Sterol Esterase
Lipolysis
Cyclic AMP-Dependent Protein Kinases
IL-1 polymorphism and periimplantitis. A literature review. (1/24)
The most important factor leading to periimplantitis with bone loss appears to be an inflammatory process due to plaque accumulation. The object of this article was to present a review of the literature on a possible correlation between IL-1 polymorphism and periimplantitis. Research was carried out in the PUBMED and WEB OF KNOWLEDGE literature databases and 27 relevant articles were found. Of these articles, 4 groups of authors came to the conclusion that no correlation exists between IL-1 polymorphism and periimplantitis. In 5 articles by 4 groups of authors, the influence of IL-1 polymorphism on periimplantitis is unclear. 9 studies prove a correlation between IL-1 polymorphism and periimplantitis, and 6 studies also document a direct linkage between gene polymorphism and periimplantitis, if certain cofactors are present. IL-1 polymorphism is frequently connected with "noninfectious periimplant bone loss". Other studies prove that the inflammatory mediators and IL-1beta were significantly elevated in the gingival crevicular fluid (GCF) of infected implants. Many studies document that IL-1 polymorphism alone cannot be considered a risk factor for bone loss, but in combination with smoking, it is closely associated with periimplant bone loss. More studies are needed to discover possible correlations between IL-1 polymorphism and periimplantitis. (+info)Unusual presentation of active implant periapical lesions: a report of two cases. (2/24)
Active implant periapical lesion (IPL) is a rare lesion which has been reported as one of the causes of dental implant failures. Usually, an affected implant shows radiolucency in the apical area, while remaining clinically stable. IPL is often accompanied by symptoms of pain, swelling, tenderness, and fistulation. In this paper, we describe two cases of IPL with very unusual findings which led to implant failure. A large IPL associated with an inflammatory cyst in the anterior maxilla, and a mandibular IPL resulting in an extra-oral fistula are presented. The etiology and treatment approaches for IPL are discussed. (+info)Interleukins IL-6, IL-8, IL-10, IL-12 and periimplant disease. An update. (3/24)
INTRODUCTION: A study is made of the usefulness of cytokines (such as interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10) and interleukin-12 (IL-12)) as markers of periimplant disease (mucositis and periimplantitis). An increase in the levels of these cytokines in dental implant crevicular fluid may give rise to a lack of osteointegration, bone loss or implant failure. OBJECTIVE: To review the literature relating IL-6, IL-8, IL-10 and IL-12 levels to dental implant surgery and periimplantitis. MATERIAL AND METHOD: A PubMed literature search was made of articles in English and Spanish, using the key words "cytokine and dental implants", cytokine and periimplantitis", "IL-6, IL-8, IL-10, IL-12 and dental implants", "IL-6, IL-8, IL-10, IL-12 and periimplantitis". Fourteen articles were found and classified into two groups relating interleukin levels to: a) periimplant disease; and b) their influence upon dental implant osteointegration without periimplant disease. CONCLUSIONS: An increase in interleukin levels is observed in patients with periimplant disease, though there is controversy over the effect of interleukins in crevicular fluid and periimplantitis in relation to implant failure or the development of periimplant disease. (+info)Development of an animal model for Aggregatibacter actinomycetemcomitans biofilm-mediated oral osteolytic infection: a preliminary study. (4/24)
(+info)Electrochemical disinfection of dental implants--a proof of concept. (5/24)
(+info)Peri-implantitis: associated microbiota and treatment. (6/24)
INTRODUCTION: Peri-implantitis is a late complication of dental implant treatment, induced by microbiological changes. Since the disorder is frequent, a review is indicated of the microorganisms that influence it and of the existing treatment options. OBJECTIVE: To conduct a literature review of the microbiota associated to peri-implantitis and the existing treatment options. MATERIAL AND METHOD: A PubMed literature search was made of the studies on the microbiota associated to dental implants in healthy patients and patients with peri-implantitis, as well as of the latest treatment developments, using the following key words: "peri-implantitis AND microbiota", "periimplantitis AND microbiota", "peri-implantitis AND treatment", and "periimplantitis AND treatment". Only clinical studies in humans were considered. The following criteria were applied for including articles in the analysis: a) for the peri-implant microbiota, the search limits were human studies after the year 2000; and b) for the treatment of peri-implantitis, the search limits were randomized and controlled clinical trials (RCTs) in humans, with a minimum follow-up of 4 months, and publication after the year 2000. RESULTS: A total of 18 articles were selected in relation to peri-implant microbiota, and 13 in relation to the treatment of peri-implantitis (8 involving nonsurgical mechanical treatments and 5 surgical procedures). CONCLUSIONS: Evaluation of the literature has shown the microbiota associated to peri-implantitis to be more complex than that found under healthy peri-implant conditions - the main flora consisting of anaerobic gramnegative bacteria. No clear criteria have been identified for the diagnosis and treatment of peri-implantitis. (+info)Failures in implants. (7/24)
(+info)Pyrosequencing reveals unique microbial signatures associated with healthy and failing dental implants. (8/24)
(+info)A sterol esterase is an enzyme that catalyzes the hydrolysis of sterol esters, which are fatty acid esters of sterols (such as cholesterol) that are commonly found in lipoproteins and cell membranes. Sterol esterases play a crucial role in the metabolism of lipids by breaking down sterol esters into free sterols and free fatty acids, which can then be used in various biochemical processes.
There are several types of sterol esterases that have been identified, including:
1. Cholesteryl esterase (CE): This enzyme is responsible for hydrolyzing cholesteryl esters in the intestine and liver. It plays a critical role in the absorption and metabolism of dietary cholesterol.
2. Hormone-sensitive lipase (HSL): This enzyme is involved in the hydrolysis of sterol esters in adipose tissue, as well as other lipids such as triacylglycerols. It is regulated by hormones such as insulin and catecholamines.
3. Carboxylesterase (CES): This enzyme is a broad-specificity esterase that can hydrolyze various types of esters, including sterol esters. It is found in many tissues throughout the body.
Sterol esterases are important targets for drug development, as inhibiting these enzymes can have therapeutic effects in a variety of diseases, such as obesity, diabetes, and cardiovascular disease.
Lipolysis is the process by which fat cells (adipocytes) break down stored triglycerides into glycerol and free fatty acids. This process occurs when the body needs to use stored fat as a source of energy, such as during fasting, exercise, or in response to certain hormonal signals. The breakdown products of lipolysis can be used directly by cells for energy production or can be released into the bloodstream and transported to other tissues for use. Lipolysis is regulated by several hormones, including adrenaline (epinephrine), noradrenaline (norepinephrine), cortisol, glucagon, and growth hormone, which act on lipases, enzymes that mediate the breakdown of triglycerides.
Cyclic AMP (cAMP)-dependent protein kinases, also known as protein kinase A (PKA), are a family of enzymes that play a crucial role in intracellular signaling pathways. These enzymes are responsible for the regulation of various cellular processes, including metabolism, gene expression, and cell growth and differentiation.
PKA is composed of two regulatory subunits and two catalytic subunits. When cAMP binds to the regulatory subunits, it causes a conformational change that leads to the dissociation of the catalytic subunits. The freed catalytic subunits then phosphorylate specific serine and threonine residues on target proteins, thereby modulating their activity.
The cAMP-dependent protein kinases are activated in response to a variety of extracellular signals, such as hormones and neurotransmitters, that bind to G protein-coupled receptors (GPCRs) or receptor tyrosine kinases (RTKs). These signals lead to the activation of adenylyl cyclase, which catalyzes the conversion of ATP to cAMP. The resulting increase in intracellular cAMP levels triggers the activation of PKA and the downstream phosphorylation of target proteins.
Overall, cAMP-dependent protein kinases are essential regulators of many fundamental cellular processes and play a critical role in maintaining normal physiology and homeostasis. Dysregulation of these enzymes has been implicated in various diseases, including cancer, diabetes, and neurological disorders.