Introduction

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 [3]. 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 [9]. 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 [13]. 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% [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) [23]. 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 [24]. 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 [27]. 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 [28]. 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 [29]. 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. 1). 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?