Pathogenesis of Periodontitis Flashcards
(36 cards)
What are features of healthy gingiva histologically?
Junctional epithelium is attached to the enamel
Oral epithelium appears to be continuous with the JE
CT will have regular appearance - dense with prominent collagen bundle fibers
JE is thin (10-20 cell layers)
Rete pegs are absent
What are the vascular features of healthy gingiva?
Number of loops in the subepithelial plexus is constant
Supraperiosteal blood vessels have anastamose with vessels from bone and PDL
Dentogingival plexus venules have no loops in health
What are the reasons for stability of clinically healthy gingiva?
Shedding of epithelial cells Intact epithelial barrier Positive flow if GCF PMNs and macrophages Protective effects of antibodies
What is the difference in the flow of gingival crevicular fluid in healthy v inflamed gingiva
Flow is slow in healthy gingiva
Much higher flow in inflamed gingiva
What are the histopathological stages in the development of gingivitis and periodontitis?
Initial lesion (subclinical stage of gingivitis) Early lesion (clinical early stages of gingivitis) Established lesion (chronic gingivitis) Advanced lesion (progression to periodontitis)
Initial lesion
Occurs within 1-4 days of plaque development Early stage of inflammation Increased permeability PMNs and monocytes are seen in the JE Increased vascular density Decreased perivascular collagen Increased GCF volume This stage is not detectable clinically
What vascular changes occur in the initial lesion?
Dilation of vessels in the dentogingival plexus is induced by vasoactive mediators (histamine, IL-1, TNF, prostaglandins)
Gaps form between capillary endothelial cells, resulting in increased permeability
Fluids and proteins can move out of the capillary
GCF flow rate increases
Gingival Crevicular Fluid
GCF is a plasma transudate (health) or inflammatory exudate (disease)
Passes through perio tissues
Can be collected from within or at the orifice of the gingival crevice
GCF constituents indicate inflammatory changes and bacterial colonization
GCF flow rate increases with inflammation
What cellular events occur during the initial lesion
Cytokine-mediated up-regulation of adhesion molecules on endothelial cells
PMNs adhere to post-capillary venules and begin to migrate
PMNs migrate through the JE to the gingival sulcus
What induces chemotaxis of PMNs?
Host factors (IL-8, C5a) Molecules released by bacteria (fMetLeuPhe)
Early lesion
Occurs within 4-7 days of plaque development
Lymphocytes and PMNs are subadjacent to the JE - make about 15% of infiltrated CT
Few plasma cells
Fibroblasts are undergoing cytopathic alterations - less collagen to make room
Inflammation is now clinically evident (redness, slight swelling)
Basal cells of JE and SE proliferate
Epithelial rete pegs invade the coronal portion of the lesion
What vascular changes occur in the early lesion?
Dentogingival plexus remains dilated
Large number of venules
Dentogingival plexus is extremely permeable following minor trauma or inflammation
As JE invades the CT, the previously inactive capillary bed opens up and proliferates into the CT papillae
Chemotaxis in the early lesion
The JE is more reactive with more projections into the CT
There is more plaque, so more toxic things
More chemotaxis
Macrophages are making pro-inflammatory cytokines
A couple of T cells are present, but no B-cells yet
Established lesion
Increased swelling seen clinically
Increased fluid exudation and leukocyte migration
Plasma cells increase around blood vessels and in coronal CT
Collage loss continues as infiltrate expands
In addition to macrophages and serum proteins, T-cells, B-cells, and plasma cells are present
What do activated T-cells produce in the established lesion?
Cytokines (IL-2, 3, 4, 5, 6, 10, and 13) Chemotactic substances (MCP, ICP, RANTES)
What do plasma cells produce in the established lesion?
Ig
Cytokines (IL-6, and TNF-a)
What do fibroblasts produce in the established lesion?
Metlloproteinases
Tissue inhibitory metalloproteinases
How does the JE convert to PE in the established lesion?
The JE and sulcular epithelium proliferate, and migrate deep into the CT
The sulcus deepens and a portion of the JE is converted into permeable pocket epithelium (PE)
The PE is not attached to the tooth surface
The PE is loaded with PMNs
Advanced lesion
Beginning and duration are not known
Similar to an established lesion with a couple of exceptions
Increased proportion of plasma cells (~50%)
Extension of lesion into alveolar bone and PDL, with significant bone loss
Continued loss of collagen fibers and matrix subadjacent to PE
Formation of periodontal pocketing and apical migration of JE to CEJ
What are the histopathological differences between advanced lesion and established lesion?
Advanced lesions switches from T- to B-cell predominance, which signals the conversion from gingivitis to periodontitis
Advanced lesions have destruction of CT attachment to the root surface and apical migration of epithelial attachment indicates the first clinical sign of periodontitis
How does bone loss occur in advanced lesions?
Bone destruction begins around the communicating blood vessels along the crest of the septum
There is apical proliferation of PE into deep CT
PE is not attached to the tooth
What are some common modifying factors?
Diabetes
Pregnancy, puberty, and menopause
Smokine
What can common modifying factors influence?
Susceptibility to gingivitis and periodontitis Plaque growth and composition Clinical presentation Disease progression Response to periodontal therapy
Diabetes’ Mellitus
Risk factor for periodontitis
Type I = impaired insulin production
Type II = deficient insulin utilizaiton
