Chapter 7 Flashcards
1
Q
what is histopathogenesis
A
- inflammatory/immune events occurring in the periodontal tissues
- microscopic changes in the lamina propria and epithelium
- development of periodontal diseases
- movement into attachment and alveolar bone
2
Q
what are page and Schroeder’s lesions
A
- classified stages in the histopathogenesis of periodontal disease
- page and Schroeder 1976
- animal models
- some adolescent specimens
- although used in periodontal literature, it is not up-to-date
- initial, early and established are gingivitis
- advance is periodontitis
- the mechanism still holds true
3
Q
what are the 4 stages of histopathogenesis
A
- initial
- early
- established
- advanced
- the stages are not mutually exclusive
- still unclear when established becomes advanced
4
Q
what is an initial lesion
A
- initial plaque accumulation at gingival margin
- initiation of inflammatory and immune response
- inflammation develops quickly
- similar to a bacteria in a cut in the skin
- within 24 hours vascular (blood vessels) changes occur in the lamina propria just beneath the junctional epithelium
- blood vessels become engorged and more blood is brought to the area
- increase permeability of the blood vessels allows fluid, proteins, and cells to migrate out into the connective tissues
- GCF flow increases in the tissues and the gingival sulcus
- while these vascular changes occur, polymorphonuclear leukocytes (PMNs) exude from blood vessels into tissues
- PMNs move through the lamina propria and accumulate in the junctional epithelium (remember that even in gingival health PMNs are still present in the JE) and the gingival sulcus
- PMNs are the first line of dense for the body (host) to eliminate the antigens
- so, PMNs dominate the initial lesion
5
Q
is the initial lesion clinically visible
A
- no
- onset of 2-4 days
6
Q
what is the early lesion
A
- if oral biofilms are not removed, early lesion develops
- 4-7 days of biofilm accumulation
- clinically visible
- all the inflammatory/immune responses seen in the initial lesion are also occurring in the early lesion but more events are happening
- blood vessels remain dilated
- clinical signs of gingival inflammation are evident at the gingival margin
- continual vasodilation
- PMNs still are migrating into the tissue
- T cells are now entering the tissue
- as the number of PMNs and T cells increase in connective tissue, collagen is reduced to make room for these cells
- junctional epithelial cells proliferate for protection
- it is uncertain how long this early lesion lasts
- 60-70% of collagen is lost in connective tissue - not the attachment
- still reversible
- initial and early, like one lesion
7
Q
what is an established lesion
A
- as oral biofilms continue, more intense reaction
- fewer T cells, more B cells, 2-3 weeks
- clinically more inflammation is present
- predominant cells exuded from blood vessels and migrating into the connective tissue are plasma cells
- makes antibodies against the antigens
- collagen destruction is still occurring with replacement with WBC
- junctional epithelium transforms into pocket epithelium
- detaches laterally
- pocket epithelium: more permeable passageway from connective tissue to gingival sulcus/pocket; deeper ridges into connective tissue; microulcerations
- established lesion can remain stable for extended periods of time or it can convert into the advanced lesion (periodontitis)
- this is still (chronic) gingivitis
- still reversible
8
Q
what is the advanced lesion
A
- the inflammatory/immune response continues
- the periodontal pocket gets deeper as the pocket epithelium distends laterally and apically
- this lesion has all of the features of the established lesion except now it is periodontitis
- alveolar and supporting bone loss
- loss of connective tissue attachment
- the inflammatory infiltrate spreads in the connective tissue
- plasma cells (B cells) are the predominant cells
9
Q
summary
A
- periodontal diseases are complex and multifactorial and caused by bacterial pathogens
- inflammatory, immune, and histopathogenic events occur simultaneously in the gingival tissues
10
Q
what is the pathogenesis of gingivitis
A
- gingival pocket/pseudo pocket
- coronal migration of the gingival margin (gingival enlargement)
- no loss of connective tissue attachment
- no apical migration of the junctional epithelium
- no alveolar or supporting bone loss
- increased height of gingiva creates an impression that a deep ‘pocket’ is present
- pocket epithelium migrate laterally
11
Q
what is the host response to gingival inflammation
A
- oral biofilms (plaque) accumulate at gingival margin
- if it remains the gingival tissues will respond
- first the tissue becomes red (erythematous)
- due to vasodilation
- more blood vessels in the area
- fluid and cells leak out into connective tissue
- gingiva becomes red
- engorgement and from the fluid leaking out
- bleeding on probing: ulceration of the epithelium
- there is no apical migration of the junctional epithelium
- no supporting and alveolar bone loss
12
Q
what is dental plaque-induced gingival diseases
A
- gingivitis caused by bacterial biofilms
- most common
- bacteria non-specific
- clinical dx
- changes in colour, contour and consistency/texture
- 1-3 weeks to see clinically - start in papilla
13
Q
how does the endocrine system affect gingival diseases
A
- altered hormonal balances cause an exaggerated response to oral biofilms
- puberty-associated gingivitis, menstrual cycle-associated gingivitis, and pregnancy-associated gingivitis
- diabetes-associated gingivitis
14
Q
what is puberty associated gingivitis
A
- elevation of estrogen and progesterone
- other risk factors:
- reduced plaque control
- mouth breathing
- tooth crowding
- tooth eruption
15
Q
what are clinical features of puberty associated gingivitis
A
- plaque at gingival margins
- intense inflammatory response
- small amount of dental plaque vs degree of inflammation
