others Flashcards
(20 cards)
Why do we get anesthetic failures?
Hargraves – Endodontic Topics Vol.2
- Anatomic causes – variations in anatomy
- Acute tachyphylaxis
- Effect of Inflammation on local tissues (pH)
- Effect of Inflammation on blood flow – vasodilation
- Effect of Inflammation on nociceptors – allodynia
- Effect of Inflammation on central sensitization
- Psychological factors
Focal Infection – Does it occur today?
No – Correlation does not mean causation !
“focal infection” term coined by WD Miller 1890 found gangrenous pulps could act as centers of infection causing alveolar abscesses.
William Hunter attributed a multitude of diseases to “focal infection”
Billings 1912 introduced “focal infection” theory to USA
Rosenow, reported that streptococci present in diseased organs could establish an infection in a distant organ after traveling through the blood stream.
No evidence - does not pass scientific scrutiny
Siqueira – endodontic infections can cause bacteremia – no evidence that organisms from RCT can cause disease in remote sites.
Wahl - defines focal infection as “a localized or generalized infection caused by dissemination of microorganisms or toxic products from a focus of infection”.
Are antibodies present in the pulp?
YES
Langeland – antigens in the root canal system can initiate an immune response with antibodies
Martin – Immunoglobulins are present in the pulp which react with microorganisms
Hahn – IgG, major class of immunoglobulins in normal and irreversible groups.
Pulver – Normal pulps do NOT have immunoglobulins-containing cells. In inflamed pulps, IgG most common, IgA, IgE, IgM containing cells are also seen.
What is the role of the neuropeptides?
Byers – injury leads to “sprouting” of CGRP fibers
Wakisaka – neuropeptides may help regulate pulpal blood flow + pain transmission
Olgart – sensory nerves may play a role in instant (increase blood flow) defense reaction in the pulp.
Hargraves – sympathetic transmission may modulate pain (capsaicin study)
Vascular response to pulpal inflammation
Kim - key components in pulpal inflammation
- microcirculation – increased PBF by C fiber stimulation (neurokinins, substance P, released from c fiber nerve terminals)
- sensory nerve activity – excitatory/inhibitory effect from increased/decreased pulpal blood flow via increased tissue pressure.(A delta fibers)
What cells are found in a periapical granuloma?
Stern’s study results – Inflammatory Cells = 52% of all cells 1. Macrophage = 24% 2. Lymphocyte = 16% 3. Plasma cells = 7% 4. PMNS = 4% Other Cells 1. Fibroblasts = 42% 2. Epithelial Cells = 5% 3. Vascular cells = 6%
Perrini – found mast cells in varying stages of activity
Pulver – found 70% IgG, 14% IgA, 10% IgE and 4% IgM
Cysts have 45% IgG, 45% IgA, 5% IgE and 5% IgM
Torabinejad – Granulomas & Cysts have T and B cells, T Cells were in greater quantity.
Cellular Activity & their Mediators
- Ito – Macrophages & Fibroblasts produce PGE2 which may contribute to the osteolytic resorption of periapical lesions.
- Hamachi – Macrophages contribute IL –1, an important activator of osteoclastic bone resorption.
- Torabinejad – NK Cells – defensive role in controlling root canal infections
- Fouad – Pulpal and periapical pathosis were independent of the presence of functional T and B cells
- Torabinejad – high concentrations of LTB4 in symptomatic human periapical lesions
Cytokines and their activity
Cytokines are soluble polypeptide products of immune cells.
Modify behavior of other cells
Produce systemic effects
Act as growth factors
- Stashenko – IL1alpha – contributes to resorptive activity
- Stashenko – IL1alpha, IL1beta, TNFalpha, PG, bradykinin, and LPS – stimulate resorption either alone or in synergistic combination.
- Safavi – TNF identified in periapical exudates from CAP
- Stashenko – IL1alpha and beta, TNF and lymphocyte-derived lymphotoxin potentially stimulate resorption and inhibit reparative bone formation
Describe the Compliment cascade
- Mediate vascular responses
a. Histamine release via C3a and C5a anaphylatoxins - Recruiting phagocytic leukocytes
- Opsonizing targets of phagocytic cells (C3b)
- Directly damaging target cells (C5-9 MAC)
Most important step is cleavage of C3
Classical pathway is activated by Ab coated targets or Ag-Ab complexes (IgM,IgG)
Alternate pathway is activated by LPS, aggregated IgM or IgG, Ag-IgG complexes, plasmin
Who studied LPS?
Schilder –
- pulpless teeth contain greater concentration than vital teeth
- symptomatic w/ AP contained greater concentrations than asymptomatic
Berganholtz –
1. endotoxic activity correlated with the presence and number of Gram – bacteria
Horiba –
- higher concentrations in symptomatic teeth than asymptomatic
- higher concentrations in teeth with radiolucencies
- higher concentrations in teeth with exudation than without
Hydrodynamic Theory of Dentinal Sensitivity
Brannstrom –
- heat causes inward fluid movement in tubules
- cold causes outward fluid movement in tubules
- concurrent distortion of odontoblastic process stimulates nerves at the pulpo-dentinal junction.
- distortion leads to impulse conduction
What lines sinus tracts?
Baumgartner –
- 100% of sinus tracts are lined with epithelium to the level of the rete ridge
- 67% had granulomatous tissue lining the tract
- 33% had epithelium lining the entire way
Harrison –
- Sinus tracts may be lined with epithelium 10%
- lined with granulation tissue 90% of the time
LA complications:
- stimulatory phase: talkativeness/agitation
- Generalized convulsive state
- CNS depression
LA toxicity treatment:
Protect patient Monitor & record vitals Provide supportive therapy Keep patient supine O2 w/ 10L flow/min Maintain BP Treat bradycardia (0.4 mg atropineIV) Transport to hospital
Pulpal Changes as related to depth of bacteria –
- Baum – found correlation between depth of penetration of bacteria and severity of inflammation
- Brannstrom – Pulpal changes occur early in caries, even in incipient lesions. Impairment of odontoblast layer, accumulation of lymphocytes
- Reeves & Stanley – Irreversible pulpitis detected when bacteria were 0.5mm from the pulp, little pathosis seen if >1mm from pulp. If bacteria invade repairative dentin – irreversible pulpitis.
- Stanley – rate of repairative dentin formation = 1.49 micrometers/day, tertiary dentin begins 19 days after operative procedures.
- Torneck – tissue from pulp exp = abscess components, nerves least effected
- Langeland – Carious exp caused increased PMSs, chronic inflammatory cells cause most cell injury.
- Classic - Seltzer/Bender – described classic caries progression to pulp
Are Mast Cells in the Pulp ?
Farnoush – yes, found in inflamed and un-inflamed pulpal tissue
Who found lymphatics in the pulp ?
Bernick – demonstrated lymphatics in the pulp
Heyerass - the pulp may have a beneficial blood flow increase during inflammation in spite of simultaneously increased tissue pressure. This supports the concept of lymphatic drainage.
Do Odontoblast process extend into the tubules?
- Sigel – odontoblastic process extends to DEJ
- Holland – Odontoblastic process extends ½ way through the tubule.
- Aubin – Odontoblastic process extends to DEJ
- Thomas – dentinal tubules are lined throughout their length by an organic structure, the lamina limitans, which can be mistaken for odontoblastic processes.
Who studied pulpal vasculature ?
Kim & Tekahashi – discovered presence of arteriovenous anastomosis and venous-venous anastomosis and u shaped arterioles (unique feature of pulpal vascular network)
Also found sympathetic adrenergic vasoconstritor fibers
Tonder – localized increased tissue pressure may persist in the inflamed area w/out a circumferential spread to the rest of the pulp. Negative feedback system prevents self-strangulation (lymphatic drainage)
Pulp Stones / pulpal calcification
- Bernick – age causes decreased vascularity, nerves, pulp chamber size and increased calcified masses in the pulp
- Hendricks-Klyvert – incidence of calcifications 8-90%
a. Pulp stones – calcifications
b. Denticles – composed of dentin
