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
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
Q
what is a chancre
A
- symptoms of syphilis
- full of spirochetes
26
Q
what are gingival diseases associated with herpes
A
- herpes simplex
- primary heretic gingivostomatitis
- varicella-zoster virus
- childhood and adulthood
27
Q
what are gingival lesions associated with fungal infections
A
- 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
Q
what are hereditary gingival fibromatosis
A
- fibrotic, enlarged gingiva
- rare occurence
29
Q
what are lesions involving the mucous membranes
A
- 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
Q
what is pemphigus vulgaris
A
- involves blistering of the outer (epidermal) layer of the skin and mucous membranes
31
Q
what can cause allergic reactions of the gingival tissues
A
- mouth rinses
- dentifrices
- chewing gum
- food/additives
- rare: sloughing of the gingiva
32
Q
what can cause physical injury to the gingival tissues
A
- thermal: hot beverages, pizza
- chemical: sloughing of tissues from oral rinses/dentifrices; aspirin burn
- physical: tooth brushing, dental floss, tooth picks
33
Q
what are the 8 non-plaque induced gingival diseases
A
- gingival diseases of specific bacterial origin
- gingival diseases of viral origin
- gingival diseases of fungal origin
- gingival lesions of genetic origin
- gingival manifestations of systemic conditions mucocutaneous disorders
- traumatic lesions
- foreign body reactions
- not otherwise specified
