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Background Although many studies have investigated the anatomy of the Medial Patello-Femoral Ligament (MPFL), some studies have even questioned its existence. In the last 20 years, there is a renewed interest on the role of the MPFL in patello-femoral instability. As a result, several studies have been published that describe the anatomy, function and possible surgical reconstruction of the MPFL. Despite the large amount of literature produced, there is still a lack of consensus on what is its real anatomy as there are currently no systematic reviews on this topic. Purposes Thus, the aim of this review is to systematically report the results in literature regarding in anatomical papers, the existence, size, insertion sites and relationships of this ligament with the other medial structures of the knee. Methods We have systematically analyzed anatomical studies currently available in literature between 1980 and December 2012. The search was carried out on Medline, Embase, Cochrane Library and Google Scholar. We checked reference lists of articles, reviews and textbooks identified by the search strategy for other possible relevant studies. Results The outcomes examined are the presence of the ligament, its size (length, width, thickness), and its patellar and femoral insertions. A total of 312 cadaveric knees were included in the 17 studies; the MPFL was identified in 99 % of cases (309). Conclusions The consensus is that the MPFL is almost always present in the dissected knees. The size and insertions of the ligament demonstrate great variation between cadavers.

IgE is an important marker for allergy and plays a central role in the induction of allergic diseases through its binding of the high affinity receptor on mast cells. Mast cells can influence B cell survival, proliferation and differentiation into CD138+ cells. Among TH2 cytokines, interleukin (IL)-4 and IL-13 are responsible for class-switching in B cells which resolves in production of allergen-specific IgE antibodies that bind to specific receptor on mast cells. IgE synthesis by B cells is regulated by CD40 ligand, IL-4 and interferon-gamma, therefore inhibition of B cell antigen-specific IgE may prevent the cleavage of CD23 from B cells, having a therapeutic impact which also includes the removal of circulating free IgE, omalizumab, corticosteroids, mast cell stabilizers, leukotriene receptor antagonist, and others. B cell differentiation into IgE-producing cells requires two signals provided by TH2 cells and IL-4, however IL-4, IL-1 and IL-10 as well as several hormones are critical for the development of TH2 cells, while cytokines, such as interferon (IFN)-alpha, IFN-gamma, IL-12 and transforming growth factor (TGF)-beta play a negative role. However, the exact mechanism of this process has not yet been defined.

Neuropeptides are involved in neurogenic inflammation where there is vasodilation and plasma protein extravasion in response to this stimulus. Nerve growth factor (NGF), identified by Rita Levi Montalcini, is a neurotrophin family compound which is important for survival of nociceptive neurons during their development. Therefore, NGF is an important neuropeptide which mediates the development and functions of the central and peripheral nervous system. It also exerts its proinflammatory action, not only on mast cells but also in B and T cells, neutrophils and eosinophils. Human mast cells can be activated by neuropeptides to release potent mediators of inflammation, and they are found throughout the body, especially near blood vessels, epithelial tissue and nerves. Mast cells generate and release NGF after degranulation and they are involved in iperalgesia, neuroimmune interactions and tissue inflammation. NGF is also a potent degranulation factor for mast cells in vitro and in vivo, promoting differentiation and maturation of these cells and their precursor, acting as a co-factor with interleukin-3. In conclusion, these studies are focused on cross-talk between neuropeptide NGF and inflammatory mast cells.

It is well established that mast cells, which are found in the tissues in the proximity of small blood vessels and post-capillary venules, play a key role in the early phase of IgE-mediated allergic reactions. A greatly expanded understanding of the biology of IL-3 has emerged since the early 1980s. IL-3 is a specific factor that stimulates the growth of hematopoietic stem and progenitor cells of a variety of lineages and can promote the proliferation of certain classes of lymphocytes distinct from those that are dependent on IL-2. IL-3 has been identified among the most important cytokines for regulation of mast cell growth and differentiation, migration and effector function activities of many hematopoietic cells. IL-3 termed multi colony-stimulating-factor (multi-CSF) or mast cell growth factor (MCGF) is a haematopoietic growth factor which stimulates the formation of colonies for erythroid, megakaryocytic, granulocytic and monocytic lineages. It is predominantly produced by activated T cells, natural killer (NK) cells and mast cells and supports the growth-promoting effects of SCF on mast cell precursors. IL-3 causes severe hypersensivity reactions and plays a pivotal role in exacerbating the inflammatory response in vivo. Here we report the interrelationship between IL-3 and mast cells.

The purpose of our study was that to systematically review the fixation techniques for the ACL reconstruction and associated clinical outcomes at the early follow-up. Systematic search on three electronic databases (Cochrane register, Medline and Embase) of fixation devices used for primary ACL reconstruction with doubled semitendinosus and gracilis and bone–patellar tendon–bone autografts in randomized clinical trials of level I and II of evidence published from January 2001 to December 2011. Therapeutic studies collected were with a minimum 12- month follow-up, and the clinical outcomes were evaluated by at least one of International Knee Documentation Committee, Lysholm and Tegner functional scales and at least one of the following knee stability tests: arthrometric AP tibial translation, Lachman test and pivot-shift test. Nineteen articles met the inclusion criteria. At the femoral side cross-pin, metallic interference screw, bioabsorbable interference screw, and suspensory device were used in 32.3, 27.3, 24.8, 15.5 % of patients, respectively. At the tibial side fixation was achieved with metallic interference screw, bioabsorbable interference screw, screw and plastic sheath, screw post and cross-pin in 38.7, 31, 15.7, 12.8, and 1.7 % of patients, respectively. Side-to-side anterior– posterior tibial translation was 1.9 ± 0.9, 1.5 ± 0.9, 1.5 ± 0.8, 2.2 ± 0.4 mm for metallic interference screw, bioabsorbable screw, cross-pin and suspensory device, respectively. At least two-third of all the patients achieved good-to-excellent clinical outcomes. Rate of failure was 6.1, 3.3, 1.7 and 1.2 % for bioabsorbable interference screw, metallic interference screw, cross-pin and suspensory device, respectively. Clinical outcomes are good to excellent in almost two-third of the patients but several pitfalls that affect the current fixation techniques as graft tensioning such as graft-tunnel motion are still unaddressed.

Microglia derive from mononuclear myeloid progenitors and are a major glial complement of the central nervous system. When microglia are activated they secrete inflammatory cytokines and toxic mediators which amplify the inflammatory response. In addition, the microglia inflammatory products are implicated in the neuronal destruction usually observed in various neurodegenerative diseases. Microglia cells express corticotropin releasing hormone (CRH) receptors, and activation of microglia by CRH releases bioactive molecules which have a biological effect in the brain and regulate several neurological diseases. CRH plays a pivotal role in stress responses and is a key mediator of the hypothalamic-pituitary-adrenocortical system. CRH is expressed in human mast cells, leading to autocrine effects and participates in inflammatory response together with neuropeptides, and stimulates mast cells. IL-33-activated mast cells release vascular endothelial growth factor in response to CRH and act synergistically to increase vascular permeability. CRH also up-regulates IL-18 expression by increasing intracellular reactive oxygen in microglia cells. Here we report the relationship between CRH, microglia and mental disorders.

Serotonin (5-HT) is an important neurotransmitter that acts in both central and peripheral nervous system, and has an impact on cell proliferation, migration and apoptosis. 5HT exerts its effects via several receptors. Treatment with anti-5-HT receptors diminish the severity of contact allergy in experimental animals, an effect mediated by mast cells; while an agonist reduces the stress level and relieves pruritus in patients with atopic dermatitis. Mast cells are important for both innate and adaptive immunity and they are activated by cross-linking of FceRI molecules, which are involved in the binding of multivalent antigens to the attached IgE molecules, resulting in a variety of responses including the immediate release of potent inflammatory mediators. Serotonin is present in murine mucosal mast cells and some authors reported that human mast cells may also contain serotonin, especially in subjects with mastocytosis. Here we report the interrelationship between mast cells, serotonin and its receptor inhibitor.