6. NEW THEORIES Trauma From DISCLUSION (2017)
The mechanics of dental occlusion and disclusion Thomas R. Katona, George J. Eckert PII: Clinical Biomechanics 2017; S0268-0033(17)30222-X
N= Force; f=Friction; R= contact force vector; U/D= Tooth moving upward or downwards
8. QUESTIONS
1. Why is inflammation
characteristically absent in TFO?
What are the prominent cellular
processes in this regard?
2. What is the role of TFO in
Periodontal Medicine?
Description: Newer theories/ mechanisms behind TFO? Types of forces causing TFO? Isometric and isotonic forces?
Frequency=Number; Intensity=Amount of force
The elapsed time in seconds, measured from the beginning of an excursive movement that is commenced with all teeth in complete intercuspation, and is made in one direction through until only canines or incisors are in contact. The schematic depicts all external forces that act on the tooth, including 4 occlusal contact forces and the tensions in the PDL oblique and apical fibers (large arrows) and the distributed tension and compression applied to the root by the PDL matrix (small arrows). . Occlusal contact forces. (A) When 2 curved surfaces contact, (B) the contact force vector (R) is the vector sum of the normal (perpendicular, N) and the force of friction (f) components, R = N + f. f acts along the contact surface, and if the impending, or actual, motion of the upper tooth is downward (or the lower tooth upward) then the sense of the friction force is toward the left and down, fD. If the motion of the upper tooth is upward (or the lower tooth downward) then the sense of the friction force, fU, is upward to the right. In both instances, the contact force is the vector sum, R = N + f. Thus, in this illustration, as the teeth occlude, the contact force on the mandibular tooth, RD, would be nearly vertical. But during disclusion, the contact force, RU, is more horizontal. (C) and (D) show the movements of the contact point, and the associated contact forces, as the teeth occlude (● ⇨ ○ in C) and disclude (● ⇨ ○ in D), respectively
NLRP3 inflammasome structure. NLRP3 inflammasome consists of three major components-the sensor NLRP3 protein, the adaptor-apoptosis-associated speck-like protein (ASC) which contains a N-terminal PYRIN-PAAD-DAPIN domain (PYD) and a C-terminal caspase recruitment domain (CARD) and the effector protein-caspase-1. Activation of NLRP3 occurs when the cell is subjected to pathogen-associated molecular patterns and damage-associated molecular patterns. The stimulated NLRP3 interacts through PYD domain with ASC and pro-caspase-1 binds to ASC via CARD to assemble into a large cytosolic complex, which triggers activation of caspase-1. Active caspase-1 cleaves the pro-inflammatory cytokines interleukin 1β (IL-1β) and IL-18 from their precursors to their biologically active forms inducing inflammation. ASC: Adaptor-apoptosis-associated speck-like protein; CARD: C-terminal caspase recruitment domain; PYD: PYRIN-PAAD-DAPIN domain; IL: Interleukin; PAMPs: Pathogen-associated molecular patterns; DAMPs: Damage-associated molecular patterns