TLR4 activation by different bacterial LPS induces production of inflammatory mediators in hPDLCs.22 Similarly, TLR2 activation results in cytokine production by PDLCs32 and gingival fibroblasts.33 Our finding is a further indication that hPDLCs cannot develop any immune tolerance state and this is additional evidence of their role in sustained inflammation in periodontal disease. This evidence concerns the gene TLR2 and periodontal disorder.