-
Clinics in Sports Medicine Jan 2020Meniscus injuries are among the most common athletic injuries and result in functional impairment in the knee. Repair is crucial for pain relief and prevention of...
Meniscus injuries are among the most common athletic injuries and result in functional impairment in the knee. Repair is crucial for pain relief and prevention of degenerative joint diseases like osteoarthritis. Current treatments, however, do not produce long-term improvements. Thus, recent research has been investigating new therapeutic options for regenerating injured meniscal tissue. This review comprehensively details the current methodologies being explored in the basic sciences to stimulate better meniscus injury repair. Furthermore, it describes how these preclinical strategies may improve current paradigms of how meniscal injuries are clinically treated through a unique and alternative perspective to traditional clinical methodology.
Topics: Adipose Tissue; Biomechanical Phenomena; Bone Marrow Cells; Cartilage; Chondrocytes; Humans; Intercellular Signaling Peptides and Proteins; Menisci, Tibial; Platelet-Rich Fibrin; Platelet-Rich Plasma; Regeneration; Stem Cell Transplantation; Synovial Membrane; Tibial Meniscus Injuries; Tissue Engineering; Tissue Scaffolds
PubMed: 31767102
DOI: 10.1016/j.csm.2019.08.003 -
Frontiers in Pharmacology 2022Insulin secretory agents are commonly used to treat type 2 diabetes. However, traditional insulin secretory agents such as sulfonylureas and glinides have side effects...
Insulin secretory agents are commonly used to treat type 2 diabetes. However, traditional insulin secretory agents such as sulfonylureas and glinides have side effects of hypoglycemia. In recent years, researchers have discovered that berberine can inhibit the voltage-gated k channels of pancreatic β cell membrane and promote insulin secretion without causing hypoglycemia, because the glucose-lowering effects of berberine are only under hyperglycemic conditions or in a high-glucose-dependent manner. In order to shed light on the glucose-lowing effects of berberine in type 2 diabetes with different baseline fasting plasma glucose (FPG) and glycosylated hemoglobin (HbA1c), we conducted a meta-analysis of randomized controlled trials. We searched eight databases, which included PubMed, EMBASE, Web of Science, the Cochrane Library, and the Chinese databases such as Sino-Med, China National Knowledge Infrastructure (CNKI), Wanfang Database, and VIP Database for Chinese Technical Periodicals, for randomized controlled trials, with berberine as the intervention and patients with type 2 diabetes mellitus as subjects, published up until November 2021. We analyzed the glucose-lowing effects of berberine, including its effects on FPG, HbA1c and 2-h plasma blood glucose (2hPBG), by calculating weighted mean differences (WMD) and 95% confidence interval (CI). To assess the safety of berberine, we analyzed the incidence of total adverse events and hypoglycemia by calculating relative risk (RR) and 95% CI. Thirty-seven studies involving 3,048 patients were included in the meta-analysis. The results showed that berberine could reduce FPG (WMD = -0.82 mmol/L, 95% CI (-0.95, -0.70)), HbA1c (WMD = -0.63%, 95% CI (-0.72, -0.53)), and 2hPBG (WMD = -1.16 mmol/L, 95% CI (-1.36, -0.96)), with all results being statistically significant. Subgroup analyses revealed that the glucose-lowering effect of berberine was associated with baseline mean FPG and HbA1c in type 2 diabetes. In addition, berberine alone or in combination with oral hypoglycemic agents (OHAs) in the treatment of T2DM did not significantly increase the incidence of total adverse events (RR = 0.73, 95% CI (0.55, 0.97), = 0.03) and the risk of hypoglycemia (RR = 0.48, 95% CI (0.21, 1.08), = 0.08). Berberine has a glucose-lowering effect, which is related to the baseline FPG and HbA1c levels of patients. Treatment with berberine may be safe since it does not increase the incidence of total adverse events and the risk of hypoglycemia. https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=292975, identifier CRD42021292975.
PubMed: 36467075
DOI: 10.3389/fphar.2022.1015045 -
International Journal of Molecular... Aug 2019A nutritional approach could be a promising strategy to prevent or slow the progression of neurodegenerative diseases such as Parkinson's and Alzheimer's disease, since...
A nutritional approach could be a promising strategy to prevent or slow the progression of neurodegenerative diseases such as Parkinson's and Alzheimer's disease, since there is no effective therapy for these diseases so far. The beneficial effects of omega-3 fatty acids are now well established by a plethora of studies through their involvement in multiple biochemical functions, including synthesis of anti-inflammatory mediators, cell membrane fluidity, intracellular signaling, and gene expression. This systematic review will consider epidemiological studies and clinical trials that assessed the impact of supplementation or dietary intake of omega-3 polyunsaturated fatty acids on neurodegenerative diseases such as Parkinson's and Alzheimer's diseases. Indeed, treatment with omega-3 fatty acids, being safe and well tolerated, represents a valuable and biologically plausible tool in the management of neurodegenerative diseases in their early stages.
Topics: Clinical Trials as Topic; Fatty Acids, Omega-3; Humans; Neurodegenerative Diseases; Observational Studies as Topic
PubMed: 31480294
DOI: 10.3390/ijms20174256 -
Journal of Applied Physiology... Jul 2021Muscle atrophy and decline in muscle strength appear very rapidly with prolonged disuse or mechanical unloading after acute hospitalization or experimental bed rest. The...
Muscle atrophy and decline in muscle strength appear very rapidly with prolonged disuse or mechanical unloading after acute hospitalization or experimental bed rest. The current study analyzed data from short-, medium-, and long-term bed rest (5-120 days) in a pooled sample of 318 healthy adults and modeled the mathematical relationship between muscle strength decline and atrophy. The results show a logarithmic disuse-induced loss of strength and muscle atrophy of the weight-bearing knee extensor muscles. The greatest rate of muscle strength decline and atrophy occurred in the earliest stages of bed rest, plateauing later, and likely contributed to the rapid neuromuscular loss of function in the early period. In addition, during the first 2 wk of bed rest, muscle strength decline is much faster than muscle atrophy: on , the ratio of muscle atrophy to strength decline as a function of bed rest duration is 4.2, falls to 2.4 on , and stabilizes to a value of 1.9 after ∼35 days of bed rest. Positive regression revealed that ∼79% of the muscle strength loss may be explained by muscle atrophy, while the remaining is most likely due to alterations in single fiber mechanical properties, excitation-contraction coupling, fiber architecture, tendon stiffness, muscle denervation, neuromuscular junction damage, and supraspinal changes. Future studies should focus on neural factors as well as muscular factors independent of atrophy (single fiber excitability and mechanical properties, architectural factors) and on the role of extracellular matrix changes. Bed rest results in nonuniform loss of isometric muscle strength and atrophy over time, where the magnitude of change was greater for muscle strength than for atrophy. Future research should focus on the loss of muscle function and the underlying mechanisms, which will aid in the development of countermeasures to mitigate or prevent the decline in neuromuscular efficiency. Our study contributes to the characterization of muscle loss and weakness processes reflected by a logarithmic decline in muscle strength induced by chronic bed rest. Acute short-term hospitalization (≤5 days) associated with periods of disuse/immobilization/prolonged time in the supine position in the hospital bed is sufficient to significantly decrease muscle mass and size and induce functional changes related to weakness in maximal muscle strength. By bringing together integrated evaluation of muscle structure and function, this work identifies that 79% of the loss in muscle strength can be explained by muscle atrophy, leaving 21% of the functional loss unexplained. The outcomes of this study should be considered in the development of daily countermeasures for preserving neuromuscular integrity as well as preconditioning interventions to be implemented before clinical bed rest or chronic gravitational unloading (e.g., spaceflights).
Topics: Adult; Bed Rest; Humans; Muscle Strength; Muscle, Skeletal; Muscular Atrophy; Neuromuscular Junction
PubMed: 33703945
DOI: 10.1152/japplphysiol.00363.2020 -
Pharmacological Reviews Apr 2021The complement system was discovered at the end of the 19th century as a heat-labile plasma component that "complemented" the antibodies in killing microbes, hence the...
The complement system was discovered at the end of the 19th century as a heat-labile plasma component that "complemented" the antibodies in killing microbes, hence the name "complement." Complement is also part of the innate immune system, protecting the host by recognition of pathogen-associated molecular patterns. However, complement is multifunctional far beyond infectious defense. It contributes to organ development, such as sculpting neuron synapses, promoting tissue regeneration and repair, and rapidly engaging and synergizing with a number of processes, including hemostasis leading to thromboinflammation. Complement is a double-edged sword. Although it usually protects the host, it may cause tissue damage when dysregulated or overactivated, such as in the systemic inflammatory reaction seen in trauma and sepsis and severe coronavirus disease 2019 (COVID-19). Damage-associated molecular patterns generated during ischemia-reperfusion injuries (myocardial infarction, stroke, and transplant dysfunction) and in chronic neurologic and rheumatic disease activate complement, thereby increasing damaging inflammation. Despite the long list of diseases with potential for ameliorating complement modulation, only a few rare diseases are approved for clinical treatment targeting complement. Those currently being efficiently treated include paroxysmal nocturnal hemoglobinuria, atypical hemolytic-uremic syndrome, myasthenia gravis, and neuromyelitis optica spectrum disorders. Rare diseases, unfortunately, preclude robust clinical trials. The increasing evidence for complement as a pathogenetic driver in many more common diseases suggests an opportunity for future complement therapy, which, however, requires robust clinical trials; one ongoing example is COVID-19 disease. The current review aims to discuss complement in disease pathogenesis and discuss future pharmacological strategies to treat these diseases with complement-targeted therapies. SIGNIFICANCE STATEMENT: The complement system is the host's defense friend by protecting it from invading pathogens, promoting tissue repair, and maintaining homeostasis. Complement is a double-edged sword, since when dysregulated or overactivated it becomes the host's enemy, leading to tissue damage, organ failure, and, in worst case, death. A number of acute and chronic diseases are candidates for pharmacological treatment to avoid complement-dependent damage, ranging from the well established treatment for rare diseases to possible future treatment of large patient groups like the pandemic coronavirus disease 2019.
Topics: COVID-19; Collectins; Complement Activating Enzymes; Complement C3; Complement Inactivating Agents; Complement System Proteins; Genetic Therapy; Humans; Inflammation Mediators; Lectins; Mannose-Binding Protein-Associated Serine Proteases; Pandemics; Rare Diseases; SARS-CoV-2; Synapses; Ficolins
PubMed: 33687995
DOI: 10.1124/pharmrev.120.000072 -
The Cochrane Database of Systematic... Apr 2021Alveolar bone changes following tooth extraction can compromise prosthodontic rehabilitation. Alveolar ridge preservation (ARP) has been proposed to limit these changes... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Alveolar bone changes following tooth extraction can compromise prosthodontic rehabilitation. Alveolar ridge preservation (ARP) has been proposed to limit these changes and improve prosthodontic and aesthetic outcomes when implants are used. This is an update of the Cochrane Review first published in 2015.
OBJECTIVES
To assess the clinical effects of various materials and techniques for ARP after tooth extraction compared with extraction alone or other methods of ARP, or both, in patients requiring dental implant placement following healing of extraction sockets.
SEARCH METHODS
Cochrane Oral Health's Information Specialist searched the following databases: Cochrane Oral Health's Trials Register (to 19 March 2021), the Cochrane Central Register of Controlled Trials (CENTRAL) (the Cochrane Library 2021, Issue 2), MEDLINE Ovid (1946 to 19 March 2021), Embase Ovid (1980 to 19 March 2021), Latin American and Caribbean Health Science Information database (1982 to 19 March 2021), Web of Science Conference Proceedings (1990 to 19 March 2021), Scopus (1966 to 19 March 2021), ProQuest Dissertations and Theses (1861 to 19 March 2021), and OpenGrey (to 19 March 2021). The US National Institutes of Health Ongoing Trials Register (ClinicalTrials.gov) and the World Health Organization International Clinical Trials Registry Platform were searched for ongoing trials. No restrictions were placed on the language or date of publication when searching the electronic databases. A number of journals were also handsearched.
SELECTION CRITERIA
We included all randomised controlled trials (RCTs) on the use of ARP techniques with at least six months of follow-up. Outcome measures were: changes in the bucco-lingual/palatal width of alveolar ridge, changes in the vertical height of the alveolar ridge, complications, the need for additional augmentation prior to implant placement, aesthetic outcomes, implant failure rates, peri-implant marginal bone level changes, changes in probing depths and clinical attachment levels at teeth adjacent to the extraction site, and complications of future prosthodontic rehabilitation.
DATA COLLECTION AND ANALYSIS
We selected trials, extracted data, and assessed risk of bias in duplicate. Corresponding authors were contacted to obtain missing information. We estimated mean differences (MD) for continuous outcomes and risk ratios (RR) for dichotomous outcomes, with 95% confidence intervals (95% CI). We constructed 'Summary of findings' tables to present the main findings and assessed the certainty of the evidence using GRADE.
MAIN RESULTS
We included 16 RCTs conducted worldwide involving a total of 524 extraction sites in 426 adult participants. We assessed four trials as at overall high risk of bias and the remaining trials at unclear risk of bias. Nine new trials were included in this update with six new trials in the category of comparing ARP to extraction alone and three new trials in the category of comparing different grafting materials. ARP versus extraction: from the seven trials comparing xenografts with extraction alone, there is very low-certainty evidence of a reduction in loss of alveolar ridge width (MD -1.18 mm, 95% CI -1.82 to -0.54; P = 0.0003; 6 studies, 184 participants, 201 extraction sites), and height (MD -1.35 mm, 95% CI -2.00 to -0.70; P < 0.0001; 6 studies, 184 participants, 201 extraction sites) in favour of xenografts, but we found no evidence of a significant difference for the need for additional augmentation (RR 0.68, 95% CI 0.29 to 1.62; P = 0.39; 4 studies, 154 participants, 156 extraction sites; very low-certainty evidence) or in implant failure rate (RR 1.00, 95% CI 0.07 to 14.90; 2 studies, 70 participants/extraction sites; very low-certainty evidence). From the one trial comparing alloplasts versus extraction, there is very low-certainty evidence of a reduction in loss of alveolar ridge height (MD -3.73 mm; 95% CI -4.05 to -3.41; 1 study, 15 participants, 60 extraction sites) in favour of alloplasts. This single trial did not report any other outcomes. Different grafting materials for ARP: three trials (87 participants/extraction sites) compared allograft versus xenograft, two trials (37 participants, 55 extraction sites) compared alloplast versus xenograft, one trial (20 participants/extraction sites) compared alloplast with and without membrane, one trial (18 participants, 36 extraction sites) compared allograft with and without synthetic cell-binding peptide P-15, and one trial (30 participants/extraction sites) compared alloplast with different particle sizes. The evidence was of very low certainty for most comparisons and insufficient to determine whether there are clinically significant differences between different ARP techniques based on changes in alveolar ridge width and height, the need for additional augmentation prior to implant placement, or implant failure. We found no trials which evaluated parameters relating to clinical attachment levels, specific aesthetic or prosthodontic outcomes for any of the comparisons. No serious adverse events were reported with most trials indicating that the procedure was uneventful. Among the complications reported were delayed healing with partial exposure of the buccal plate at suture removal, postoperative pain and swelling, moderate glazing, redness and oedema, membrane exposure and partial loss of grafting material, and fibrous adhesions at the cervical part of previously preserved sockets, for the comparisons xenografts versus extraction, allografts versus xenografts, alloplasts versus xenografts, and alloplasts with and without membrane.
AUTHORS' CONCLUSIONS
ARP techniques may minimise the overall changes in residual ridge height and width six months after extraction but the evidence is very uncertain. There is lack of evidence of any differences in the need for additional augmentation at the time of implant placement, implant failure, aesthetic outcomes, or any other clinical parameters due to lack of information or long-term data. There is no evidence of any clinically significant difference between different grafting materials and barriers used for ARP. Further long-term RCTs that follow CONSORT guidelines (www.consort-statement.org) are necessary.
Topics: Adult; Alveolar Process; Alveolar Ridge Augmentation; Bias; Biocompatible Materials; Bone Regeneration; Bone Remodeling; Confidence Intervals; Dental Implantation, Endosseous; Heterografts; Humans; Middle Aged; Organ Sparing Treatments; Randomized Controlled Trials as Topic; Time Factors; Tooth Extraction; Tooth Socket; Treatment Outcome
PubMed: 33899930
DOI: 10.1002/14651858.CD010176.pub3 -
Orphanet Journal of Rare Diseases Mar 2015Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is a rare autosomal recessive disorder of the urea cycle. HHH has a panethnic distribution, with a... (Review)
Review
BACKGROUND
Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is a rare autosomal recessive disorder of the urea cycle. HHH has a panethnic distribution, with a major prevalence in Canada, Italy and Japan. Acute clinical signs include intermittent episodes of vomiting, confusion or coma and hepatitis-like attacks. Alternatively, patients show a chronic course with aversion for protein rich foods, developmental delay/intellectual disability, myoclonic seizures, ataxia and pyramidal dysfunction. HHH syndrome is caused by impaired ornithine transport across the inner mitochondrial membrane due to mutations in SLC25A15 gene, which encodes for the mitochondrial ornithine carrier ORC1. The diagnosis relies on clinical signs and the peculiar metabolic triad of hyperammonemia, hyperornithinemia, and urinary excretion of homocitrulline. HHH syndrome enters in the differential diagnosis with other inherited or acquired conditions presenting with hyperammonemia.
METHODS
A systematic review of publications reporting patients with HHH syndrome was performed.
RESULTS
We retrospectively evaluated the clinical, biochemical and genetic profile of 111 HHH syndrome patients, 109 reported in 61 published articles, and two unpublished cases. Lethargy and coma are frequent at disease onset, whereas pyramidal dysfunction and cognitive/behavioural abnormalities represent the most common clinical features in late-onset cases or during the disease course. Two common mutations, F188del and R179* account respectively for about 30% and 15% of patients with the HHH syndrome. Interestingly, the majority of mutations are located in residues that have side chains protruding into the internal pore of ORC1, suggesting their possible interference with substrate translocation. Acute and chronic management consists in the control of hyperammonemia with protein-restricted diet supplemented with citrulline/arginine and ammonia scavengers. Prognosis of HHH syndrome is variable, ranging from a severe course with disabling manifestations to milder variants compatible with an almost normal life.
CONCLUSIONS
This paper provides detailed information on the clinical, metabolic and genetic profiles of all HHH syndrome patients published to date. The clinical phenotype is extremely variable and its severity does not correlate with the genotype or with recorded ammonium/ornithine plasma levels. Early intervention allows almost normal life span but the prognosis is variable, suggesting the need for a better understanding of the still unsolved pathophysiology of the disease.
Topics: Aging; Humans; Hyperammonemia; Mutation; Origin Recognition Complex; Ornithine; Protein Conformation; Urea Cycle Disorders, Inborn
PubMed: 25874378
DOI: 10.1186/s13023-015-0242-9 -
Frontiers in Pharmacology 2017Bilirubin is a highly-hydrophobic tetrapyrrole which binds to plasma albumin. It is conjugated in the liver to glucuronic acid, and the water-soluble glucuronides are... (Review)
Review
Bilirubin is a highly-hydrophobic tetrapyrrole which binds to plasma albumin. It is conjugated in the liver to glucuronic acid, and the water-soluble glucuronides are excreted in urine and bile. The membrane transporters of bilirubin diglucuronide are well-known. Still undefined are however the transporters performing the uptake of bilirubin from the blood into the liver, a process known to be fast and not rate-limited. The biological importance of this process may be appraised by considering that in normal adults 200-300 mg of bilirubin are produced daily, as a result of the physiologic turnover of hemoglobin and cellular cytochromes. Nevertheless, research in this field has yielded controversial and contradicting results. We have undertaken a systematic review of the literature, believing in its utility to improve the existing knowledge and promote further advancements. We have sourced the PubMed database until 30 June 2017 by applying 5 sequential searches. Screening and eligibility criteria were applied to retain research articles reporting results obtained by using bilirubin molecules in membrane transport assays or by assessing serum bilirubin levels in experiments. We have identified 311 articles, retaining 44, reporting data on experimental models having 6 incremental increases of complexity (isolated proteins, membrane vesicles, cells, organ fragments, rodents, and human studies), demonstrating the function of 19 membrane transporters, encoded by either or genes. Three other bilirubin transporters have no gene, though one, i.e., bilitranslocase, is annotated in the Transporter Classification Database. This is the first review that has systematically examined the membrane transporters for bilirubin and its conjugates. Paradoxically, the remarkable advancements in the field of membrane transport of bilirubin have pointed to the elusive mechanism(s) enabling bilirubin to diffuse into the liver as if no cellular boundary existed.
PubMed: 29259555
DOI: 10.3389/fphar.2017.00887 -
Frontiers in Immunology 2022Transplant-associated thrombotic microangiopathy (TA-TMA) is an increasingly recognized complication of allogeneic and autologous hematopoietic cellular therapy (HCT),... (Review)
Review
Transplant-associated thrombotic microangiopathy (TA-TMA) is an increasingly recognized complication of allogeneic and autologous hematopoietic cellular therapy (HCT), associated with significant morbidity and mortality. Although the central drivers of the disease are thought to be endothelial damage and complement activation, no specific diagnostic biomarkers have been identified. TA-TMA is typically diagnosed using criteria comprised of non-specific clinical and laboratory features. Some patients will have a self-remitting course, but more than half develop multi-organ dysfunction or die, making prognostic biomarkers critical. Prevention of TA-TMA, an approach central to other HCT complications such as graft-versus-host disease, is largely untested in part due to a lack of identified early high-risk biomarkers. We conducted a systematic review to summarize the diagnostic, early risk, and prognostic biomarkers of TA-TMA. We screened the titles and abstracts of 1524 citations. After screening out duplications, we read the abstracts of 979 papers and fully reviewed 132 full-text publications. Thirty-one publications fulfilled the inclusion criteria of more than five patients with TA-TMA and a reported measure of association with diagnosis, prognosis, or risk of later development of the disease. Fourteen studies (45%) were with adults, 12 (39%) were with children <18 years old, three included both children and adults, and two did not report age. There were 53 biomarker or biomarker signature entries, and a total of 27 unique biomarkers. Only four biomarkers reported sensitivity and specificity. The single biomarker with the most robust data was sC5b-9, which conferred diagnostic, prognostic, and risk implications. Studies of combinations of biomarkers were rare. No meta-analyses were performed because of significant heterogeneity between studies. The limitations of studies included small sample size, study designs with a high risk of bias (i.e., case-control), the timing of sample collection, and the selection of controls. Furthermore, only two (6%) studies included a training and validation cohort. Cut-off points are needed to stratify groups, as most biomarkers do not have normal values, or normal values cannot be assumed in the HCT setting. In the future, multi-institutional, collaborative efforts are needed to perform rigorously designed, prospective studies with serially enrolled patients, with samples collected at the time of TA-TMA diagnosis, careful selection of controls, and validation of selected biomarkers and cut-off points in a separate cohort.
Topics: Adult; Child; Humans; Adolescent; Prognosis; Prospective Studies; Biomarkers; Graft vs Host Disease; Thrombotic Microangiopathies
PubMed: 36818475
DOI: 10.3389/fimmu.2022.1064203 -
Frontiers in Surgery 2020Bone augmentation techniques have increasingly been indicated for re-creating adequate bone height and volume suitable for dental implant sites. This is particularly...
Bone augmentation techniques have increasingly been indicated for re-creating adequate bone height and volume suitable for dental implant sites. This is particularly applicable in the severely atrophic posterior maxilla where sinus perforation (ruptured Schneiderian membrane) is a very common complication and sinus floor elevation or lift is frequently considered a standard procedure. The augmentation of the maxillary sinus can be performed with or without grafting biomaterials. Herein, numerous biomaterials and bone substitutes have been proposed, primarily to sustain the lifted space. In addition, cytokines and growth factors have been used to stimulate angiogenesis, enhance bone formation as well as improve healing and recovery period, either as the sole filling material or in combination with bone substitute materials. Within such, is the family of autologous blood extracts, so-called platelet concentrates, which are simply the "product" resulting from the simple centrifugation of collected whole blood samples of the patient, immediately pre-surgery. Platelet-Rich Fibrin (PRF), a sub-family of platelet concentrates, is a three-dimensional (3-D) autogenous biomaterial obtained, without including anti-coagulants, bovine thrombin, additives, or any gelifying agents during the centrifugation process. Today, it is safe to say that, in implant dentistry and oral and maxillofacial surgery, PRFs (particularly, the pure platelet-rich fibrin or P-PRF and leukocyte and platelet-rich fibrin or L-PRF sub-classes) are receiving the most attention, essentially due to their simplicity, rapidness, user-friendliness/malleability, and cost-effectiveness. Whether used as the sole "bioactive" filling/additive material or combined with bone substitutes, the revolutionary second-generation PRFs have been very often associated with clinical results. Hence, this review aims to provide a 10-years update on the clinical effectiveness of L-PRF when applied/used as the "sole" biomaterial in maxillary sinus augmentation procedures. An electronic search using specific keywords for L-PRF and maxillary sinus augmentation was conducted in three main databases (PubMed-MEDLINE database, Google Scholar and Cochrane library) for the period between January 2009-February 2020. The quest yielded a total of 468 articles. Based on the pre-established inclusion/exclusion criteria, only seven articles were deemed eligible and included in the analysis. Surprisingly, of the 5 studies which used de-proteinized bovine bone mineral (DBBM) in combination with L-PRF, 60% acclaimed no significant effects and only 40% declared positive effects. Of the two articles which had used allogenous bone graft, 50% declared no significant effects and 50% acclaimed positive effects. Only one study had used L-PRF as the sole grafting material and reported a positive effect. Likewise, positive effects were reported in one other study using L-PRF in combination with a collagen membrane. Due to the heterogeneity of the included studies, this review is limited by the inability to perform a proper systematic meta-analysis. Overall, most of the published studies reported results of L-PRF application as a grafting material (sole or adjuvant) in maxillary sinus augmentation and dental implant restorative procedures. Yet, distinct technical processing for L-PRF preparation was noted. Hence, studies should be approached with caution. Here in, in sinus lift and treatment of Schneider membrane, the formation of mature bone remains inconclusive. More studies are eagerly awaited in order to prove the beneficial or detrimental effects of PRFs, in general and L-PRFs, in specific; especially in their tissue regenerative potential pertaining to the promotion of angiogenesis, enhancing of cell proliferation, stimulation of cell migration and autocrine/paracrine secretion of growth factors, as well as to reach a consensus or a conclusive and distinct determination of the effect of leukocytes (and their inclusion) on inflammation or edema and pain; a call for standardization in PRFs and L-PRFs composition reporting and regimenting the preparation protocols.
PubMed: 33330603
DOI: 10.3389/fsurg.2020.537138