After The Domestic Rabbit T.M.J Indirect Damage Injects The Anti-VEGF Reagent Effect In Its Ticulare The Research

The research indicated that,T.M.J after receives a time more serious indirect damage to be possible to send the joint the damage, arthrocleisis or osteoarthropathy formation. How regardless of the course of an illness does transfer turns over to, follows the inflammation and the vascularization. This research through carries on the indirect damage after domestic rabbit T.M.J to inject Anti-VEGF in its ticulare (VEGF is presses one of main factors which blood vessel produces) the reagent, thus further studies oppresses the anti-vascularization factor regarding the T.M.J indirect damage organization's influence.VEGF at first discovery is by the tumor cell secretion one kind of protein, it can increase the partial blood vessel to the blood circulation in the macro-molecule permeability, calls it the blood vessel insightful factor (vascular permeability factor VPF).At present thought VEGF belongs to the secretive glycoprotein, is promotes the blood vessel endothelial cell mitosis, the multiplication and the migration specificity factor, can strengthen the blood vessel permeability, induces the new vascularization, the increase organization blood stream irrigation and the improvement organization lacks blood condition .VEGF in extremely low density ( < 1nmol/L) can play the effective promotion blood vessel permeability role, its function intensity is equal to histamine 5 ten thousand times.Research demonstrations and so on Brown damages latter 2～3 day in the wound namely to have the special high permeability vascularization, and continues above 7 day.VEGF mainly through the upward endothelial cell surface conformity element acceptor expression, lures to be called the bone bridge the agglutination glycoprotein and it union, the promotion endothelial cell migration.lt also can increase the intercellular space adherency member and the blood vessel cell adherency member level and on the induction endothelial cell its ligand and the acceptor expression, and surrenders to the state the serine protein enzyme activity, thus degrades the too dense extracellular matrix ingredient, promotes the vascularization.The maxillofacial damage, after specially the mandible department suffers the external force attack often indirectly to create the temporomandibular joint (TMJ) damage, so that causes the condyloid bone fracture, damage osteoarthropathy, in the joint the fiber proliferation the arthrocleisis and so on the complications and the sequela. Although the pathological change extension turns over to many and varied, but the common synovitis,bone degrades,osteophyte formation and under superfluously the cartilage the bone board accumulation characteristic value change obtained the widespread approval.Regardless of what kind of pathological change follows the inflammation blood vessel to produce this pathology process.The detailed process produces which about the blood vessel had the literature to report that, but the blood vessel production possibly is the inflammation important maintenance factor is not the inflammation start factor.In the joint continues the inflammation to be possible to cause the joint organization destruction and finally to cause a series of pathology process which the bone repairs.The newborn blood vessel to the macro-molecule material permeability increase, promotes dropsy to form like the soluble E selective protein adherency factor to express the promotion inflammation cell in the newborn blood vessel to invade Run highly, not only that the newborn blood vessel has to the inflammation region transportation inflammation and the nutrients can maintain the inflammation reflection, the newborn blood vessel lacks the nerve and the peptide class material adjustment factor, thus lacks to the inflammation blood vessel control action.The blood vessel production invades Run through the increase inflammatory cell also to be possible to stimulate the blood vessel production indirectly.The synovitis early time stage blood vessel production may promote the acute inflammation to turn over to the chronic inflammation extension finally to cause the organization destruction and the proliferation.But took promotes important factor VEGF which the blood vessel produces (blood vessel bast growth factor) in the joint disease occurrence development function more and more to be valued researcher's.Recently studies factors and so on confirmation mechanical stress and oxygen deficit may stimulate the joint organization cell to express blood vessel original factors and so on the VEGF, thus promotion blood vessel production.This research through and injects VEGF to the wound arthritis joint in to oppress the anti-reagent regularly (the VEGF multi-clone immune body), attempts to disturb the blood vessel to produce this pathology process, through to tests the result statistics analysis and the deduction recognized this experiment has achieved the anticipated effect.At present, might cause the temporomandibular joint osteoarthropathy (TMJOA) and other clinical illness mechanism regarding the indirect TMJ damage still knows not clear.Some research believed that, the damage destroyed or has suppressed the condyle suddenly cartilage multiplication ability, caused the cartilage matrix to carry on the nature to lose, thus caused the clinical various illness.But not yet sees the related experimental study report at present. But regarding TMJ serious damage treatment also many by surgery primarily.Through this experimental research, hoped can establish one about the TMJ indirect damage multi-dimensional cause of disease and the treatment way.Methods1 Examines 32 domestic rabbit TMJ with the conventional organization HE staining method the joint synovial membrane and the articular cartilage.2 Using Safranin O the staining method examination domestic rabbit TMJ articular cartilage, and examines with the spectrophotometer Extinction3 Application pathology damage index, joint synovial membrane blood vessel density integral and articular cartilage content.Results1 passes through conventional HE staining method examination domestic rabbit TMJ the articular cartilage pathology damage index.The articular cartilage experimental group's mean value and the standard deviation are 1.25±0.46/4 the week, 2.00±0.53/8 week.Control group's mean value and the standard deviation are 2.88±0.35/4 the week, 3.25±0.46/8 week. Carries on the statistical inference after the galley proof application factor T-test 4 week and 8 week-long P values is smaller than 0.05.2 passes through conventional HE the staining method examination domestic rabbit TMJ synovial membrane the blood vessel density integral.The joint synovial membrane experimental group's mean value and the standard deviation are 5.25±0.71/4 the week, 6.13±0.83/8 week.Control group's mean value and the standard deviation are 19.25±1.28/4 the week, 29.00±1.85/8 week.Carries on the statistical inference after the galley proof application factor T-test 4 week and 8 week-long P values is smaller than 0.05.3 passes through Safranin O special staining examination domestic rabbit TMJ the articular cartilage cartilage content.The articular cartilage experimental group's mean value and the standard deviation are 2.48±0.21/4 the week, 2.89±0.14/8 week.Control group's mean value and the standard deviation are 1.59±0.29/4 the week, 1.75±0.16/8 week. Carries on the statistical inference after the galley proof application factor T-test 4 week and 8 week-long P values is smaller than 0.05. conclusionThis experiment through conventional and special staining method examination domestic rabbit pathology damage index, joint synovial membrane blood vessel dense integral and articular cartilage content.The above findings showed the control group cartilage content and the disturbance group cartilage content both comparison has the remarkable difference, P< 0.05.Two groups have the inflammation index also to have statistics difference, obviously applies oppresses the anti-blood vessel production reagent to be possible obviously to enhance the TMJ indirect damage the articular cartilage content, prompts the blood vessel inhibitor to break the TMJ articular cartilage to destroy.