Matrix metalloproteinases, their physiological inhibitors and osteoclast factors are differentially regulated by the cytokine profile in human periodontal disease.
OBJECTIVE
Inflammatory reactions raised in response to periodontopathogens are thought to trigger pathways of periodontal tissue destruction. We therefore investigated the expression of matrix metalloproteinases (MMPs) and the osteoclastogenic factor receptor activator of nuclear factor-kappaB ligand (RANKL), their respective tissue inhibitors of metalloproteinases (TIMPs) and osteoprotegerin (OPG) in different forms of human periodontal diseases (PDs), and the possible correlation with the expression of inflammatory and regulatory cytokines.


METHODS
Quantitative polymerase chain reaction (real-time PCR) was performed with gingival biopsies mRNA from aggressive (AP) and chronic periodontitis (CP) patients.


RESULTS
Periodontitis patients exhibit higher expression of all analyzed factors when compared with healthy tissues. The expression of MMPs and RANKL were similar in AP and CP, as well as the expression of TNF-alpha. On the other hand, the expression of TIMPs and OPG was higher in CP, and was associated with lower IFN-gamma and higher IL-10 expression, compared with AP.


CONCLUSIONS
It is possible that the pattern of cytokines expressed determines the stable or progressive nature of the lesions and regulates the severity of PD, driving the balance between MMPs and TIMPs, RANKL and OPG expression in the gingival tissues controlling the breakdown of soft and bone tissues and, consequently, the disease severity.
Garlet
Gustavo P
GP
Department of Biochemistry and Immunology, University of Ribeirao Preto-UNAERP, Dentistry School, Av.Bandeirantes 3900, 14049-900 Ribeirao Preto, SP, Brazil.
Martins
Walter
W
Fonseca
Benedito A L
BA
Ferreira
Beatriz R
BR
Silva
João S
JS
D000328:Adult; D002352:Carrier Proteins / Q000378:metabolism*; D002908:Chronic Disease; D016207:Cytokines / Q000378:metabolism; D004812:Epidemiologic Methods; D005786:Gene Expression Regulation; D006023:Glycoproteins / Q000378:metabolism*; D006801:Humans; D020782:Matrix Metalloproteinases / Q000378:metabolism*; D008562:Membrane Glycoproteins / Q000378:metabolism*; D053244:Osteoprotegerin; D010510:Periodontal Diseases / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D053245:RANK Ligand; D012333:RNA, Messenger / Q000378:metabolism; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear / Q000378:metabolism*; D018124:Receptors, Tumor Necrosis Factor; D019714:Tissue Inhibitor of Metalloproteinases / Q000378:metabolism*
D002352:Carrier Proteins; D016207:Cytokines; D006023:Glycoproteins; D008562:Membrane Glycoproteins; D053244:Osteoprotegerin; D053245:RANK Ligand; D012333:RNA, Messenger; D053246:Receptor Activator of Nuclear Factor-kappa B; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; C505686:TNFRSF11A protein, human; C506030:TNFRSF11B protein, human; C505688:TNFSF11 protein, human; D019714:Tissue Inhibitor of Metalloproteinases; D020782:Matrix Metalloproteinases