暗瘡對大部份人來說可謂是一道萬惡的存在，尤其是愛靚唔愛命的女士們的公敵。676Please respect copyright.ＰＥＮＡＮＡeeyxUAoiB2
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在講述暗瘡的形成之前，我們首先需要了解一下皮膚的背景資料。676Please respect copyright.ＰＥＮＡＮＡRvGthwcB9L
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（圖1）皮膚是人類最大的器官，它是我們一道抵禦外來物入侵的防線，同時亦提供了一個優良環境給予各式各樣的細菌及真菌成長及聚居。676Please respect copyright.ＰＥＮＡＮＡEk5rqiEao7
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除皮膚表層外，那些細菌及真菌亦可聚居在髮囊、負責散熱的汗腺及負責分泌油脂的皮脂腺裡頭。676Please respect copyright.ＰＥＮＡＮＡHefGmYfqvM
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（圖2）皮膚最外層的細胞全都是已死的細胞(Dead Cells)，學名為Enucleated keratinocytes。676Please respect copyright.ＰＥＮＡＮＡUBQ5BkTjAR
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這些已死的細胞會不斷脫落，大概每日總共會脫落50億這些已死的細胞，而下層已死的細胞會逐漸補上，日復如是。676Please respect copyright.ＰＥＮＡＮＡkaix5QjWMO
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（圖3）暗瘡的形成，與那些表層細胞有著莫大的關係。676Please respect copyright.ＰＥＮＡＮＡddTEsIjuh8
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以下為形式暗瘡的簡略三步曲：676Please respect copyright.ＰＥＮＡＮＡu1OpzWWK3i
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1.皮膚表面已死細胞脫落到髮囊裡頭。676Please respect copyright.ＰＥＮＡＮＡTuDc99CvH1
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2.皮脂腺釋出油脂，因已死細胞阻窒通道，導致油脂無法離開，久而久之便成為黑頭。676Please respect copyright.ＰＥＮＡＮＡWg5mz1D3Mc
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3.聚居在油脂腺的細菌分解油脂為更簡單結構的油脂物，而這些油脂物觸動發炎反應，造就暗瘡的誕生。676Please respect copyright.ＰＥＮＡＮＡRqymGGQSnp
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（圖4）青春期荷爾蒙作怪，油脂分泌特別旺盛，所以年青人特別容易生暗瘡。676Please respect copyright.ＰＥＮＡＮＡGJtCUrLZZl
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但是，有些人就算做足日常護理都會特別容易生暗瘡，而有些不愛日常臉部護理的懶鬼就死都唔會生暗瘡，裡頭究竟是甚麼原因呢？676Please respect copyright.ＰＥＮＡＮＡbGq6ZDgrci
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（圖5）大量的研究指出，Cutibacterium acnes (C. acnes)是人體皮膚最常見且數量眾多的一種細菌，亦是暗瘡促成的元兇。676Please respect copyright.ＰＥＮＡＮＡ7mxblj2Z9e
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易生暗瘡以及不易生暗瘡的人，C. acnes 數量並沒有太大的分別，但品種上有著一道顯著的分別。676Please respect copyright.ＰＥＮＡＮＡUUOX9dytRS
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易生暗瘡人皮膚上的C. acnes 品種更有效率代謝皮脂腺所釋出的油脂，亦即是更容易促成發炎反應形成暗瘡。676Please respect copyright.ＰＥＮＡＮＡ99FmMrzuxa
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（圖6）現時治理暗瘡的手法大多會用上benzoyl peroxide或retinoic acid，目的是刺激皮膚及減低油脂的分泌。676Please respect copyright.ＰＥＮＡＮＡUTXw19xJbE
隨著科技的進步及對皮膚細菌的認識，科學界有著思想上的轉變，認為改變皮膚上的細菌群組才是對付暗瘡治標且治本的方法。676Please respect copyright.ＰＥＮＡＮＡLoyIh3ZEed
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現時只至有三種治理暗瘡的嶄新手段正進行臨床階段之中。676Please respect copyright.ＰＥＮＡＮＡd7VXDWwkFt
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1.把不易生暗瘡的人皮膚表面上的C. acnes放到易生暗瘡人士上，企圖以良幣消除劣幣的方式取代舊有的C. acnes。676Please respect copyright.ＰＥＮＡＮＡgkDwiJRNgQ
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2.把失去化謝油脂能力的C. acnes取代舊有的C. acnes。676Please respect copyright.ＰＥＮＡＮＡfQ4kbliLms
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3.把懂得釋放抑制發炎化應化學物的C. acnes取代舊有的C. acnes。676Please respect copyright.ＰＥＮＡＮＡCE8GEN07iA
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今年的十月相信會有這些臨床研究的進一步結果的分析，但願這種治療方式會為暗瘡人士帶來一股新希望。676Please respect copyright.ＰＥＮＡＮＡPqcfy1bUt9
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