of PRP for KOA has further indicated both the efficacy and safety of PRP treatment. Although research has shown a tendency toward better efficacy at earlier stages of osteoarthritis (OA), evidence exists to indicate positive effects at all stages of OA.
In summary, since KOA is an extremely prevalent condition that can be a challenge to treat, it is imperative that safe and effective nonoperative treatment methods be available to individuals that are suffering from this condition.
Osteoarthritis (OA) is the most common form of arthritis, affecting more than 30 million adults in the USA, or approximately 23% of the adult population [1, 2]. In 2013, OA was the second most expensive condition treated in US hospitals, accounting for more than US$16.5 billion spent in hospital cost . The knee joint is the most common joint affected by osteoarthritis [4, 5], making osteoarthritis of the knee (KOA) a considerable health concern.
Treatment of KOA is difficult due to the avascular and aneural nature of adult knee cartilage, which results in a low regenerative capacity, and thus limited healing potential for the joint [6, 7]. The exact mechanism and pathophysiology of KOA is still unclear; however, it is clear that OA is the result of a long chain of events rather than just being “wear and tear” of the joint [7, 8]. While loss and breakdown of articular cartilage is the endpoint of this process, the entire process and progression of OA involves a combination of mechanical, cellular, and biochemical processes . The joint destruction that occurs in the early stages of OA leads to an imbalance of the inflammatory mediators of the joint, resulting in further cartilage degeneration, degeneration of the extracellular matrix, systemic inflammation, chondrocyte apoptosis, osteophyte formation, and bone remodeling [9–12].
As of today, there are no definitive curative therapies for OA, meaning that treatment focuses on ways to treat patient symptoms and slow the progression of the degenerative process . Thus, treatment goals for OA focus on activity modification, relieving pain and stiffness, improving joint function, improving quality of life, correcting potential deformities in the joint, and delaying or avoiding the need for total knee arthroplasty (TKA) [14–16]. While TKA is effective in treating late stage KOA, it is estimated that 10- and 20-year survivorship rates are approximately 95 and 85% [17, 18]. Furthermore, it is estimated that up to one third of TKA recipients experience chronic pain postoperatively [19, 20], resulting in a reported poor outcome rate of 20% . Therefore, it is imperative that KOA be identified and treated in the stages before TKA is the only option.
The current nonpharmacological treatments for patients with symptomatic KOA begin with patient education and self-management of risk factors for OA, exercise, weight loss, physical therapy, and the use of orthotics [21, 22]. Pharmacological options include topical anti-inflammatory gels; oral non-steroid anti-inflammatory drugs (NSAIDs); oral supplements, such as glucosamine and chondroitin sulfate; and injection therapies [21, 22]. The four main injection therapies currently utilized are corticosteroids, viscosupplementation with hyaluronic acid (HA), platelet-rich plasma (PRP), and autologous mesenchymal stem cells (MSCs) . For patients that do not respond to the nonpharmacological and pharmacological treatment methods, surgical options including arthroscopic surgery, osteotomy, and knee arthroplasty can be considered.
PRP is an autologous blood product that is created by first obtaining a small amount of blood through peripheral venesection, concentrating that blood sample through centrifugation, and then administering the concentrated plasma product back into the patient via an intra-articular (IA) injection . The concentrated plasma product contains a high concentration of platelets (at least two times greater than whole blood), which have critical roles in maintaining tissue homeostasis and regulating the inflammation and coagulation responses of the body [25, 26], such as chondrocyte apoptosis inhibition, bone and vessel remodeling, inflammation modulation, and collagen synthesis . Because of these properties, PRP has emerged as a viable treatment method for individuals suffering from KOA. The purpose of this article is to update the reader on the current information that is available regarding PRP, including the basic science involved with PRP’s effect on OA, and how PRP compares to other treatment modalities.
How is PRP made?
Not all PRP is the same, and preparation methods lack a standardized protocol . After a blood sample is collected from the patient, that sample is run through a centrifuge, which separates the samples cellular products based on different specific gravity . One primary difference in PRP systems involves this centrifugation, which can involve either one or two spins through the system. Systems utilizing one spin, such as autologous conditioned plasma (ACP) (Arthrex, Naples, Florida) and Cascade PRP (MTF Biologics, Edison, New Jersey), separate the sample into a plasma layer containing platelets and a separate layer containing red and white blood cells (Fig. ). These one-spin systems typically result in platelet concentrations that are 1 to 3 times greater than whole blood; furthermore, the one-spin systems are efficient because they typically have short preparation times (under 10 min), which can remove the need for an anti-coagulant to be added to the preparation to prevent clotting. PRP systems that utilize two spins, like the Biomet GPS (Zimmer Biomet, Warsaw, Indiana) and MagellanPRP (Isto Biologics, Hopkinton, Massachusetts), focus on separating the blood sample into three layers: a layer with red blood cells, a buffy coat layer containing platelets and white blood cells, and a platelet depleted plasma layer. The focus of the two-spin systems is to concentrate the buffy coat layer, which contains higher platelet concentrations (> 5× whole blood) than the one-spin systems. Due to the nature of the two-spin cycle, the preparation times for these products are longer, typically 30 min or greater, often requiring the use of an anti-coagulant to prevent the sample from clotting during the preparation process.
How does PRP work?
Platelets and growth factors
Platelets are anucleated cells that are derived from megakaryocytes . When platelets are activated, growth factors contained in the α-granules of the platelet respond in a localized, site specific manner . This process is quick, with almost 70% of the growth factors contained within the α-granule being secreted in the first 10 min . These growth factors, along with coagulation factors, cytokines, chemokines, and other proteins stored within the platelet, have been shown to stimulate chondrocyte and chondrogenic MSC proliferation, promote chondrocyte cartilaginous matrix secretion, and diminish the catabolic effects of pro-inflammatory cytokines [32–36].
The major growth factors and growth factor families from PRP that are involved with OA treatment include tissue growth factor-β (TGF-β), insulin-like growth factor 1 (IGF-1), bone morphogenetic proteins (BMP), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), fibroblast growth factor (FGF), and hepatocyte growth factor (HGF). TGF-β has been identified as one of the most important factors in cartilage regeneration because of its role in the proliferation and differentiation of chondrocytes [37, 38]. TGF-β induces chondrogenic differentiation of MSCs [39, 40] and also antagonizes the suppressive effects of IL-1, a pro-inflammatory cytokine responsible for stimulating catabolic factors, and predisposing intracapsular structures for further degradation [26, 41]. IGF-1 is an important component in cartilage processes, promoting chondrocyte mitosis and extracellular matrix synthesis . BMP assists in chondrocyte migration , and FGF has a major role in cartilage repair [4, 32]. PDGF assists in the regeneration of articular cartilage by increasing chondrocyte proliferation and plays a role in all cells of mesenchymal origin [40, 43, 44]. VEGF effects vascular structure formation and regeneration, and has been shown to be essential in reestablishing nutrient flow [26, 45].
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By Mark D. Coggins, PharmD, BCGP, FASCP
Today’s Geriatric Medicine
Vol. 13 No. 2 P. 14
Neuropathic pain (NP) is a common and difficult-to-treat symptom of nerve damage. Patients suffering from this chronic pain condition are at risk of incurring increased health care expenditures and experiencing significant reductions in quality of life. Patients with NP often report job loss or significant changes to their careers, limited social interactions, decreased quality time with family, and feelings of hopelessness and depression due to their disease.1 Furthermore, current treatment approaches for NP, which focus on symptom management, are frequently inadequate.
Advancements in stem cell research are promising and may lead to new treatment modalities for NP.
NP symptoms are frequently described as burning, electric, tingling, and shooting. Hallmarks of NP include allodynia (pain resulting from a stimulus that normally does not elicit a painful response) and hyperalgesia (greater pain than normally would be expected from a painful stimulus).
Symptoms of neuropathy range from mild to disabling and may include a loss of reflexes, problems feeling pain, changes in temperature, numbness and tingling, and pain that is often worse at night.2 Symptoms are often sudden and unpredictable and follow different patterns that vary over a period of days, weeks, or years.1,2
Approximately 30% of cases of neuropathy are the result of diabetes, and about 60% to 70% of people with diabetes have mild to severe forms of damage to sensory, motor, and autonomic nerves that cause such symptoms as numb, tingling, or burning feet; one-sided bands of pain; and numbness and weakness on the trunk or pelvis.2
More than 100 types of neuropathy have been identified, each with its own characteristic set of symptoms and prognosis.2 Causes of NP include chronic medical conditions (eg, diabetes), physical injury (eg, fractures, spinal cord injury), alcoholism, amputation (resulting in phantom pain), use of some chemotherapeutic agents (eg, Cisplatin, Vincristine), radiation therapy, trigeminal neuralgia, infections (eg, shingles, HIV), central nervous system disorders (eg, Parkinson’s disease, multiple sclerosis), kidney and liver disorders, nutritional deficiencies and imbalances (eg, B12 deficiency, excess B6), autoimmune disorders (eg, Guillain-Barré syndrome, rheumatoid arthritis, lupus), and some cancers/tumors. In some cases, NP is idiopathic.1-3
Existing treatments and approaches to NP focus on palliative management of symptoms. There are no drugs available that can restore nerve function. The management of NP is challenging, as this type of pain is frequently refractory to existing treatments.4 It’s been reported that in clinical trials, no more than one-half of patients with NP experience clinically meaningful pain relief.3 Similarly, several studies of individuals with NP living in the community have shown patients on average experience pain of moderate severity despite taking prescribed medications for their pain.4
Medications commonly used include analgesics such as opioids (eg morphine, methadone, tramadol) and over-the-counter pain medications (eg, NSAIDs), antidepressants (eg, amitriptyline, nortriptyline, venlafaxine, duloxetine), anticonvulsants (eg, gabapentin, pregabalin), muscle relaxers (eg, cyclobenzaprine), and topical agents such as lidocaine creams or patches. In addition to medications, nondrug therapies and lifestyle modifications such as exercise, physical therapy, acupuncture, and limiting physical activity may also be utilized to manage symptoms.
Stem cell transplantation has the potential to repair, restore, replace, and regenerate cells, and may be able to treat a number of different medical conditions and diseases. Research increasingly is evaluating the use of stem cells for the treatment of NP. Unlike existing treatments that focus only on symptom management, stem cell transplantation may be able to replace damaged nerve cells, possibly offering a cure.
Stem cells, sometimes referred to as “master cells,” are the foundation for every organ and tissue in the human body. These include embryonic stem cells and tissue-specific adult stem cells. Due to the ethical issues associated with the use of embryonic stem cells, most of the research being done involves the use of adult stem cells. Regardless of the type used, stem cells have the unique ability to self-renew (make copies of themselves) and differentiate (develop into more specialized cells).
Stem cells can be transplanted in a number of different ways, including local delivery, intrathecal or intracerebroventricular administration, IV injection, intranasal delivery, and endogenous mobilization by drugs for chronic intractable pain treatment.
In early research, it had been thought that stem cells would need to be administered intrathecally to reduce pain as IV administration appeared to result in the stem cells becoming trapped in the lungs, preventing their migration to the site of injury. However, more recent evidence suggests this lung trapping effect may be transient.
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Neuropathic pain is a chronic condition that is heterogeneous in nature and has different causes. Different from and more burdensome than nociceptive pain, neuropathic pain more severely affects people’s quality of life. Understanding the various mechanisms of the onset and progression of neuropathic pain is important in the development of an effective treatment. Research is being done to replace current pharmacological treatments with cellular therapies that will have longer lasting effects. Stem cells present an exciting potential therapy for neuropathic pain. In this review, we describe the neuroprotective effects of stem cells along with special emphasis on the current translational research using stem cells to treat neuropathic pain.
Keywords: Adult stem cells, Cellular therapy, Neuropathy, Stem cell-microenvironment interactions
In 2008, the International Association for the Study of Pain formed a special interest group to redefine neuropathic pain as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system” [1
]. Neuropathy is heterogeneous in nature; however, neuropathic lesions may be characterized into four broad categories: focal or multifocal lesions of the peripheral nervous system, generalized lesions of the peripheral nervous system (polyneuropathies), lesions of the central nervous system, and complex neuropathic disorders () [2
Although categorized as chronic pain, neuropathic pain is regarded as more severe than other types of chronic pain. This is due to the increased disruption of both physical and mental quality of life when compared with other chronic pain syndromes. People with chronic neuropathic pain report a higher severity of pain and significantly worse scores for all interference items of the Brief Pain Inventory than non-neuropathic chronic pain patients. Also, those with chronic neuropathic pain report mean scores for the Neuropathic Pain Scale significantly higher than those with non-neuropathic chronic pain, even after adjusting for pain severity, age, and sex .
Types of Pain
Neuropathic pain presents itself in many different forms. Spontaneous sensations include paroxysmal pain (shooting pain that lasts several seconds) and superficial pain (an ongoing, burning sensation). Evoked pain includes mechanical allodynia (pain caused by normally nonpainful pressure), heat or cold allodynia (pain caused by normally nonpainful hot/cold stimuli), hyperalgesia (increased sensitivity to a normally painful stimulus), and temporal summation (increasing pain sensation from repetitive application of identical stimuli) .
Neuropathic pain differs from nociceptive pain in that nociceptive pain is caused by tissue damage, whereas neuropathic pain is produced by nerve damage. In particular, pain signaling areas of the peripheral or central nervous system are injured, causing neuropathic pain. In nociceptive pain, tissue damage causes the generation of prostaglandins that cause vasodilation, increased blood flow, inflammatory exudates, and the sensitization of nociceptive nerve endings. In neuropathic pain, signals are generated by the injured nerve, sent to the brain, and interpreted as pain. Nociceptive pain is proportional to the intensity of the stimulus; neuropathic pain is not—a small stimulus may provoke increased sensations of pain .
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Experts are looking at the potential of stem cell therapy in developing new therapies aimed at conditions that do not respond well to treatment, such as non-small cell lung cancer.
Non-small cell lung cancer (NSCLC) is one of the two main types of lung cancer. Evidence suggests that roughly 80–85%Trusted Source of lung cancer is NSCLC. It occurs when cells that line the lungs grow abnormally.
Lung cancer is one of the most common cancersTrusted Source worldwide and is the leading cause of cancer-related death, representing about 25%Trusted Source of cancer deaths. Most lung cancer-related deaths are due to treatment failure and the spreading of cancer cells to distant sites (metastasis).
Current research proposes that NSCLC’s resistance to treatment and fast progression is due to the presence of specific types of cancer cells, called cancer stem cells (CSCs), which have the ability of normal stem cells, allowing them to divide and proliferate.
Stem cell therapy is a field of regenerative medicine that utilizes people’s own cells to promote healing, repair damaged tissue, and help boost the immune response to fight off cancer cells and infections.
In this article, we look at whether stem cell therapy is a viable treatment for NSCLC along with other new treatment breakthroughs.
Currently, there are limited studies that prove the effectiveness of using stem cell therapy in treating NSCLC, and the majority of these are still under clinical trials. Growing evidence suggests that stem cell therapy may also have some potential to treat other lung conditions, such as chronic obstructive pulmonary disease (COPD).
While a few clinical studies suggest some promise of stem cell therapy in treating NSCLC, more research is necessary due to potential concerns regarding the effectiveness and safety of the therapy. At present, many experts do not recommend this therapy due to the potential risks, lack of proven benefits, and costs.
However, researchers continue to investigate the potential benefits. For example, a 2021 study indicates that mesenchymal stem cells may be able to inhibit NSCLC cells in a lab setting. An animal study also found that giving human-induced neural stem cells intravenously to mice was safe and reduced NSCLC tumor cells by seeking and killing them.
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