Pulpal inflammatory pauv hloov yuav ua rau muaj kev puas siab puas ntsws ntawm cov hlab ntsha intradental. Vasodilation, nce vascular permeability thiab extravasation yuav ua rau muaj zog intrapulpal siab. Qhov no tuaj yeem ua rau lub paj hlwb ua haujlwm tsis tu ncua.
Dab tsi yog qhov ib txwm muaj lub siab Intrapulpal?
Ib txwm pulpal siab yog nyob nruab nrab ntawm 14.1- 32.6 cmH2O6, 8, 9thaum lub permeability ntawm dentin nyob ntawm tus naj npawb ntawm cov hniav hauv ib cheeb tsam thiab txoj kab uas hla ntawm cov hniav.
Pulp capillary siab yog dab tsi?
Ntau cov ntshav pulpal ntws thiab pulpal capillary siab yog ob qho tib si siab ( 20–60 ml min- 1 (100 g pulp)−1 thiab 35 ± 0.8 mmHg, ntsig txog) (Matthews & Andrew, 1995), thiab pulpal IFP, sib piv rau lwm cov ntaub so ntswg, zoo tshaj atmospheric siab (6–60 mmHg) (Heyeraas & Berggreen, 1999).
Kev tiv thaiv ntawm cov hniav puas yog dab tsi?
Defensive/reparative: the formation of reparative or tertiary dentin (los ntawm odontoblasts); Formative: cov hlwb ntawm cov tawv nqaij tsim cov dentin uas nyob ib puag ncig thiab tiv thaiv cov ntaub so ntswg.
Cov tshuaj tiv thaiv ntawm cov nqaij mos rau caries stimuli yog dab tsi?
Nyob rau hauv teb rau qhov kev thuam thuam, lub plab-dentin complex pib ob leeg innate22 thiab yoog lub cev tiv thaiv kab mob23 Innate tiv thaiv ua lub luag haujlwm tseem ceeb hauv cov caries ntiav tom qab thawj zaug enamel caries ncav cuag lub dentinoenamel hlws ris. Thaum lub sijhawm pib no, cov lus teb ntawm pulpal yuav yog qib qis thiab ntev.
