Parodontitida je chronické multifaktoriální onemocnění, jehož výsledkem je progresivní destrukce závěsného aparátu zubů. Z hlediska etiologie je důležitá zejména přítomnost paropatogenů a vnímavost hostitele. Vzhledem k velmi omezeným možnostem ovlivnění vnímavosti hostitele zůstává metodou léčby subgingivální ošetření – mechanické očištění povrchu kořenů zubů od zubního kamene a plaku, často v kombinaci s antibiotiky nebo antiseptiky, aplikovanými lokálně nebo systémově. Při systémové aplikaci antibiotik byly popsány vedlejší účinky (průjmy, zvracení, kovová pachuť), nárůst bakteriální rezistence a možný výskyt alergických reakcí. Navíc v horizontu týdnů až měsíců dochází k rekolonizaci parodontu původními, agresivními bakteriemi, a tudíž jejich použití nemá dlouhodobý efekt. Hledají se proto nové terapeutické postupy pro snížení virulence paropatogenů nebo jejich eliminaci. Do popředí se dostávají teorie zabývající se orálním mikrobiomem a vlivem nedostatku „prospěšných“ bakterií. Ve většině studií se prokazuje pozitivní vliv probiotik z hlediska mikrobiologického, imunologického, ale i klinického. Cílem sdělení je seznámit čtenáře se současnými poznatky a možnostmi využití probiotik při léčbě parodontitidy.
Periodontitis is a chronic multifactorial disease, that results in the progressive destruction of periodontal attachment. Periopathogens and host susceptibility are of great importance in the etiology of the disease. However, there are very few ways of affecting the host ́s susceptibility, therefore deep scaling remains the golden standard of the treatment. Deep scaling is a mechanical debridement of root surfaces, often with a combination of antibiotics and/or antiseptics applied locally or systematically. Antibiotics, when used systematically, may have side effects (diarrhea, nausea, vomiting, metallic taste), an increase of bacterial resistance, and possibly allergic reactions. Moreover, in a matter of weeks or months, a re-colonization of periodontal pockets with aggressive bacteria occurs, so their use does not have a long-term effect. Thus, new therapeutic approaches are being sought to reduce the virulence or eliminate periopathogens. Theories dealing with the oral microbiome and the influence of the lack of ”beneficial“ bacteria became a matter of interest and most of studies have shown a positive microbiological, immunological, and even clinical effect of probiotics. The aim of this review is to familirize the use of probiotics in treatment of periodontitis.
- Keywords
- Lactobacillus reuteri,
- MeSH
- Chronic Periodontitis * classification physiopathology therapy MeSH
- Immunomodulation immunology MeSH
- Gingival Hemorrhage drug therapy MeSH
- Humans MeSH
- Periodontal Pocket drug therapy MeSH
- Probiotics administration & dosage pharmacology MeSH
- Dental Plaque drug therapy MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Propeptide blocks the active site in the inactive zymogen of cathepsin D and is cleaved off during zymogen activation. We have designed a set of peptidic fragments derived from the propeptide structure and evaluated their inhibitory potency against mature cathepsin D using a kinetic assay. Our mapping of the cathepsin D propeptide indicated two domains in the propeptide involved in the inhibitory interaction with the enzyme core: the active site "anchor" domain and the N-terminus of the propeptide. The latter plays a dominant role in propeptide inhibition (nanomolar Ki), and its high-affinity binding was corroborated by fluorescence polarization measurements. In addition to the inhibitory domains of propeptide, a fragment derived from the N-terminus of mature cathepsin D displayed inhibition. This finding supports its proposed regulatory function. The interaction mechanisms of the identified inhibitory domains were characterized by determining their modes of inhibition as well as by spatial modeling of the propeptide in the zymogen molecule. The inhibitory interaction of the N-terminal propeptide domain was abolished in the presence of sulfated polysaccharides, which interact with basic propeptide residues. The inhibitory potency of the active site anchor domain was affected by the Ala38pVal substitution, a propeptide polymorphism reported to be associated with the pathology of Alzheimer's disease. We infer that propeptide is a sensitive tethered ligand that allows for complex modulation of cathepsin D zymogen activation.
- MeSH
- Amino Acid Motifs MeSH
- Financing, Organized MeSH
- Glycosaminoglycans metabolism MeSH
- Protease Inhibitors chemical synthesis metabolism MeSH
- Catalytic Domain MeSH
- Cathepsin D antagonists & inhibitors chemistry metabolism MeSH
- Humans MeSH
- Models, Molecular MeSH
- Molecular Sequence Data MeSH
- Peptide Fragments antagonists & inhibitors chemical synthesis metabolism MeSH
- Peptide Mapping MeSH
- Enzyme Precursors antagonists & inhibitors chemistry metabolism MeSH
- Amino Acid Sequence MeSH
- Sequence Homology, Amino Acid MeSH
- Protein Binding MeSH
- Check Tag
- Humans MeSH
