• periodontitis
• CD14
• polymorphism
• lipopolysaccharide

Periodontitis, a chronic inflammation of the tissues surrounding the teeth, is a common disease affecting all populations. The main aetiology remains a bacterial infection that leads to gingival inflammation, loss of alveolar bone, and tooth loss.¹ Although the presence of pathogenic micro-organisms is required to trigger this process, the amplification and progression of the disease is believed to rely heavily on the production of host mediators in response to bacteria and/or their metabolic products.² The CD14 molecule, described as the major endotoxin receptor, is one of the receptors which act on the recognition of lipopolysaccharides (LPS, endotoxin) and gram positive or mycobacterial cell wall components and thus can initiate the innate immune response to bacterial invasion.^3–5 It is constitutively expressed primarily on the surface of monocytes, macrophages, neutrophils, and gingival fibroblasts (mCD14).⁶ In addition, a soluble form of CD14 (sCD14) is abundant in serum and is apparently derived both from the secretion of CD14 and from enzymatically cleaved glycosyl-phosphatidylinositol anchored mCD14.⁷ Besides the role of CD14 in the host defence, several other biological functions have been found. CD14 is involved in the phagocytosis of gram negative bacteria,⁸ LPS mediated bone resorption,⁹ and monocyte-endothelial cell interactions. Furthermore, changes in CD14 expression and serum sCD14 levels seem to be associated with a number of pathological states including periodontal diseases.¹⁰

CD14 production is genetically regulated. The gene for the CD14 receptor is on chromosome 5 (region q23-21), consists of ≈3900 bp organised in two exons, and encodes a protein of 375 amino acids.¹¹ In the promoter region of the CD14 gene, a C to T transition was identified at position –159 upstream from the major transcription site, which is near to an SP1 binding site that has a major influence on the monocyte …