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Estimated HIV infected world wide?
2.3-2.8 became infected in 2009
HIV induced oral lesions in adults?
- Candidiasis (erythematous/pseudomembraneous)
- Hairy leukoplakia
- Kaposi sarcoma
- non-hodgkin's lymphoma
- periodontal disease (NUG/NUP)
risk in inverse to CD4 count
Name the 8 identified Herpes viruses?
Pathophysiology of HSV-1?
Primary infection: virus transported via retrograde axonal transport to regional sensory ganglia (V), where latency begins
can be shed in saliva
Clinically aparent recurrent infections are estimated to occur in __% to __% of indviduals harboring latent HSV-1.
Triggers to HSV?
- Irritation by dental instruments
Three clinical forms of recurrent HSV-1?
- 1. Herpes labialis
- 2. Intraoral recurrence (gingiva or hardpalate)
- 3. Recurrence mimicking a primary infection
HSV-1 proposed as a potential etiologic factor of pulpal necrosis
VZV establishes latency where?
Neuronal ganglia (cranial nerve, dorsal root, and autonomic ganglia)
An estimated 13% of zoster cases involve the head and neck.
may lead to pulpal death
failure of epithelial root sheath differentiation
most cases molar
How does taurodontism complicate endo?
ID of canal can be compromised
Affected teeth more prone to manipulative fracture
Three types of Dens in dente?
- 1. Enamel lined
- 2. Enamel lined blind sac that invades the root
- 3. Invades the root and has secondary foramen
Prevalence of dens-in-dente?
involves maxillary lateral incisors
Clinical significance of densindente?
- 1. inc risk of bacteria induced necrosis
- 2. NRSCT difficult due to complexity
use CaOH, ultrasonics, GP warm vertical
Den evaginatus prevalence?
premolar and molar
Clinical significance of dens evaginatus?
narrow shelf of enamel, easily penetrated
Types of DI?
DI Type 1: assoc with osteogen imperfecta, type 1 collagen defect
DI Type II/III: DSPP gene defect
Type II most common 1:6000-8000
Clinical findings of DI?
Amber-brown to blue-gray hue, cracking or loss of enamel, attrition.
Radio Type I/II: bulbous crown structure, cervical constriction, short roots, obliterated pulp chamber
Radio Type III: pulp chamber normal or enlarged, PARLs present
Paget disease of bone (PDB) is a...
heterogenous, focal, progressive bone disease characterized by active bone turnover
men over 40 (1%)
Affected sites for PDb?
pelvis, skull, vertebra, femur, and tibia
Affected bones of PDB manifest an initial ______ phase, followed by a mixed __________/__________, which progresses to a disorganized __________ phase
Clinical signs of PDB?
osseous distortion or expansion, mild to moderate depp aching bone pain
vestublar involvment in 89%
Dental abnormalities of PDB?
Malocclusion, hypercementosis, tooth mobility, root resorption, pulp calcification, osteomyelitis, poor fitting prsthesis,
PDB is cotton wool appearance
PDB radiographic findings?
Hypercementosis, local thickened PDL space, root resorption, pulpal obliteration
Hyperparathyroidism is generalized widening PDL space
Most prevalent form of rickets is caused by mutations affecting the PHEX gene, termed X-linked hypophosphatemia.
XLH dental findings?
- Enlarged pulp chamber and pulp horns
- hypocalcified dentin
- short roots
- poor defined lamina dura
- hypoplastic alveolar ridge
What is pathognomonic for XLH?
Promininent pulp horns extending up to the dentinoenamel junction
causes spontaneous dental abscesses
Most serious type of thalassemia?
Beta, known as Cooley anemia
A characteristic "rodent" or "chipmunk" facies may be observed (maxillary protusion or expansion, bossing of skull, prominent cheek bones)
Percent of AA heterozygous for SCA trait?
Sickle red cell lifespan?
Percent of patients with head and neck manifestations?
Risk of osteomyelitis of the jaws in SCA?
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