Platelet-rich plasma for regeneration of neural feedback pathways around dental implants: a concise review and outlook on future possibilities

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Maximizing neuroprotection: where do we stand?

Damien P KufflerInstitute of Neurobiology, University of Puerto Rico, San Juan, Puerto RicoAbstract: Brain and spinal cord traumas include blunt and penetrating trauma, disease, and required surgery. Such traumas trigger events such as inflammation, infiltration of inflammatory and other cells, oxidative stress, acidification, excitotoxicity, ischemia, and the loss of calcium homeostasis, all of which cause neurotoxicity and neuron death. To prevent trauma-induced neurological deficits and death, each of the many neurotoxic events that occur in parallel or sequentially must be minimized or prevented. Although neuroprotective techniques have been developed that block single neurotoxic events, most provide only limited neuroprotection and are only applied singly. However, because many neurotoxicity triggers arise from common events, an approach for invoking more effective neuroprotection is to apply multiple neuroprotective methods simultaneously before the many neurotoxic triggers and cascades are initiated and become irreversible. This paper first discusses some triggers of neurotoxicity and neuroprotective mechanisms that block them, including hypothermia, alkalinization, and the administration of adenosine. It then examines how the simultaneous application of these techniques provides significantly greater neuroprotection than is provided by any technique alone. The paper also stresses the importance of determining whether the neuroprotection provided by these techniques can be further enhanced by combining them with additional techniques, such as the systemic administration of glucocorticoids. Finally, the paper stresses the absolute critical importance of applying these techniques within the “golden hour” following trauma, before the many neurotoxic events and cascades are manifest and before the neurotoxic cascades become irreversible.Keywords: adenosine, hypothermia, alkalinization, glucocorticoid

Variables affecting the potential efficacy of PRP in providing chronic pain relief

Damien P Kuffler Institute of Neurobiology, Medical Sciences Campus, University of Puerto Rico, San Juan, PR, USA Abstract: Although chronic pain affects about 1% of the US population, it remains largely resistant to treatment. Despite great variability in pain outcomes, the application of autologous platelet-rich plasma (PRP) has become increasingly popular in attempts to reduce chronic pain. The variability in PRP efficacy raises the question of whether PRP actually has an analgesic capacity, and if so, can that capacity be made consistent and maximized. The best explanation for the variability in PRP analgesic efficacy is the failure during PRP preparation and application to take into account variables that can increase or eliminate its analgesic capabilities. This suggests that if the variables are reduced and controlled, a PRP preparation and application protocol can be developed leading to PRP inducing reliable, complete, and long-term pain relief. The goal of this study was to examine some of the variables that influence platelets and see how they might be controlled to increase the analgesic potential of PRP. Among the variables examined are the physiological status of the patient, methods used to prepare PRP, and methods of PRP application. The goal of modifying these variables is to minimize platelet serotonin content, maximize platelet content of factors that reduce inflammation and pain, while maintaining their bioactivity, maximize platelet capacity to aggregate at injury sites, induce rapid and simultaneous release of their contents, and optimize PRP application protocols. It is concluded that controlling some or many of these variables will lead to PRP that induces reliable, maximum, and long-term relief of chronic pain. Keywords: analgesia, anti-inflammation, chronic pain, cytokines, inflammation, nerve trauma, neuropathic pain, platelet-rich plasma, pro-inflammation&nbsp

Differing efficacies of autologous platelet-rich plasma in reducing pain following rotator-cuff injury in a single patient

Damien P Kuffler Institute of Neurobiology, Medical Sciences Campus, University of Puerto Rico, San Juan 00901, Puerto Rico Abstract: Rotator-cuff tears (RCTs) are typically associated with chronic pain. The most common treatment for reducing pain is the injection of cortisone into the injury site. An alternative and increasingly used technique is the injection of autologous platelet-rich plasma (PRP). A limitation of cortisone is its pain relief is short-lived, while PRP has the limitation of providing pain relief to only about 50% of patients, making its efficacy questioned, although when it is effective, its efficacy is longer than cortisone. Little is known about what accounts for these limitations. This paper presents results from a patient with RCTs causing excruciating pain who received an injection of PRP into that shoulder resulting in complete pain elimination that was ongoing at 2 years and 2 months. When 7-month severe posttrauma pain associated with the RCT developed in the contralateral shoulder, PRP prepared the same way and injected by the same person who performed the first injection provided no pain relief. However, a subsequent single cortisone injection resulted in complete pain elimination, which was ongoing at >15 months. These observations indicate that PRP can have inconsistent effects in reducing pain, not only between patients but also within the same patient. Further, although the pain relief induced by cortisone is normally not long-lasting, when given following a PRP injection, it can induce complete pain relief lasting >15 months. This paper discusses possible reasons for the variability in PRP efficacy on pain relief and addresses the possibility that when administered together, PRP and cortisone may act in a complementary manner, leading to significantly greater and longer-lasting pain relief. Keywords: PRP, corticosteroids, RCTs, pain, pain reduction, platelets, inflammation, nerve injur

Can mammalian vision be restored following optic nerve degeneration?

Damien P Kuffler Institute of Neurobiology, School of Medicine, University of Puerto Rico, San Juan, Puerto Rico Abstract: For most adult vertebrates, glaucoma, trauma, and tumors close to retinal ganglion cells (RGCs) result in their neuron death and no possibility of vision reestablishment. For more distant traumas, RGCs survive, but their axons do not regenerate into the distal nerve stump due to regeneration-inhibiting factors and absence of regeneration-promoting factors. The annual clinical incidence of blindness in the United States is 1:28 (4%) for persons >40 years, with the total number of blind people approaching 1.6 million. Thus, failure of optic nerves to regenerate is a significant problem. However, following transection of the optic nerve of adult amphibians and fish, the RGCs survive and their axons regenerate through the distal optic nerve stump and reestablish appropriate functional retinotopic connections and fully functional vision. This is because they lack factors that inhibit axon regeneration and possess factors that promote regeneration. The axon regeneration in lower vertebrates has led to extensive studies by using them as models in studies that attempt to understand the mechanisms by which axon regeneration is promoted, so that these mechanisms might be applied to higher vertebrates for restoring vision. Although many techniques have been tested, their successes have varied greatly from the recovery of light and dark perceptions to partial restoration of the optomotor response, depth perception, and circadian photoentrainment, thus demonstrating the feasibility of reconstructing central circuitry for vision after optic nerve damage in mature mammals. Thus, further research is required to induce the restoration of vision in higher vertebrates. This paper examines the causes of vision loss and techniques that promote transected optic nerve axons to regenerate and reestablish functional vision, with a focus on approaches that may have clinical applicability. Keywords: vision, RGC, axon regeneration, optic nerve trauma, restoration of visio

Stimulus Intensity modifies Saccadic Reaction Time and Visual Response Latency in the Superior Colliculus.

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