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    • Koebnerisin (S100A15): A novel player in the pathogenesis of rosacea. J Am Acad Dermatol. 2019 Jun;80(6):1753-1755 Authors: Batycka-Baran A, Hattinger E, Marchenkov A, Koziol M, Bieniek A, Szepietowski J, Ruzicka T, Wolf R PMID: 31103159 [PubMed - in process] {url} = URL to article
    • Related Articles Combined treatment of recalcitrant papulopustular rosacea involving pulsed dye laser and fractional microneedling radiofrequency with low-dose isotretinoin. J Cosmet Dermatol. 2019 May 18;: Authors: Kwon HH, Jung JY, Lee WY, Bae Y, Park GH Abstract BACKGROUND: While a considerable number of cases with papulopustular rosacea (PPR) are resistant to conventional medications, therapeutic regimens are not currently established. Pulsed dye laser (PDL) and fractional microneedling radiofrequency (FMR) have previously demonstrated satisfactory results for anti-angiogenesis, anti-inflammation, and dermal remodeling. AIMS: To evaluate the efficacy and safety of novel combination regimen with low-dose oral isotretinoin, PDL, and FMR in the treatment of recalcitrant PPR. PATIENTS AND METHODS: A retrospective study was undertaken for recalcitrant PPR patients to evaluate the clinical course of novel combination regimen. Twenty-five PPR patients who had failed in previous first-line therapies were enrolled. They were treated with three sessions of PDL and FMR consecutively at 4-week intervals, maintaining daily oral administration of 10 mg isotretinoin for 8 weeks. Objective assessments, erythema index measurement, and patients' subjective satisfaction were evaluated at each visit and 16 weeks after the final treatment. RESULTS: At the final follow-up visit, the number of papules and pustules decreased by 71%, and erythema index by 54% compared with baseline (P < 0.05 for both). Physician's global assessment based on rosacea severity score and patients' subjective assessments paralleled with these results. No serious side effect was observed during whole study periods. CONCLUSION: This novel combination regimen demonstrated satisfactory efficacy with reasonable safety profiles for the treatment of recalcitrant PPR. PMID: 31102325 [PubMed - as supplied by publisher] {url} = URL to article
    • A paper in 2017 continues to explain the quandary. "Many studies have shown higher density of the parasites in diseased inflammatory skin than in normal skin, but whether it is the cause or result of the inflammation remains unclear." [6]  A paper in 2018 may help to resolve this issue because for the first time it has been discovered that Demodex mites secrete bioactive molecules that reduced TLR2 expression in sebocytes. [7] So while the jury is still out on this subject, What do you think?  Which comes first, the demodex or the rosacea? Does it even matter? With your above statement I highlighted and giving my view on this topic which comes first, I am also stating the same thing that I think demodex came first well it is not experiment or evidence based but with the experience I have had. Human Permanent Ectoparasites; Recent Advances on Biology and Clinical Significance of Demodex Mites: Narrative Review Article With this journal which you quoted in your article , "Many studies have shown higher density of the parasites in diseased inflammatory skin than in normal skin, but whether it is the cause or result of the inflammation remains unclear." So I was elaborating this sentence that higher density might be the result of inflammation (inflammatory immune response) and then subsequently the cause of inflammation. So I explained this with the term “reciprocal correlation”. And let’s say if the higher density is the result of inflammation, so the altered cutaneous immune responses are the cause of persistent inflammation and that is what I was trying to state in my post but then I read the above journal in detail after your question and I found the confirmation of my  expression with these sentences of journal   “ Studies indicate increased number of D. folliculorum in immunocompromised patients”  and “It remains to be determined which kind of cellular immunity may foster mites’ proliferation” and my statement “the false immune response(altered immune response) might be the cause of increasing number of demodex”  state the same thing. Thank you for questions because what I was stating is experience based but after thoroughly reading the reference journals from your article I found the confirmation of the same thing.    
    • That is difficult to follow. In a paper by Powell, et al, it is stated that the mites "secrete bioactive molecules that reduced TLR2 expression in Sebocytes." The 'bioactive molecules' that the mites secrete keep the innate immune system from reacting to the mites when in normal numbers on normal skin, so my question is what causes the demodex to proliferate in greater numbers to what you say,  "cause inflammatory immune response and inflammatory immune response" ?   Could you better explain what you mean by "self-antigen presentation to immune cells rather than non-self which is false immune response? ?
    • In my view, normal skin also has demodex mites but less in number so they can't activate pro-inflammatory cytokines but when the number is more they activate it. so logically when the normal skin flora has demodex before rosacea has occured so demodex apparently came first and because demodex mites cause inflammatory immune response and inflammatory immune response is not just related to mites but self-antigen presentation to immune cells rather than non-self which is false immune response or we call it autoimmune response and attacks to healthy cells and so the false immune response might be the cause of increasing number of demodex .So demodex and rosacea have reciprocity with each other to increase its effects and outcomes.
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