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
16
Q
what is menstrual cycle gingivitis
A
- similar features to puberty gingivitis
- not every female
- increased estrogen and progesterone levels
- clinical features: intense inflammatory response initially occurring at interdental papillae, improves post ovulation
17
Q
what is pregnancy gingivitis
A
- again elevated estrogen and progesterone levels
- intensity of inflammation is related to OHI
- 30-100%
- especially seen if there is pre-existing gingivitis
- 2nd tri and most severe in the 8th
- condition regresses postpartum
- increased tooth mobility is seen caused by ‘looseness’ of the PDL
- does not cause inflammation, aggravates the inflammation
- increased permeability of blood vessels
- increase in progesterone: redness, edema, increased GCF flow
- elevated levels of prevotella intermedia (in all hormonal-associated gingivitis)
- growth increases
- uses progesterone levels for growth
18
Q
what is a pregnancy tumor called
A
- pyogenic granuloma
19
Q
what causes diabetes gingivitis
A
- gingival tissue changes due to elevation of blood glucose levels (hyperglycaemia)
- microvascular changes
- altered wound healing
- similar to plaque-induced gingivitis
- most common in children with poorly controlled type 1 diabetes mellitus
20
Q
what is leukaemia associated gingivitis
A
- abnormal proliferation of white blood cells
- inflammation starts at IP and spreads to AG
21
Q
what are drug influenced enlargements
A
- etiology is unclear
- excessive production of collagen or less collagenase
- gingival overgrowth
- gingival hyperplasia
- looks similar
- increase number of fibroblasts
- controversial whether influenced by plaque accumulation
22
Q
what are calcium channel blockers
A
- amlodipine (norvasc)
- felodipine (plendil)
- nicardipine (Cardene, carden SR)
- nifedipine (Procardia, adalar)
- nimodipine (nimotop)
- nisoldipine (sular)
- nitrendipine (Cardif, nitrepin)
- lacidipine (motens)
- lercanidipine (zanidip)
23
Q
what are oral contraceptive associated gingivitis
A
- oral contraceptives – estrogen and progesterone
- initial clinical studies done in 1960s had high concentrations of hormones
24
Q
what are gingival diseases of specific bacterial origin
A
- gingival lesions (infections) caused by gonnorhea, treponema pallidum
- seen in immunocompromised patient
- gingival lesions appear
- fiery red
- edematous
- painful elcerations
25
what is a chancre
- symptoms of syphilis
| - full of spirochetes
26
what are gingival diseases associated with herpes
- herpes simplex
- primary heretic gingivostomatitis
- varicella-zoster virus
- childhood and adulthood
27
what are gingival lesions associated with fungal infections
- candidiasis
- gingiva of immunocompromised patients
- red band
- linear gingiva erythema
- Linear Gingival Erythema (HIV patient)
- several different types of fungi, can cause deep fungal infections like:
- histopasmosis
- cryptococcosis (pigeon droppings)
28
what are hereditary gingival fibromatosis
- fibrotic, enlarged gingiva
| - rare occurence
29
what are lesions involving the mucous membranes
- erosive lichen planus
- benign mucous membrane pemphigoid
- bullous pemphigoid
- pemphigus vulgaris
- multifactorial etiology: no specific bacteria found, autoimmune
- gingival involvement may show as a desquamative gingivitis: peeling (desquamation) of the oral epithelium, exposure of a red, painful underlying connective tissue surface
30
what is pemphigus vulgaris
- involves blistering of the outer (epidermal) layer of the skin and mucous membranes
31
what can cause allergic reactions of the gingival tissues
- mouth rinses
- dentifrices
- chewing gum
- food/additives
- rare: sloughing of the gingiva
32
what can cause physical injury to the gingival tissues
- thermal: hot beverages, pizza
- chemical: sloughing of tissues from oral rinses/dentifrices; aspirin burn
- physical: tooth brushing, dental floss, tooth picks
33
what are the 8 non-plaque induced gingival diseases
1. gingival diseases of specific bacterial origin
2. gingival diseases of viral origin
3. gingival diseases of fungal origin
4. gingival lesions of genetic origin
5. gingival manifestations of systemic conditions mucocutaneous disorders
6. traumatic lesions
7. foreign body reactions
8. not otherwise specified
Periodontics
flashcards
Decks in class (9)
# Cards
