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Spring 2016 Lit ABE Lit
Terms in this set (29)
1. Pulp Anatomy
What are the various experimental techniques that have been used to demonstrate pulp anatomies?
What are the advantages and disadvantages of each technique?
Green; Meder-Cowherd; Krell
Green- Stained w/ red dye. Vertical x-sections. Viewed with a microscope.
Disadvantage: Cannot accurately get all canals in the same orientation
Meder-Cowherd- micro-CT: morphology and incidence of the apical constriction in palatal canals.
Advantages: allows a 3D image, tooth has not been damaged from sectioning
Krell- Resin casts. Disadvantage: Resin may not flow into small spaces
Describe the apical termination area of root canals?
Meder-Cowherd; Dummer; Gani
Meder-Cowherd- 65% of MxM palatal roots did not have apical constriction
Dummer- mean distance from anatomical apex to apical foramen was 0.89mm. 4 types of ACs: 1.) Single 45% 2.) Tapering 30% 3.) Multi- 20% 4.) Parallel 5%
Gani- MxM apical 3mm: P- circular, MB- flat, MB2- circular, DB- circular/flat
What are the most common anatomies/variations in? Why are there variations between studies?
Nosrat; Stropko; Vertucci; Meder-Cowherd
Nosrat- MdM Middle M 20% incidence
Stropko- MB2: Mx1M- present 73% of the time and joined with MB1 45% when present. Mx2M- present 50% of the time and 55% joined with MB1
Vertucci- Mx2PM most variable RC anatomy. Differences in findings because of materials and class schemes
Meder-Cowherd- Variations due to different visualization techniques (staining, sectioning, CT)
What roots commonly show two cnals and what is their relationship?
Skidmore- Md1M: Mesial root- 93% had 2 canals & converge 40% of the time; Distal root- 30% 2 canals & converge 60% of the time
Vertucci- 2 canals found in Mx1M MB root, MxPM, Md Canines, Md1&2M M roots
What are various methods for determining numbers of canals clinically? Are they accurate?
Krasner; Vertucci; Green
Krasner- following root development fusion lines and knowing the chamber floor anatomy laws, # of canals can be determined
Vertucci- study angled RGs looking for fast break
Green- knowledge of canal anatomy
Accessory canals (Lateral canals):
de Deus; Vertucci
de Deus- 27%, mostly apical 1/3, could lead to Endo-Perio issues
Vertucci- 20-60% observed & mostly in apical 1/3
What is the relationship between canal anatomy and morphology and the outline form for access preparations?
Krasner- outline at CEJ was the most consistent landmark observed.
Law ORIFICE location #1: located at jxn of walls-floor
#2: located at vertices of floor-wall line angles
2. Pulp Histology
What are the cellular and extracellular elements of the pulp?
Walton & Pashley; Zerlotti
Walton & Pashley- NON INFLAMM: FibroB and odontoB. INFLAMM: Macrophages, PMNS, lymphocytes, plasma cells and mast cells. 1* EC component-Collagen fibers synth. by ODB and FB. Ground substance: gel-like mass- bulk of pulp w/ complex proteins, carbons and water. Transport and support
Zerlotti- Cells- Endothelial vessels and nerves, FB, ODB, inflamm. ExCellular- glycoproteins, Muco polysacch, proteins w/ large amounts of lysine-hydroxylysine
What are the functions of the pulp?
Walton & Pashley; Pimenta
Walton & Pashley- 1
formation of dentin, 2
nutrition, 3* innervation and defense
Pimenta- Lymph vessels operate to limit the initial effects of inflamm and allow active drainage
What are some of the defense cells in the uninflamed pulp?
Couve; Walton & Pashley; Bernick
Couve- ODB layer connected by gaps jxns serve as 1st line defense. ODB also recognize pathogens and activate immune response
Walton & Pashley- OBD secrete dentin in response to noxious stimuli
Bernick- Lymphocytes have been observed in lumina of lymph vessels
Describe the ultrastructure and function of ODBs?
Walton & Pashley; Couve
Walton & Pashley- 1st cell encountered. Tall pseudostratified columnar in coronal and cuboidal in radicular and almost single, squamous near apex. Can modify dentin structure (peritubular dentin deposition) leading to complete occlusion of tubule- decreased permeability
Couve- highly polarized, pseudostrat. columnar and single layer apically. Extensions into predentin layer. Secrete dentin over lifetime and active in pulpal innervation and defense
What is the extent of the ODB process into dentin?
Holand; Sigal; Walton & Pashley
Holland 1985- Depends on research techniques used. More research required.
Sigal- SEM & immunofluorescence 3rdM- ODB process to the DEJ
Walton & Pashley- extend to the inner third of dentin only
What are the general patterns of nerve supply in the pulp and dentin? Does it change with aging?
Johnsen- UnMyel enter first and 3-4x in quantity (max # at eruption). Myel reach max # post-apical closure.
Fan out towards pulp-dentin border. Most nerve endings at pulp horn, then central, radicular least
Byers- Few terminal branches in root, most form plexus of Rashckow and terminate in ODB layer, predentin and as far as 120um in D tubules. Reactive dentin poorly innervated. Nerves mineralize with aging.
What are the general patterns of vasculature, both blood and lymphatics?
Bernick- lymph vessels originate as "blind sacs" along ODB layer--> small vessels-->larger vessels that accompany blood vessels-->exit thru Apical Foramen and empty in PDL lymph. Blood vessels few in immature and increase Apical-->coronal as matures. Rich network in subODB layer
Walton- Substances placed in pulp chamber were found in regional lymph nodes. A-V shunts disperse blood at periphery of pulp
What are changes that occur as pulp progresses from young to aged?
Bernick- reduction in chamber size and deposition of calcified masses. Blood vessels and nerves calcify and #'s decrease. Increased fibrosis
Zerlotti- decrease ratio GS to collagen, decrease solubility, chemical reactivity and water content
Are there changes in pulp structure/fxn with inflammation?
Pimenta- increase lymph vessels to remove excess interstitial fluid and limit effects of tissue pressure
Walton- may lead to pulp stones; PMNs phagositze bacteria and dead pulp cells; increased pressure but not enough for strangulation of pulp
Describe the ultrastructure and fxn of the fibroblast at the various stages of development and the fibroclast?
Walton & Pashley; Tran-Hung; Han
Walton- FB synthesize and secrete collagen
Tran-Hung- FB secrete angiogenic factors at sites of pulp injury
Han- Immature FB at proximal end, mature in mid-pulp; incisal fibrocytes become less active and organelles shrink
3. Pulp Phys I: Blood Supply
What techniques have been used to study pulpal rxns to various stimuli?
Giovanella; Kim; Walton & Langeland
Giovanella- pulse oximetry showed reduction in pulp O2 SAT with PD attachment loss shows perio dz correlates w/ level of pulp O2 SAT
Kim- blood flow changes using radiolabeled microspheres
Walton & Langeland- applied sealer to vital pulp stumps and observed migration
What local factors affect pulpal blood flow?
Giovanella; Kim; Krell
Giovanella; Kim; Krell
Giovanella- PD attachment loss associated with pulp O2 SAT
Kim- neuropeptides are released during noxious stimulation and they alter vascular fxn leading to increase in tissue pressure
Krell- artherosclerotic monkeys had no changes in pulpal vasculature
Describe Starling's Law.
Van Hassel- relationship between hydrostatic and osmotic pressures determining direction of fluid movement across vessel walls
What evidence supports the presence of a lymphatic system in the dental pulp?
Walton & Langeland
Walton & Langeland- sealer particles on vital pulp were found in lymph nodes= indirect evidence of lymphatic drainage
Describe the fxn of the architecture of pulpal vasculature.
Kim- transport nutrients and remove metabolic waste
Bernick- during inflamm,, vasodilation leads to increased tissue pressure; lymphatics regulate fluid pressure build up
Describe the "strangulation theory." Does it occur?
Kim- pressure from inflammation closes off all blood vessels leading to necrosis; coronal pulp inlfamm, is localized and apical blood flow NOT affected. Strangulation does not occur
Heyeraas- During inflamm, Net colloid osmotic pressure, lymph flow and capillary draingage prevent strangulation
Describe the mechanism of pulp death and recovery
Kim- Noxious stimuli leads to inflamm mediator and neuropeptide release causing increased tissue pressure. Tissue pressure elevation in low compliance systems (such as the pulp) lead to a decrease in PBF (contrary to other tissues). Without the removal of inflamm mediators, vessel damage goes unchecked slowly leading to pulp necrosis
Kim- Recovery of the pulp can occur (HYPOTHETICALLY) by shunting blood in the apical 1/3 by means of AV anastomoses AND U-turn arterioles
4. Pulp Phys II: Nerve Supply
Three main theories of dentin sensitivity:
1.) Direct innervation- EM have shown nerve fibers in some tubules, but not extending to DEJ
2.) Odontoblastic Receptor- OBstic processes act as receptors for conduction and transmission of impulses. Transmission from OB to nerve has yet to be shown
3.) Hydrodynamic Theory- (BRANNSTROM) postulates that rapid inward/outward movement of dentinal/pulpal fluid causes displacement of dentinal tubules contents, distorting mechanoreceptors
What are the effects of various stimuli to dentin on pulpal nerves?
Munoz- inflamm (caries, cavity prep, ortho forces) results in sprouting of afferent fibers and release of neurogenic mediators
Fried- occlusal forces, attrition, and aging lead to increased reactive dentin and axonal atrophy
What is the response of Na channels to inflammation?
Henry- deep caries resulted in demyelinization of pulpal nerves and decreased Na channels
Rogers- Voltage gated Na channel expression is increased and appears to play a major role in inflamm pain
What neural effects are seen with inflammatory mediators- neuropeptides?
Munoz; Hargreaves; Fristad
Munoz- CGRP, SP and NKA generate vasodilation and increase PBF and exert long -lasting control
Hargreaves- activations of PGE2 and TRPV1 have been implicated in the generation of inflammatory pain
Fristad- rapid release of SP and CGRP from sensory nerves after dentin prep leads to vasodilation and increased PBF
Describe possible factors involved in dentin sensitivity
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