Quiz 4 Flashcards
(23 cards)
What is the key to effective treatment?
What is the key to accurate diagnosis?
What are the five steps that make up the science of recognizing disease?
- Accurate Diagnosis
- Understanding the pathological process occurring to tissues
- Chief complaint (subjective), medical/dental history (subjective), oral examination (objective), correlate findings, formulate diagnosis.
What are the 5 Subjective tests/Dental History tests?
- Localization of pain
- Commencement/First symptoms
- Intensity (wake at night)
- Provocation/Relief
- Duration
What are the 5 Objective test?
- Palpation
- Percussion
- Mobility
- Periodontal exam
- Pulp tests
What is an inflamed pulp with dentinoclastic activity?
What is long term, low grade pulpal irritation, where dentin formation obliterates the pulp?
What is discrete calcified bodies with no pathological significance?
- Internal Resorption
- Calcific Metamorphosis
- Pulp Stones
STDs, HIV/AIDS and Diabetes are all considered what type of problem?
- Hematologic
There are 5 classifications of pulpal disease, what are they?
- Reversible Pulpitis
- Irreversible Pulpitis
- Pulpal Necrosis
- Previously Initiated Pulpal Therapy
- Normal
What Pulpal Disease has: • Stimulation uncomfortable but reverses quickly • Caries, exposed dentin (most), recent dental treatment, defective restorations, trauma • RCT generally not needed
- Reversible Pulpitis
What Pulpal Disease has: • Symptomatic—Intermittent or spontaneous pain • Stimulation results in heightened and prolonged response • Minimal or no radiographic changes • Pulp will eventually become necrotic • Asymptomatic—Caries possibly into pulp space (best time to treat) • RCT needed
- Irreversible Pulpitis
What Pulpal Disease has:
• Only classification describing histological status of pulp (or lack there of)
• Subsequent to Irreversible pulpitis (Symptomatic or assymptomatic)
• Following complete pulpal necrosis, symptoms usually subside until disease extends into PA tissues
• Cold test—no response
• Heat—sometimes exacerbates pain due to
expansion of gases or fluids
• RCT needed
- Pulpal Necrosis
What dominate intraradicular infections? What are the most common bacteria in Endotontic Infections? What is the main source of microbial irritation to dental pulp and periradicular tissues? What is the goal in vital cases to prevent infection? What is the goal in non-vital cases to remove all microorganisms? True or False, direct pulp exposure to microorganisms is a pre-requisite for pulpal response and inflammation? Primary RTC infections are mostly monomicrobial or polymicrobial? Which are considered the facultative bacteria for these infections?
- Obligate Anaerobes
- Gram Negative
- Dental Caries
- Asepsis
- False
- Polymicrobial Obligate Anaerobes
- Strep, Entero, Lacto and Entero. Faecalis (usually secondary infections)
There are two different types of sensory nerves to the teeth (A-Fibers and C-Fibers), what makes them different?
- A-Fibers (Delta Fibers): Sharp and quick pain. Myelinated and threshold is low.
- C-Fibers: Burning and aching. Not myelinated and threshold is high.
What are the 5 pathways of pulpal disease?
- Dentinal Tubules
- Direct Pulp Exposure
- Caries (most common)
- Latrogenic (restorative procedure gone wrong)
- Trauma
Pulpal necrosis only occurs if periodontal disease/pockets reach the ______ _______ due to damage of blood vessels.
- Apical Foramen
What is when microbes are transported in the blood to areas of tissue damage and is the reason that traumatized teeth become infected?
- Anachoresis or Chemotaxis
What are the three pulpal reactions to protect the pulp against caries? **(Pulp is the only CT in the body with the ability to protect itself)
- Decrease in dentin permeability
- Tertiary dentin formation
- Inflammatory/Immune responses
Response to trauma:
• Increased blood flow leads to vasodilation and an increased
capillary pressure, which leads to increase capillary filtration
which leads to increased tissue pressure resulting in pulpal pain!
• This increased pressure outside the vessels compresses the
thin-walled venous vessels which leads to a decreased blood flow
and increased filtration, strangulating the pulpal vessels
• Occurs only at site of injury—can remain localized for some time
especially if irritant is removed
• If injurious irritant is strong and long lasting, the inflammation will
spread throughout the pulp (from periphery to central to root to
periapical tissues = pulpal necrosis
What are the 5 classifications of Periapical Pathosis?
- SAP: Symptomatic Apical Periodontitis
- AAP: Asymptomatic Apical Periodontitis
- AAA: Acute Apical Access
- CAA: Chronic Apical Abscess
- Condensing Osteitis
What classification of Periapical Pathosis that involves:
• First extension of pulpal inflammation into
periradicular tissues
• Spontaneous pain
• Acute pain to biting or percussion
• Hot, cold, electric sensitivity (pulpitis)
• May or may not respond to Pulp Vitality Tests
• May or may not have PA radiolucency (yet)
• Widened (thickened) PDL • Histology—PMNs and macrophages
• May have liquefaction necrosis
- SAP: Symptomatic Apical Periodontitis
What classification of Periapical Pathosis that involves:
• Caused by Pulpal Necrosis
• Generally assymptomatic
• Little or no pain
• No response to Pulp Vitality Tests
• Slightly sensitive to palpation
• Widened PDL to Extensive lesion (starting lesion at least)
• Granuloma—PMNS, Mast Cells, Macrophages,(no
epithelium)
• Apical Cyst—Stratified squamus epithelium surrounded by
CT containing all cellular components found in granuloma
(Granuloma that contains a cavity lined with
epithelium—Epithelial Cell Rests of Malessev or Hertwigs
root sheath)
• 59%–granuloma, 22%–cysts, 12%–scars, 7%–?
- AAP: Asymptomatic Apical Periodontitis
What classification of Periapical Pathosis that involves:
• Localized or diffuse liquefaction lesion of
pulpal origin
• Destroys periapical tissues
• Disintegrating PMNs
• Necrotic pulp
• Abcess within a granuloma
• Rapid onset of acute spontaneous pain to percussion and
biting and palpation
• Moderate to severe discomfort and swelling—intra and
sometimes extraoral
• Purulence (pus), sinus tract • Surrounding the abscess is granulomatous tissue (an
abscess within a granuloma) • Lymphadenophy—submandibular and cervical • Periapical Radiolucency
• No response to Pulp Vitality Tests
• Varying degree of mobility • Frequently febrile
- AAA: Acute Apical Access
What classification of Periapical Pathosis that involves: • Inflammatory lesion of pulpal origin • Long standing lesion • Same histology as AAA • Generally assymptomatic • Not sensitive to biting • May feel different to percussion • No response to pulp vitality tests • Apical radiolucency • Mucosal or facial sinus tract
- CAA: Chronic Apical Abscess
What classification of Periapical Pathosis that involves:
• Variant of AAP
• Increase in trabecular bone (response to
persistant irritation in pulp) • Mostly mandibular posterior teeth
• May or not be painful
- Condensing Osteitis
When should a Root Canal Therapy be used?
• Hyperplastic Pulpitis—Pulp Polyp • Irreversble Pulpitis—Symptomatic or Assymptomatic • Necrotic Pulp • Symptomatic Apical Periodontitis—SAP • Assymptomatic Apical Periodontitis—AAP • Acute Apical Abcess—AAA • Chronic Apical Abcess—CAA • Condensing Osteitis
