Study Notes
3/30/17
Bulla
- Circumscribed, elevated lesions (+5mm), contains serious fluid - blister
Lobule
- Lobe that is part of a whole ; fused together
Macula
- Freckle flat, different colour
Papule
- Circumscribed lesion ( -1cm), elevated
Pedunculated
- Stemlike or stalk base
Pustules
- Circumscribed elevated contained pus
Sessile
- Base of a lesion flat or broad instead of stemlike
Vesicle
- Small, elevated lesion less than 1cm contains serious
Nodule
- Solid lesion up to 1cm- can occur above or beneath the skin
Erythema
- Redness
Pallor
- Paleness
Corrugated
- Wrinkled
Fissure
- Groove with depth
Papillary
- Small, nipple-shaped projections in clusters
Wound healing
Primary repair
- Edges are brought together (coapt)
- Clean cut
- Surgical incision little loss of tissue
Secondary repair
- Biggest scar
- Abrasion -edges are far apart (tooth extraction)
- 4-5 days to re-epithelialize (1mm/day)
- Connective tissue (1mm/2-3 days)
Tertiary repair
- Granulation form inside out
- Large scar
- Delayed healing
- Wound kept open to allow for drainage
- Health granulation bed formed may be closed with sutures
Guided tissue regeneration
- Cotex on root
- Putting back original tissue/cells
- Allows the PDL to come out of tissues
- GCT fills in
- Bone regrows to some degree
-
Biologic width
- Must be maintained
- PDL/GCT/JE
Regeneration
- Repair with the same cells (re-populating) no scar
Repair
- Repair with new cells (scar)
Stages of wound healing
1. Haemostasis (stop bleeding)
a. Vasoconstriction
b. Platelet activation
c. Coagulation
2. Inflammation INITIATES HEALING PROCESS -info below
3. Proliferative
a. Revascularisation/ angiogenesis
b. Granulation
c. Epithelialisation
d. contraction
e. Initial tissue granulation tissue (immature cells)
f. Epithelial cells prepare new tissue at the same time granulation tissue
is building connective tissue
g. +7 days fibrin digested by tissue enzymes off
h. Surface appears redder (thinner epithelium)
i. +14 days scar if formed, mature granulation tissue
4. Remodelling
a. Initial granulation and fiber is remodeled
b. Wound is healed and the initial scar tissue is reconstructed
Healing takes about 2 weeks
2. inflammation
Occurs almost simultaneously in epithelium and connective tissue
- Epithelium is faster
Acute inflammation
- Neutrophils (PMNS)
- Emigrate by chemotaxis
B-lymphocytes are in saliva
Integrins on the surface of the leukocyte bind to adhesion molecules on the inner
surface of the vascular endothelial cells.
Leukocytes flatten out and squeeze between endothelial cells to leave blood vessels
(diapedesis) and enter tissue
Neutrophils decrease in number
Macrophages, lymphocytes and plasma cells predominate with CHRONIC
INFLAMMATION
3 systems
1. Kinin system
a. Increased blood vessel dilation/increased vessel permeability
2. Clotting mechanism
a. The clot contains fibrin, clumped red blood cells (RBCs), and activated
platelets.
3. Complement system
a. Plasma protein
b. Polysaccharides found on the surface of bacteria can activate the
system
c. Specific immune response can activate the system
Mediators of inflammation
- Endotoxin
o Produced by cell walls of GRAM NEGATIVE bacteria
o Chemotactic factor, can activate complement, function as an antigen
+damage+bone+tissue
- Lysosomal enzymes
o Similar chemical composition and action as those released by WBC
Manifestations of inflammation
1. Fever
a. Pyrogens
i. Fever producing substances produced by WBC and pathogens
ii. Act on hypothalamus
iii. Hypothalamus increased body temp by prostaglandins
2. Leukocytosis (osis always means increase) -penia means decrease
a. Increased number of WBC from 4000-10000
b. Neutrophil is the primary cell
3. Elevated C-reactive protein-produced in liver
a. Interacts with complement system
b. Chronic increased level is associated with caridio. Disease
4. Lymphadenopathy
a. Enlarged lymph nodes
b. Hyperplasia
i. Increase in number of cells
c. Hypertrophy
i. Enlargement of individual cells
NB:
Oral mucosa less prone to scar tissue than skin
Complications in wound healing
1. Dehiscence (burst)
a. Too few capillaries = ischemia
b. Develop into ulcer
2. Scar herniation (bulge)
a. Build from too much collagen are either hypertrophic scars or keloids
b. Overgrowth of healed area
3. Contractures
a. Excess scars from tight ridges along the skin and permanently interfere
with normal movement
b. Scar tissue is larger
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Microphnathia
- Abnormally small jaw
- Primarily mandible -maybe because it develops by its self (max develops with
the face)
- May be hereditary
- Orthognathic surgeon -surgeon of the jaw
Macrognathia
- Abnormally large jaw
- Primarily mandible
- Resulting in Class III malocclusion
- Hereditary
- Pituitary gigantism
- Pagets disease
- Acromegaly
Agnostic (A-means without)
- Without a jaw
Cleft Palate
- Develops in weeks 7-9
- Cleft soft palate if untreated problems with speech and swallowing develop
- Extension from lip through soft palate and uvula
Fordyces granules (lips) **
- Misplaced sebaceous glands
- Ectopic misplaced
- Normally around hair follicles, lips and buccal mucosa
Congenital lip pits
- Mandible forms in one piece-slows towards the middle -forms pits
- Commissural lip pits max joins the man (corner of the mouth)
Irritation fibroma
- Result from trauma
- Check biting
- Lots of keratinized tissue
Epilus fissuratum
- From ill fitting dentures
Papillary hyperplasia
- Denture induced hyperplasia
- Projection are fibrous connective tissue
- Superficial infection of candida albicans
Gingival enlargement
- Chronic inflammation
- Hormone changes
- Medications
Chronic hyperplastic pulpitis
- Pulp is inflamed due to carries
- Chronic is treated by extraction and endodontic treatment