Carranza periodontology Flashcards
(323 cards)
1
Q
What is the turnover time for junctional epithelium?
A
4 to 6 days
2
Q
Under normal circumstances, the gingival sulcus should be how deep?
A
0 mm (or close to it), but this is only possible in germ-free animals, lab settings
-the histologic depth of a sulcus does not need to be exactly equal to the depth of penetration of the periodontal probe
3
Q
Attached gingiva: width?
A
distance between MGJ and projection on the external surface of the bottom of the sulcus, or periodontal pocket (different than width of keratinized gingiva), is different throughout the mouth
The width of attached gingiva increases with age (?)
4
Q
What are the layers of stratified squamous epithelium?
A
Stratum corneum
Stratum granulosum
Stratum spinosum
Stratum basale
5
Q
What is the difference between orthokeratinized, parakeratinized, and nonkeratinized epithelium?
A
Ortho- no nuclei in the stratum corneum and well-defined stratum granulosum (only some areas of gingiva are this)
Para- stratum corneum retains pyknotic nuclei, keratohyaline granules dispersed (not giving rise to a granulosum)
Non- has neither corneum or granulosum, superficial cells have viable nuclei
6
Q
What does gingival epithelium consist of (cells)?
And what is the principle cell type of this tissue?
A
Overlying stratified squamous epithelium, underlying central core of connective tissue (primarly composed of collagen fibers and ground substance)
KERATINOCYTE
(also has nonkeratinocytes, including langerhans cells, merkel cells, and melanocytes)
7
Q
How are keratinocytes interconnected?
A
By desmosomes (structures on the cell periphery)- tonofilaments Less frequently, they can have tight junctions, in which the membranes of the adjoining cells are fused (ions and small molecules can pass between cells)
8
Q
Melanocytes are what kind of cells?
And are located in what layers of the gingival epithelium?
A
- Dendritic cells
- basal and spinous layers
9
Q
What enzyme is closely related to the degree of keratinization? (contained in the upper layer of the stratum spinosum)
A
Lysosomes
Keratinization begins in the stratum spinosum!
10
Q
What are Langerhans cells and where are they located?
A
Located among keratinocytes at suprabasal levels
Are modified monocytes (macrophages with possible antigenic properties), antigen presenting cells for lymphocytes
11
Q
What are Merkel cells?
A
located in deeper layers of epithelium
harbor nerve endings, connected to adjacent cells by desmosomes
TACTILE PERCEPTORS
12
Q
How is the epithelium joined to the underlying connective tissue?
A
Basal lamina
13
Q
Oral epithelium (outer) is how keratinized? (which is the most, and which is the least?)
A
Para or keratinized, majority is para
-palate, gingiva, ventral aspect of tongue, cheek (from most to least)
-degree of keratinization diminishes with age and onset of menopause
14
Q
Sulcular epithelium!
-What type?
- what cell is missing in this?
- acts as?
A
Thin, non-keratinized stratified squamous (lacking granulosum and corneum), but keratinizes if exposed to the oral environment
-No Merckel cells normally
-semipermeable membrane through which injurious bacterial products can pass into the gingival and tissue fluid
15
Q
Junctional epithelium
1-consists of?
2- is how thick?
3-is thickest at what point?
4- where is the apical termination in healthy tissue?
A
1-stratified squamous nonkeratinizing epithelium
2- 3-4 layers in early life, but layers increase with age
3- tapers from its coronal end, so only a couple cells wide at its apical termination
4- Apical termination is at the cementoenamel junction in healthy tissue
16
Q
Junctional epithelium is formed by the confluence of what?
A
The REE and oral epithelium (but REE is not essential for its formation)
17
Q
What cells are consistently present in junctional epithelium?
A
PMNs!, with a substantial increase seen with accumulation of dental plaque and gingival inflammation
18
Q
How is the junctional epithelium attached to the tooth surface?
A
By means of an internal basal lamina, which consists of a lamina densa (next to enamel), and lamina lucida (to which hemidesmosomes are attached)
Organic strands from enamel appear to extend into lamina densa
19
Q
Who is the father of dentistry?
A
Pierre Fauchard
20
Q
Attachment of junctional epithelium to the toth is reinforced by?
A
Gingival fibers, for this reason, junctional epi and gingival fibers are considered as a functional unit, called the dentogingival unit
21
Q
So, how does junctional epithelium contribute to defense?
A
epithelial barrier
allows access of gingival fluid, inflammatory cells, and components of host defense to the gingival margin
Exhibit rapid turnover!
22
Q
Development of the gingival sulcus: proceeds how?
A
after enamel formation is complete, it is covered with the REE, and when tooth penetrates the oral environment, the REE unites with the oral epithelium and transforms into the junctional epithelium
-as tooth erupts, this united epithelium condenses along the crown, and the ameloblasts (inner layer of REE) gradually become squamous epi cells
-transformation of REE into Junctional eli occurs in an apical direction
23
Q
How do keratinization and gingivitis affect mitotic rate?
A
Higher mitotic rate in nonkeratinized areas
Also higher rate with gingivitis
24
Q
What layers does new cell formation occur in?
A
Spinosum and basale
25
How do epi cells participate in immunity?
Increased proliferation
alteration of cell-signaling events
changes in differentiation and cell death
alteration of tissue homeostasis
26
What is a cuticle?
| And what are three coatings of developmental origin in the tooth?
1- thin, acellular structure with a homogenous matrix
| 2- REE, coronal cementum, dental cuticle
27
What is the main route of diffusion for gingival fluid?
Thru the basement membrane, thru the relatively wide intracellular spaces of the junctional epithelium, and then into the sulcus
-Is a transudate to exudate (exudate in inflammation)
28
Gingival connective tissue!
1- Major components?
2-CT of gingiva is known as?
3- Contains what two layers?
1- collegen fibers, fibroblasts, vessels, nerves and matrix
2- Lamina Propria
3- papillary layer (subjacent to epithelium, papillary projections)
Reticular layer, contiguous with periosteum
29
What type of collagen forms the bulk of lamina propria?
Type 1
30
Gingival fibers: arranged in what three groups?
1- Gingivodental group: on facial, lingual and interproximal surfaces, embedded in cementum just beneath the epi at the base of the sulcus
2- Circular group: encircle the tooth in a ringlike fashion, course through the connective tissue of the marginal and interdental gingiva
3- Transseptal group: located interproximally, extend between cementum of approximating teeth
31
Connective tissue of marginal gingiva! Contains collagen fiber bundles (type 1!) called gingival fibers! Functions are???
1- brace marginal gingiva firmly against tooth
2- provide the rigidity necessary to withstand mastication forces
3- unite the free marginal gingiva with the cementum of the root and the adjacent attached gingiva
32
What is the preponderant cellular element in gingival connective tissue?
What do they do?
Fibroblast
-they synthesize collagen and elastic fibers, as well as the glycoproteins and glycosaminoglycans of the amorphous intercellular substance
-also regulate collagen degradation through phagocytosis and secretion of collagenases
33
What cells are numerous in the CT of oral mucosa and gingiva?
Mast cells!
| Also has fixed macrophages, histiocytes, adipose cells, and eosinophils (rare)
34
Does gingival epithelium (epithelial cells) play a role in immunity?
Yes, active role in innate host defense
35
Junctional Epithelium
* Adheres to enamel; collar-like band of stratified squamous (non-keratinized)
* Forms base of sulcus; separates PDL from oral environment
* widest at bottom of sulcus (15-20 cells); narrows apically
* Part of host defense to plaque or bacteria insult; fluid constantly flowing as part of defense (exudate)
36
Three reasons junctional epithelium prevent pathogenic bacterial flora
1- Firmly attached to tooth surface, so epi barrier
2- allows access of gingival fluid, inflammatory cells, and host defenses
3- rapid turnover
37
after enamel formation is complete, the enamel is covered by the REE (reduced enamel epithelium), which is attached to tooth by basal lamina and hemidesmosomes. When the tooth penetrates the oral mucosa, the REE unites with the oral epi and forms the junctional epithelium
continually self-renewing structure with mitotic activity occurring in all cell layers
38
Gingival fluid (sulcular fluid)
transudate or exudate
in health, amount is very small, increases with disease/inflammation
Main route of diffusion: through the basement membrane, through the wide intracellular spaces of the junctional epithelium, and then into the sulcus
39
Gingival connective tissues
```
Main components:
collagen fibers (60%), fibroblasts (5%), vessels, nerves, and matrix (35%)
```
Fibroblast is main cellular element, mesenchymal origin
40
Connective tissue of the gingiva is known as the lamina propria: consists of what two layers?
1- Papillary layer: subjacent to epithelium, consists of papilllary projections b/w rete pegs
2- Reticular layer- contiguous with periosteum of alveolar bone]=
41
Gingival fibers: arranged in what three groups?
1- Gingivodental group: facial, lingual and interproximal surfaces, embedded in cementum just beneath the epi at the base of the sulcus
2- Circular group: encircle the tooth in a ringlike fashion, marginal and interdental gingiva
3- Transseptal group: located interproximally, extend between cementum of approximating teeth
42
Three sources of blood supply to the gingiva
1- Supraperiosteal arterioles
2- Vessels of the PDL
3- Arterioles which emerge from the crest of the interdental septa
43
Active eruption vs passive eruption
Active- movement of the teeth in the direction of the occlusal plane (apposition of bone accompanies this stage)
Passive= exposure of the teeth by apical migration of the gingiva
(anatomic crown/root vs clinical crown root)
44
RANKL vs OPG
```
RANKL= activates osteoclasts
OPG= antagonizes RANKL binding
```
45
Definition of periodontitis
"an inflammatory disease of the supporting tissues of the teeth caused by specific microorganisms, resulting in progressive destruction of the PDL and alveolar bone with increased probing depth formation, recession, or both."
46
Chronic periodontitis
Localized: less than 30% of sites
Generalized: >30% of sites
47
Endodontic-Periodontal lesions
Pulpal necrosis precedes periodontal changes. A periapical lesion may drain into the oral cavity thru the PDL and resulting in destruction of the PDL and alveolar bone
48
Periodontal-Endodontic lesions
Bacterial infection from a periodontal pocket may spread thru accessory canals to the pulp; infection may reach the pulp thru the apical foramen too!
49
Combined endo-perio lesions
when pulpal necrosis and a periapical lesion appear on a tooth that is also periodontally involved
ENDO SHOULD ALWAYS BE CONTROLLED FIRST!
50
Most reliable study design?
Most common study design?
1. Randomized controlled trials
| 2. Case-control and cohort studies
51
Measuring the occurrence of diseases
| 1- Prevalence?
1- Number of individuals that have a particular condition within a defined population
52
Risk?
probability that an individual or a site will develop a particular condition or disease during follow-up
When risk is reported, it should be accompanied by a specific time period
53
Odds
is the probability that an event happened divided by the probability that an event did not happen
This is often easier to estimate that probabilities, so often reported in studies
54
Incidence rates
This reflects the number of disease occurrences per time unit per person
They apply an element of time (The denomenator is time)
55
Gingival crevicular fluid
| Can normally change with circadian rhythms, sex hormones, smoking, mechanical stimulation
1- cellular elements include bacteria, desquamated epi cells, and leukocytes (PMNs, lymphocytes, monocytes)
2- Higher glucose in GCF than in serum (4X)
3- TP much lower in GCF, doesn't change with inflammation
4- Total amount of GCF is greater with inflammation
56
First stages/manifestations of gingivitis
vascular changes, dilated capillaries and increased blood flow, not clinically apparent (subclinical) Leukocytes (PMNs) leave capillaries (migrate, diapedesis)
57
What is Stage II gingivitis?
Stage II gingivitis or early lesion occurs approx. 1 week after plaque accumulation. It is marked clinically by erythema, BOP due to increased proliferation of capillaries and capillary loops btw rete ridges. Predominant leukocytes now become lymphocytes (T cells). Increased collagen destruction of circular and dentogingival fiber grps.
58
What is stage III gingivitis?
Established lesion gingivitis is marked by impaired venous return due to engorged and congested blood vessels which leads to anoxemia. Characterized by the presence of plasma cells and B lymphocytes and IgG. This occurs typically 2-3 weeks after plaque accumulation.
59
Stage IV gingivitis
Fibrosis of gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage. Plasma cells dominate connective tissue and neutrophils dominate the junctional epi
60
Localized marginal gingivitis
confined to one or more areas of marginal gingiva
61
Localized diffuse gingivitis
extends from margin to the mucobuccal fold in a limited area
62
Localized papillary gingivitis
confined to one or more interdental spaces in a limited area
63
Generalized marginal gingivitis
involves gingival margins in relation to all the teeth, interdental papilla usually affected
64
generalized diffuse gingivitis
involves entire gingiva
65
Histologic evaluations on animals showed what in the early stages of gingivitis?
expression of cytokines responsible for connective tissue breakdown (MMPs) is ubiquitous
66
Actual vs apparent position of gingiva
Actual= level of the coronal end of the epithelial attachment on the tooth
Apparent= level of the crest of the gingival margin
Severity of recession measured by actual position!
67
Drugs responsible for drug induced gingival enlargement?
Calcium channel blockers, anticonvulsants, immunosuppressants
68
Pericoronitis
* Inflammation of a gingival flap (operculum -- little flap of skin that goes over tooth) over the crown/occlusal surface of an erupting tooth (i.e. third molar)
* Debris/food trapped ® inflammation ® +/- infection
69
Pemphigoid
applies to a number of cutaneous, immune-mediated, subepithelial bullous diseases characterized by a separation of the basement membrane zone
70
Healthy gingiva microorganisms?
| Disease gingiva?
```
Healthy= coccoid cells and straight rods
Diseased= increased numbers of spirochetes and motile rods
```
71
Formation of periodontal pocket
host's immunoinflammatoryresponse unleashes mechanisms that lead to collagen and bone destruction; related to various cytokines
72
Two mechanisms associated with collagen loss
1- collagenases and other enzymes become extracellular and destroy collagen (these enzymes are called MMPs)
2- Fibroblasts phagocytized collagen fibers
73
Extension of the juctional epithelium along the root requires?
The presence of healthy epithelial cells, so marked degeneration of junctional epi impairs rather than accelerates pocket formation
74
Soft tissue wall of a periodontal pocket
C.T. edematous and densely infiltrated with plasma cells, lymphocytes, and PMNs. B.V.'s increased in number and are dilated and engorged. Necrotic foci are seen. Junctional epi at base of pocket in much shorter than a normal sulcus. Most severe degeneration is along the lateral wall of the pocket
75
Are sharpey's fibers affecting in a periodontal pocket?
Yes, undergo degradation. Bacteria then penetrate root, and can been seen up to the CDJ
Cementum is very thin in cervical regions, so scaling and root planing may remove it completely, exposing dentin
76
Dominant microorganism in root surface caries?
Actinomyces viscosus
77
Transeptal fibers in suprabony vs infrabony pockets?
```
Suprabony= arranged horizontally in the space b/w the base of the pocket and alveolar bone
Infrabony= oblique rather than horizontal, extend from cementum beneath base of pocket along the alveolar bone and over crest to the cementum of adjacent tooth
```
78
Bone destruction in periodontal disease
Not a process of bone necrosis, involves the activity of living cells along viable bone. Osteoclasts. (# of osteoclasts does not correlate with amount of inflammation, but does correlate with distance from the apical border of the inflammatory infiltrate to the alveolar bone crest)
79
Buttressing bone formation
areas of bone formation found immediately adjacent to sites of active bone resorption and along trabecular surfaces at a distance from the inflammation
80
How does the periodontium respond to an increase in the magnitude of occlusal forces?
With a widening of the pdl space, an increase in the # and width of PDL fibers, and an increase in density of the alveolar bone
Constant pressure on bone is more injurious than intermittent force
81
Traumatic occlusion defined by?
whether it produces periodontal injury! (not how the teeth occlude)
82
slightly excessive pressure?
| VS. slightly excessive tension?
1- stimulates resorption of alveolar bone, widening of PDL space (severe pressure causes undermining resorption, necrosis of PDL and bone)
2- causes elongation of the PDL and apposition of alveolar bone, enlarged blood vessels (severe tension causes resorption of bone and widening of PDL)
83
Areas of periodontium most susceptible to injury from excessive occlusal forces?
Furcations
84
Red complex in people?
P. Gingivalis, tannerella forsythia, and treponema denticola
85
attachment loss and bone loss are associated with what bacteria?
Increase in gram negative, anaerobic
86
Specific plaque hypothesis for chronic periodontal disease?
implies that although a general increase occurs in the proportion of gram-neg microorganisms in teh subgingival plaque, it is the presence of increased proportions of the "red complex" that precipitates attachment and bone loss
87
dentogingival junction
- anatomical and functional interface between the gingiva and the tooth structure
- 3 epithelial types within:
1) gingival
2) sulcular
3) junctional
- forms from the epithelial cuff
- under healthy cnditions it is bounded laterally by the oral sulcular epithelium and the enamel of the tooth.
- its coronal border is the free gingival margin and its apical aspect is the coronal aspect of hte junctional epithelium.
- AKA bounded by the histological sulcus in absolute health
88
Junctional epi as a function of attaching to the tooth
Unique epi structure b/c surface cells are specialized to attach to the tooth, so unlike other epi cells in body, it cannot slough. Cells at basal layer continually divide and move to within two or three cell layers of the tooth surface and then migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus to be sloughed off in the gingival crevice
89
extracellular spaces of junctional epi compared to other epi?
Extracellular spaces b/w the junctional epi are greater than other tissues, with intercellular spaces comprising about 18% of the volume.
Making junctional epi LEAKY
90
Early lesion of periodontitis?
-after 1 wk of plaque build-up -vasodilation, increased GCF flow, transmigrating neutrophils increase -predominant cells are neutrophils and lymphocytes (T-cells) -collagen fibers begin to be destroyed in areas apical and lateral to the junctional epi -edema of gingival tissues
91
Established lesion of periodontitis
chronic gingivitis -significant inflammatory cell infiltrate -collagen depletion continues -neutrophils accumulate and are a major releaser of MMPs -Junctional and sulcular epi form a pocket epithelium that is not firmly attached to the tooth, has large #s of neutrophils, and is permeable -Still reversible!
92
Advanced lesion of periodontitis
-marks transition from gingivitis to perio -neutrophils dominate in pocket epi, and plasma cells dominate in connective tissues -Junctional epi migrates apically to the collagen depleted areas below it -Osteoclastic bone resorption starts, bone retreats from advancing inflammatory front to prevent spread of bacteria into bone
93
Lipopolysaccarides
found on outer membrane of gram-neg bacteria -act as endotoxins -elicit strong immune responses -immune system reacts with toll-like receptors (TLRs) which recognize MAMPs (microbe-associated molecular patterns) -particular key importance in initiating and sustaining inflammatory responses
94
Bacterial enzymes and noxious products
Noxious agents: ammonia, hydrogen sulfide, butyric and propionic acid -these have a profound affect on host cells Bacteria also produce proteases, which breakdown structural proteins of the periodontium -gigipains
95
Key mediators that orchestrate host responses are?
Cytokines MMPs Prostanoids
96
Cytokines
- soluble proteins and act as messengers to transmit signals from one cell to another - bind to receptors on target cells and initiate intracellular signaling cascades -can work in a positive feedback cycle -produced by a large number of cells (lymphocytes, neutro, macro, fibroblasts, epi cells, ...) -mediate connective tissue and alveolar bone destruction thru induction of fibroblasts and osteoclasts to produce proteolytic enzymes (MMPs)
97
Prostaglandins
-group of lipid compounds derived from arachidonic acid -arachidonic acid metabolized by COX-1 and 2 to generate the prostanoids PGs are mediators of inflammation -PGE2 results in vasodilation and induces cytokine production COX2 is upregulated by cytokines and LPS PGE2 results in induction of MMPs and osteoclastic bone resorption
98
MMPs (matrix metalloproteinases)
-proteolytic enzymes that degrade extracellular matrix such as collagen, gelatin, and elastin -produces by many cells -secreted in a latent form (inactive) and activated by proteolytic cleavage, which is achieved with proteases (like cathepsin G, made by neutophils) -inhibited by the tetracycline class of Ab's
99
Cells primarily responsible for PGE2 production are?
Macrophages and fibroblasts
100
How does the epithelium play an active role in innate immunity?
-by expressing antimicrobial peptides, called defensins -secrete chemokines to attract neutrophils
101
Bone resorbs so that there is always a width of ? of noninfiltrated connective tissue overlying the bone?
0.5 to 1 mm
102
Key system for controlling bone turnover?
rank/rankl/opg
103
RANK
-cell surface receptor expressed by osteoclast progenitor cells as well as mature osteoclasts
104
RANKL
ligand that binds to RANK and is expressed by bone marrow stromal cells, osteoblasts, and fibroblasts
105
Bonding of RANKL to RANK results in?
osteoclast differentiation and activation and thus bone resorption
106
OPG?
another ligand that binds to RANK
-produced by bone marrow stromal cells, osteoblasts, and PDL fibroblasts.
-inhibits differentiation of osteoclasts
107
What regulates the expression of RANKL and OPG?
IL-1beta
TNF-alpha
- T cells express RANKL
- In periodontitis, there is increased levels of IL-1b and TNF-a and increasing numbers of T-cells
108
What mediates the resolution of inflammtion?
Lipoxins, resolvins, protectins (proresolving lipid mediators)
109
Lipoxins
lipoxygenase-derived eicosanoids and are generate from arachidonic acid
-inhibit neutrophil recruitment, chemotaxis, and adhesion
-signal macrophages to phagocytose the remnants of apopotic cells without generating an inflammatory response
110
Resolvins and protectins
Resolvins- derived from omega-2 FA's (EPA, DHA), inhibit neutrophil infiltration and migration, inhibit production of proinflammatory mediators, and have antiinflammatory effects
111
Innate immunity
saliva, GCF, epithelial keratinocytes, commensal microflora
112
Clinical ebb and flow of periodontitis is a reflection of fluctuations in?
Adaptive immunity
113
Pathogen recognition and activation of cellular innate responses
Macrophages and dendritic cells express a range of PRRs (pattern recognition receptors) that interact with MAMPs (microbe associated molecular patterns) to signal immune responses
EX: TLRs with bacterial LPS
Some non-immune cells also express PRRs, like epi cells and fibroblasts
114
Adaptive immunity
Slower than innate, relies on interactions b/w antigen-presenting cells and T and B lymphocytes
115
Population of leukocytes in periodontium of gingivitis and stable periodontal lesions is?
Population in active periodontitis?
T cells, clustered around blood vessels
| 2- B-cells and plasma cells, associated with pocket formation and progression of disease
116
Antigen presenting cells of the periodontium?
B-cells, macrophages, and two types of dendritic cells (dermal dendritic cells, langerhans cells)
They express MHC Class II molecules
Expression of MHC can be induced in other cells as well
117
Significance of antibodies in periodontitis?
Unclear, not sure if they have a protective function or if they participate in disease pathogenesis
118
Calculus?
Mineralized dental plaque, hardened by precipitation of mineral salts from saliva (supragingival) and CGF (subgingival)
-generally starts extracellulary, but can start intracellulary
119
Materia alba
white or cream-colored cheesy mass that can collect over dental biofilm on unclean, neglected teeth; it is composed of food debris, mucin, and bacteria.
120
Biofilms
composed of microbial cells encased within a matrix of extracellular polymeric substances (EPS) such as polysaccharides, proteins, and nucleic acids
Plaque is a biofilm
Intercellular matrix consists of organic and inorganic materials derived from saliva, GCF, and bacterial products
121
Organic constituents of the biofilm matrix?
polysaccharides, proteins, glycoproteins, lipid material, and perhaps DNA
122
What are the primary inorganic components of plaque?
Calcium and phosphorous (traces of sodium, potassium and flouride)
Dental plaque is composed primarily of microorganisms!
123
Phases of the process of plaque formation
1- formation of pellicle on tooth surface (bacteria adhere to acquired enamel pellicle)
2- initial adhesion/attachment of bacteria (interaction between microbial cell surface adhesin molecules and receptors in the salivary pellicle)
3- colonization and plaque maturation
124
Old vs new plaque, bacterial growth rate
Growth much slower in older plaque, because nutrients become limiting for much of the plaque biomass
125
Viruses replicate only in?
When they are present within eukaryotic or prokaryotic cells (not on their own)
126
Non-specific plaque hypothesis
maintains that periodontal disease results from the "elaboration of noxious products by the entire plaque flora"
- but this relies on quantities of plaque causing disease, which does not appear to be the case
127
Ecologic plaque hypothesis
both the total amount of plaque and the specific microbial composition of plaque may contribute to the transition from health to disease
-eliminating the disease-inducing stimulus, whether it is microbial, host, or environment, will help restore microbial homeostasis
128
Beneficial species of bacteria in the host: how do they affect the pathogenic spp?
1- passively occupying a niche
2- actively limiting a pathogen's ability to adhere to appropriate tissue surfaces
3- adversely affecting the vitality or growth of pathogens
4- affecting the ability of a pathogen to produce virulence factors
5- degrading virulence factors produce by pathogens
129
Rads tend to over or under estimate the amount of bone loss?
Underestimate
130
Healing after periodontal therapy: regeneration
regeneration occurs thru growth from the same type of tissue that has been destroyed
131
what replaces? 1-gingival epi 2- PDL
| 3-bone and cementum?
1- Epithelium
2- connective tissue
3- connective tissue (precursor of both), osteoblasts and cementoblasts
132
Healing after periodontal therapy. Repair
simply restores the continuity of the diseased marginal gingiva and reestablishes a normal gingival sulcus
133
Perio pocket healing, what is the result of healing by these cells? oral epithelium, gingival connective tissue, bone, and PDL
1- epi. result will be long junctional epithelium
2- C.T. result will be fibers parallel to the tooth surface and remodeling of the alveolar bone with no attachment to the cementum
3- Bone. root resorption and ankylosis
4- PDL, new formation of cementum and periodontal ligament!
134
Action of power scalers, how does water play a role?
Acoustic streaming: unidirectional flow caused by ultrasound waves
Acoustic turbulence: created when the movement of the tip causes the coolant to accelerate, producing an intensified swirling effect
Cavitation: formation of bubbles in water caused by the high turbulence, bubbles implode and produce shock waves in the liquid
135
Sonic units work at what frequency?
2000 to 6500 cycles per second and use a low or high speed air source from the dental unit
Tip travels in an elliptical or orbital stroke pattern
136
Magnetostrictive ultrasonic devices work in what frequency range?
18,000 to 50,000 cycles per second
| Vibrations travel from the metal stack to a connecting body that causes vibration of the working tip
137
Piezoelectric ultrasonic units work in what frequency range?
18,000 to 50,000 cycles per second
ceramic disks in handpiece power the piezoelectric technology
Move in a linear pattern
138
Tetracyclines
concentrates in periodontal tissues
-anticollagenase effects
- bacteriostatic, effective against rapidly multiplying bacteria
- more affective against gram-positive than gram-negative
- high concentration in gingival crevice
139
Metronidazole
bactericidal to anaerobic organisms and believed to disrupt bacterial DNA
-nitroimidazole compound
140
Penicillins
-bactericidal! Inhibit bacterial cell wall production
141
Amoxicillin
- bactericidal
- extended spectrum from penicillin, includes gram positive and negative
-susceptible to penicillinase (b-lactamase produced by bacteria that breaks up penicillin)
142
Amoxicillin-Clavulanate Potassium
resistant to penicillinase
143
Cephalosporin
Similar in structure and action to penicillins
| -B-lactams
144
Clindamycin
effective against anaerobic bacteria and has a strong affinity for osseous tissue
-
145
Host modulation therapy: NSAIDS
- inhibit prostaglandin formations (PGE2) which is produced by neutrophils, fibroblasts, macrophages, and epi cells in response to bacterial LPS
- PGE2 upregulates bone resorption by osteoclasts and inhibits fibroblast fxn (which modulates immune response)
-Use has not taken off because of side effects
146
Host modulation therapy: bisphosphonates
- bone seeking agents that inhibit bone resorption by disrupting osteoclast activity
- possess anticollagenase properties and interfere with osteoblast metabolism and secretion of lysosymal enzymes
- unwanted effects include inhibiting bone calcification and inducing changes in WBC counts, also, avascular necrosis of jaws
- none are currently being used
147
Host modulation therapy: Sub-antimicrobial dose doxycycline
- twice daily for up to 3 months, up to a max of 9 months
| - exerts its effect by enzyme, cytokine, and osteoclast inhibition (not antibiotic!)
148
Locally applied host modulation therapies
enamel matrix proteins
bone morphogenic proteins
growth factors
tetracyclines
149
Maximum intercuspation definition (also centric occlusion)
- position of mandible when there is maximum interdigitation and occlusal contacts b/w max and mand teeth
150
Centric relation (Definition)
The position of the mandible when both condyle-disc assemblies are in their most superior position in their respective glenoid fossa and against the slope of the articular eminence of each respective temporal bone
151
Gingival curettage vs subgingival curettage
Gingival= removal of the inflamed soft tissue lateral to the pocket wall and the junctional epi
Subgingival=performed apical to the junctional epi and severing the C.T. attachment down to the alveolar crest
*need to remove inflamed granulation tissue is questionable
152
Curettage!
- does not eliminate the causes of inflammation, so should always be proceeded by scaling and root planing
- cutting edge is always against the tissue, inserted to engage the inner lining of the pocket wall and is carried along the soft tissue (usually horizontally)
- ultrasonic instruments can do this with vibrations that disrupt tissue continuity
- Excisional new attachment procedure=knife used to make internal bevel incision and remove tissue
153
Healing after curettage
restoration and epithelialization of the sulcus require 2-7 days
-restoration of the junctional epithelium occurs in animals as early as 5 days after treatment
-immature collagen fibers appear within 21 days
154
Apically displaced flaps
-advantage is preserving the outer portion of the pocket wall and transforming it into attached gingiva, so increases width of attached gingiva while eliminating pocket!
155
Internal bevel incision benefits
1- removes pocket lining
2- conserves the relatively uninvolved outer surface of the gingiva
3-produces a sharp, thin flap margin for adaptation to the bone-tooth junction
156
Modified Widman Flap
designed for exposing root surfaces and removal of pocket lining, not intended to reduce or eliminate pocket depth
-internal bevel incision, similar to envelope flap
-sling sutures used to close
157
Undisplaced (unrepositioned) flap
improves accessibility for instrumentation and removes pocket wall, so reduces or eliminates pocket
-essentially an excisional procedure of the gingiva
- commonly performed
- internal bevel gingivectomy
158
What # wall defect usually needs to be recontoured surgically?
one wall defects (sometimes two walls as well)
159
Positive vs negative architecture
```
Positive= radicular bone apical to the interdental bone
Negative= interdental bone more apical than the radicular bone
```
160
Osteoinduction vs osteoconduction vs osteogenesis
```
Induction= molecules in the graft (BMPs) convert the neighboring cells into osteoblasts which in turn form bone
Conduction= physical effect by which the matrix of the graft forms a scaffold that favors outside cells to penetrate the graft and form new bone
```
Genesis= formation of new bone by cells contained within the graft
161
Demineralized freeze-dried bone grafts
demineralization in hydrochloric acid exposes the components of bone matrix, which are closely associated with collagen fibrils and have been termed bone morphogenic proteins (BMPs)
162
BMPs
growth factor
-BMP-2, one of strongest bone producing varieties
- induce diffentiation of mesenchymal stem cells to become bone producing osteoblast cells, so they are differentiation factors
- binds tightly to collagen within minutes
163
Enamel matrix proteins
- purified enamel matrix proteins have been extracted from porcine developing enamel
- use for perio tissue regeneration has been mixed
- mainly amelogenin protein, which is secreted by hertwig's root sheath and induce acellular cementum formation
- EMDOGAIN- gel, mostly amelogenin
not osteoinductive, but osteopromotive (stimulates bone formation when combined with FDBA)
164
Components of Gingival Crevicular Fluid
- majority are enzymes
- cellular elements
- electrolytes (K, Na, Ca)
- organic compounds (proteins, less than in serum) (Glucose, much higher (3-4x) than in serum)
165
What are the cellular elements of GCF?
Bacteria
Desquamated epithelial cells
Leukocytes (migrate thru sulcular epithelium)
166
Is protein content of GCF correlated to level of disease?
No
167
Does GCF have cell or humoral immune responses?
BOTH
168
The role of antibodies in gingival defense mechanisms is difficult to ascertain, but what is the consensus?
1- a reduction in antibody response is detrimental
| 2-antibody response plays a protective role
169
The amount of GCF changes how in inflammation?
amount is greater when inflammation is present, and is sometimes proportional to the severity of infection
170
What drugs have been shown to be excreted thru the GCF?
Tetracyclines, metronidazole
171
Leukocytes in the dentogingival area?
Mostly PMNs
Are always present, even without disease
There are some mononuclear cells as well (58% B lymphocytes, 24% T, 18% phagocytes)- That is a higher ratio of T:B lymphocytes than in peripheral blood
-leukocytes are also found in saliva, and their main entry into the oral cavity is thru the sulcus
172
Saliva!
| What are the inorganic factors present in saliva that influence bacteria?
Ions and gases, bicarb, sodium, potassium, phosphates, calcium, flourides, ammonium, and carbon dioxide
173
Saliva!
| What are the organic components of saliva that influence bacteria?
Lysozyme, lactoferrin, myeloperoxidase, lactoperoxidase, and agglutinins (glycoproteins, mucins, macroglobulins, fibronectins, antibodies)
174
What is lysozyme?
hydrolytic enzyme that cleaves the linkage between structural components of the glycopeptide muramic acid-containing region of the cell wall of certain bacteria in vitro
Works on both gram positive and negative!
175
Myeloperoxidase?
enzyme similar to salivary peroxidase, released by leukocytes, bactericidal for actinobacillus
176
Lactoperoxidase-thiocyanate system in saliva?
bactericidal to some strains of lactobacillus and streptococcus by preventing accumulation of lysine and glutamic acid
177
What is the preponderant immunoglobulin found in saliva?
IgA (IgG is more prevalent in GCF)
178
The major enzyme in saliva is?
Parotid amylase
179
What is the most important salivary buffer in saliva?
Bicarbonate-carbonic acid system
180
In clinically normal gingiva of humans, what is the basis of inflammatory cells?
Mostly T cells, very few B cells or plasma cells
181
Stage 1 of gingivitis
Is subclinical
-vascular changes
-in response to microbial activation of resident leukocytes
182
What determines how stage 1 gingivitis will progress?
The character and intensity of the host immune response (i.e., can it get back to a normal state, or will it progress to chronic inflammation)
183
Stage 1 gingivitis, microscopic level changes
changes in blood vessels and adherence of neutrophils to bv walls (happens within 2 days to 1 week of plaque accumulation)
-Leukocytes migrate out of the vessels and are seen in increased quantities in the CT, junctional epi, and gingival sulcus
-exudation of fluid from gingival sulcus seen
184
Stage 2 gingivitis (the early lesion)
evolves within about a week of plaque accumulation
| -
185
Microscopic changes with stage 2 gingivitis?
leukocyte infiltration in CT beneath junctional eli, consisting mainly of lymphocytes (T CELLS)
-junctional epi may begin to show development of rete pegs or ridges
- collagen destruction increases (70% destroyed around the cellular infiltrate)- circular and dentogingival fibers appear to be most affected
- PMNs release their lysosomes in association with the ingestion of bacteria
186
Stage 3 gingivitis
| Established lesion
- Characterized by a predominance of plasma cells and B cells (IgG class)
- Increased plasma cells differentiate this stage!
- basal lamina destroyed in some areas
- COllagen fibers destroyed
- blood vessels become engorged and congested
187
How do established gingivitis lesions progress?
Some remain stable and do not progress over months or years!
| Some become more active and convert to destructive lesions
188
Stage 4 gingivitis, or the advanced lesion, or phase of periodontal breakdown
fibrosis of gingiva and widespread manifestations of inflammatory and immunopathologic tissue damage
-plasma cells dominate CT and neutrophils dominate junctional epithelium
189
What are the two earliest signs of gingival inflammation?
1-increased gingival crevicular fluid
| 2- bleeding from sulcus on gentle probing
190
Histologic evaluations on animal specimens revealed that in early stages of gingivitis, what is ubiquitous?
expression of cytokines responsible for connective tissue breakdown (MMPs!)
191
How does gingivitis differ in children vs adults?
Response in children is dominated by T cells (not B cells), very few plasma cells
Could explain why gingivitis in children rarely progresses to periodontitis
192
Healthy gingiva is associated with what microorganisms?
And diseased gingiva?
1- mostly coccoid cells and straight rods
| 2- increased numbers of spirochetes and motile rods
193
Pocket formation starts as?
inflammatory change in the ct wall of the gingival sulcus
-degeneration of ct due to cellular and fluid inflammatory exudate, and just apical to junctional epithelium, collagen fibers are destroyed
194
what causes pain on probing of periodontal pockets?
ulceration of inner aspect of pocket wall
195
What are two mechanisms associated with collagen loss?
1-collagenases and other enzymes secreted by vaious cells in healthy and inflamed tissue (such as fibroblasts, PMNs, macrophages)- these enzymes are called MMPs
2-fibroblasts phagocytize collagen fibers
196
explain the gradual movement of the pocket
PMNs invade the coronal aspect of junctional epi due to inflammation, and once these occupy about 60%, the tissue detaches from the tooth surface. At the same time, as a result of collagen destruction, the apical cells of the junctional epi proliferate along the root, resulting in an apical shift
197
Extension of junctional epi along the root requires?
healthy epithelial cells!
| -If there is necrosis of the junctional epi, this impairs pocket formation and ulcerative gingivitis results
198
Soft tissue wall of a periodontal pocket
C.T. edematous and densely infiltrated with plasma cells, lymphocytes, and PMNs. B.V.'s increased in number and are dilated and engorged. Necrotic foci are seen. Junctional epi at base of pocket in much shorter than a normal sulcus. Most severe degeneration is along the lateral wall of the pocket
199
What are the different areas that can be seen within a periodontal pocket wall?
1-areas of relative quiescence
2-areas of bacterial accumulation
3-areas of emerging leukocytes
4-areas of leukocyte-bacterial interaction
5-areas of intense epithelial desquamation
6-areas of ulceration
7- areas of hemorrhage
200
What predominates in an edematous pocket wall vs a fibrous pocket wall?
1-inflammatory fluid and cellular exudate predominate, wall is bluish red, soft, spongy, and friable
2- newly formed ct cells and fibers predominate, and the wall is more firm and pink
201
What does the root surface look like in a periodontal pocket?
- as pocket deepens, collagen fibers embedded in the cementum are destroyed and collagen becomes exposed to the oral environment
- Sharpey's fibers degenerate
- becomes an environment favorable to bacteria penetration
- viable bacteria have been found in 87% of the roots of periodontally diseased teeth!
- can result in cementum breakdown and areas of necrotic cementum
202
What is an area of increased mineralization in a periodontal pocket?
probably a result of an exchange, on exposure to the oral cavity, of minerals and organic components at the cementum-saliva interface
-SO, the mineral component of cementum increases (calcium, magnesium, phosphorus, fluoride)
-may offer increased resistance to decay
203
Areas of demineralization?
often related to root caries
| -root surface caries tend to progress around, rather than into, the tooth
204
What is the dominant microoganism in root surface caries?
Actinomyces viscosus
205
What zones are found at the bottom of a periodontal pocket?
1. Cementum covered by calculus
2. Attached plaque (covers calculus and extends apically, about 100 to 500 micrometers)
3. Unattached plaque (extends apically to attached plaque)
4. attachment of junctional epi to the tooth (in normal sulci is 500 micrometers, in pocket is reduced to 100 micrometers or so)
5. semidestroyed connective tissue fibers- may be apical to junctional epi
206
Microscopic differences in supraboney vs infraboney pockets
- relationship of soft tissue wall of the pocket to alveolar bone
- pattern of bone destruction
-direction of transseptal fibers of the PDL
207
Micro-organisms that occupy periodontal abscesses are usually?
gram-negative anaerobic rods
208
After inflammation reaches the boneby extension from the gingiva, what happens?
-it spreads to the marrow spaces and replaces the marrow with a leukocytic and fluid exudate, new blood vessels, and proliferating fibroblasts
209
Where does resorption of the bone in periodontal disease begin?
In the marrow spaces, causing thinning of the surrounding bony trabecular and enlargement of the marrow spaces, followed by destruction of the bone and reduction in bone height
210
Is bone destruction in periodontal disease a function of bone necrosis?
NO
| It involves the activity of living cells along viable bone
211
The amount of inflammatory infiltrate correlates with the degree of bone loss, but not with the number of -------?
Osteoclasts!
However, the distance from the apical border of the inflammatory infiltrate to the alveolar bone crest correlates with both the number of osteoclasts on the alveolar crest and the total number of osteoclasts
212
Microbiologically, periods of destructive activity in periodontal disease are associated with?
increase of the loose, unattached, motile, gram-negative, anaerobic pocket flora
Periods of remission have a dense, unattached, nonmotile, gram positive flora with a tendency to mineralize
Also, hypothesized that it goes from a T cell lesion to a predominantly B cell lesion
213
How does bone destruction progress in periodontal disease?
bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts and stimulate gingival cells to release mediators that have the same effect
-Plaque products and inflammatory mediators can also directly inhibit osteoblasts
214
What are the host factors released by inflammatory cells that play a role in periodontal disease?
Prostaglandins (and their precursers)
IL-1alpha, IL-beta
TNF-alpha
215
What is buttressing bone formation?
areas of bone formation found immediately adjacent to sites of active bone resorption
216
Central vs peripheral buttressing bone formation
Central- occurs within the jaw
| Peripheral- occurs on the external surface
217
How does the periodontium respond to an increase in the magnitude of occlusal forces?
With a widening of the PDL space, and an increase in the number and width of PDL fibers, and an increase in the density of alveolar bone
218
What is more injurious to periodontium, constant or intermittent pressure?
CONSTANT
219
What is the criterion that determines whether an occlusion is traumatic?
Whether it produces periodontal injury (not how the teeth occlude)
220
What areas of the periodontium are most susceptible to injury from excessive occlusal force?
furcations
221
Stage 1: injury
(stages of tissue response to increased occlusal forces)
1- If offending force is chronic, how does the ligament respond?
widened at the expense of the bone, resulting in angular bone defects without periodontal pockets, tooth becomes loose!
222
Under forces of occlusion, tooth rotates around a fulcrum (or axis of rotation)
1-In single rooted teeth, this is where?
2- In multirooted teeth?
1- in the junction between the middle 1/3rd and apical 1/3rd
| 2- middle of the inter-radicular bone
223
What does slightly excessive pressure cause?
| How about greater pressure?
1- resorption of alveolar bone, widending of the PDL
2-compression of fibers, areas of hyalinization, areas of necrosis of the PDL; increased resorption of alveolar bone and resorption of the tooth surface occur
224
What does slightly excessive tension cause?
| Severe tension?
elongation of PDL fibers, apposition of alveolar bone, enlarged bv's
2- widening of PDL, thrombosis, hemorrhage, tearing of the PDL, and resorption of bone
225
What causes undermining resorption?
pressure severe enough to force the root against the bone
226
Stage 2, repair (of trauma from occlusion)
when bone is resorbed by excessive occlusal forces, the body attempts to reinforce it with buttressing bone formation
227
Stage 3, adaptive remodeling
| -what happens to the PDL here IF the repair can't keep up with the injury?
- widened PDL, funnel shaped at crest, and angular defects in the bone, with no pocket formation
228
What are the effects of insufficient occlusal forces?
| What situations can cause it?
insufficient stimulation causes thinning of periodontal ligament
atrophy of fibers
osteoperosis of bone
reduction in bone height
hypofunction from open bite, lack of antagonistic tooth, unilateral chewing
229
Does trauma from occlusion affect the gingiva?
No
Blood supply not affected to marginal gingiva
Does not cause pockets, gingivitis, or increase in GCF flow
230
What bacteria are part of the red complex in people?
Tannerella forsythia
Treponema denticola
porphyromonus gingivalis
231
The TMJ is formed by what bones?
the head of the mandibular condyle fits into the articular fossa of the temporal bone
232
Centric relation is?
clinically determined relationship of the mandible to the maxilla when both condyle-disc assemblies are positioned in their most superior position in the maxillary fossa and against the slope of the articular eminence of the temporal bone
233
The junctional epithelium is a unique epithelial entity in that it?
The surface cells are specialized for the purpose of attachment to the tooth, so there is no opportunity for sloughing! cells at basal layer instead just continually divide and move to within two or three cell layers of the tooth surface and migrate coronally, parallel to the tooth surface to eventually reach the floor of the sulcus and be sloughed into the gingival crevice
234
ALSO, what are teh intercellular spaces like in junctional epi compared to other epithelium?
much greater, comprise about 18% of the volume of the epithelium, it's "leaky"
235
Connective tissue of the dentogingival complex? (type 1 and 3 fibers)- included are?
1- dentogingival fibers (from cementum to free and attached gingiva)
2-alveologingival fibers (extend from alveolar crest into free and attached gingiva)
3-circular fibers (wrap around tooth, maintain close adaptation of the free gingiva to the tooth)
4- dentoperiosteal fibers (from cementum, over alveolar crest, insert into alveolar process)
5- transseptal fibers (run interdentally, cementum to cementum, over the alveolar crest)
236
Even in healthy gingiva, there are always what?
inflammatory cells, particularly neutrophils, also lymphocytes and macrophages
237
Repeat, the initial lesion of gingivitis?
Slight elevation of vascular permeability and vasodilation
GCF flow out of sulcus
Migration of leukocytes (mostly neutrophils) thru the gingival ct, across the junctional epithelium, and into the sulcus
238
Repeat, the early lesion of gingivitis?
Increased vascular permeability, GCF flow, vasodilation
large numbers of leukocytes infiltrating (mostly neutrophils, lymphocytes)
Degeneration of fibroblasts
Collagen destruction
Proliferation of junctional and sulcular epithelium into collagen-depleted areas
239
Repeat, the established lesion of gingivitis?
dense inflammatory cell infiltrate (plasma cells, lymphocytes, neutrophils)
accumulation of inflammatory cells in ct
elevated release of MMPs and lysosomal contents from neutrophils
significant collagen depletion and epi proliferation
formation of pocket epithelium containing large numbers of neutrophils
240
Repeat, the advanced gingivitis lesion
predominance of neutrophils in pocket epithelium
dense inflammatory cell infiltrate (mostly plasma cells)
apical migration of junctional eli
continued collagen breakdown
osteoclastic resorption of alveolar bone
241
What are the predominant infiltrating cell types in the early lesion of gingivitis?
neutrophils and lymphocytes (mostly T cells)
242
In the advanced lesion, what cells predominate in the pocket epithelium vs the connective tissues?
Pocket- neutrophils
| CT- plasma cells
243
Virulence factors come from both the host and the bacteria.
Microbial virulence factors are?
LPS
Bacterial enzymes and noxious products
microbial invasion
fimbriae
244
Host-derived inflammatory mediators?
Cytokines
Prostaglandins
MMPs
245
LPS
Lipopolysaccharides
Where are they found?
What do they act as?
How do immune systems in animals recognize these?
1-Outer membrane of gram-negative bacteria
2- endotoxins
3- TLR's (toll-like receptors)
(porphyromonas gingivalis has an atypical form of LPS that is recognized by TLR2 and 4 (they are usually only recognized by 4)
246
TLRs recognize what?
MAMPs (microbe-associated molecular patterns)
| -causes an increase in production of inflammatory mediators and differentiation of immune cells
247
LTA?
another component of gram-positive cell walls, lipoteichoic acid
Signals through TLR-2
248
Some examples of bacterial enzymes and noxious products?
```
NH3 (ammonia)
Hydrogen sulfide (h2S)
```
Short-chain carboxylic acids, such as butyric acid and proprionic acid
249
What does butryic acid do?
induces apotosis in T-Cells, B-cells, fibroblasts, gingival epi cells
250
Plaque bacteria also produce what? that causes tissue breakdown of the periodontium
Proteases
251
Host response: cytokines
These bind to cell surface receptors, trigger a sequence of intracellular events that lead ultimately to the production of protein by the target cell, which alters that cell's behavior
252
What cell types produce cytokines?
large number, including inflammatory cells, as well as resident cells in the periodontium (fibroblasts, epi cells)
253
How can cytokines mediate connective tissue and alveolar bone destruction?
by the induction of fibroblasts and osteoclasts to produce MMPs
254
What are the most important cytokines in periodontal disease?
IL-1Beta
| TNF-alpha
255
Prostaglandins
| These are?
1-a group of lipid compounds derived from arachidonic acid
| 2- Arachidonic acid is metabolized by COX-1 and 2 to generate a series of prostanoids (which includes prostaglandins)
256
What does PGE2 result in?
vasodilation and induces cytokine production
257
COX2 is upregulated by?
IL-1B, TNF-alpha, and bacterial LPS
258
What specifically does PGE2 result in?
induction of MMPs and osteoclastic bone resorption, major role in tissue damage!
259
What cells produce MMPs?
variety, neutro, macro, fibroblasts, epi cells, osteo blasts and calsts
260
What do MMPs degrade?
Collagen, gelatin, elastin
261
MMPs are secreted in what form?
And what activates them?
What produces the activation factor?
1- Latent
2-proteolytic cleavage by proteases (such as cathepsin G)
3- Neutrophils
262
What are some key inhibitors of MMP?
proteinase inhibitors such as glycoprotein alpha1-antitrypsin and alpha2-macroglobulin (large plasma protein produced by the liver)
263
What effect do tetracyclines have on MMPs?
inhibitory!
264
IL-1Beta
What antagonizes IL-1Beta
key role in inflammation, innate immune response
2- PGE2, platelet-activating factor, nitrous oxide
Plays a big role in the pathogenesis of periodontal disease!
3- IL-1Ra
(IL-18 might also play a large role in perio dz)
265
TNF-alpha
| along with IL-1B is a big player in perio
Induces MMP secretion! (IL-1B doesn't)
Less potent affect on osteoclasts than IL-1B
Secreted particularly by macrophages in response to LPS
266
IL-6
Also plays a big role in perio, but not as big as IL-1B and TNF-a
Stimulated by cytokines like the above
267
What are the cells mainly responsible for PGE2 production?
Macrophages and fibroblasts
268
What effects does PGE2 have?
Contributes signficantly to bone loss
| Induces secretion of MMPs and osteoclastic bone resorption
269
In healthy tissues, MMPs are mainly produced by?
fibroblasts
270
What are TIMPS?
Tissue inhibitors of metalloproteinases
271
What are the predominant MMPs in periodontal diease?
MMP-8 and MMP-9
Secreted by neutrophils
Very effective at degrading type 1 collagen (most abundant type in periodontal ligament)
272
MMP and bone destruction? expressed by?
osteoclasts
| cathepsin K is a protease that also plays a role in bone destruction
273
What antimicrobial peptides are expressed by epi cells? (making them an important part of innate immunity?)
Defensins
| Epi cells also secrete chemokines to attract neutrophils
274
What bad things do neutrophils do?
Release large quantities of MMPs and other destructive enzymes
275
Bone resorption ceases when there is what distance between sites of bacteria in the pocket and bone?
And bone resorbs so that there is always a width of noninfiltrated ct of ----- overlying the bone?
2. 5 mm
| 0. 5 mm
276
What two critical factors determine whether bone loss occurs?
concentration of inflammatory mediatros in the gingival tissues must be sufficient to activate pathways that lead to bone resorption
Inflammatory mediators must penetrate to within a critical distance of the alveolar bone
277
What regulates the expression of RANKL and OPG?
IL-1beta
TNF-alpha
- T cells express RANKL
- In periodontitis, there is increased levels of IL-1b and TNF-a and increasing numbers of T-cells
278
What resolves inflammation?
Lipoxins, resolvins, protectins
279
Lipoxins1- Their presence indicates?
2- They are derived from?
3-They inhibit what?
4- They signal macrophages to do what?
1- resolution of inflammation2- arachidonic acid, they are eicosanoids
3- neutrophil chemotaxis, recruitment, and adhesion
4- phagocytose the remnants of apototic cells without generating an inflammatory response
280
Resolvins1- derived from?
2- their effects are?
They are highly potent!!!
1- omega 3 fatty acids, eicosapentaenoic and docosahexaenoic acids2- Inhibit neutrophil infiltration and transmigration, inhibit production of proinflammatory mediators, and have potent anti-inflammatory and immunoregulatory effects
281
Infection of host cells by P. Gingivalis involves?2- It is initiated through what?
1- the action of proteases and cell surface fimbriae2- thru signalling via interaction of bacterial components with surface integrins, PAR1 and 2, and TLR
282
P. Gingivalis has also been shown to be able to migrate thru the basement membrane of epithelial layers and invade connective tissue
facilitated by bacterial-derived proteases and host proteases derived from infiltrating neutrophils
283
What do epithelial cells produce and secrete in response to periodontal bacteria?
MMPsrange of cytokines (IL-1B, TNF-a, IL-6)...
284
Sentinel cells of the immune system that are stimulated with periodontal bacteria include?
Macrophages and dendritic cells, which express and PRR, which interact with MAMPs of bacteria and signal immune responses
285
The interaction of what adhesion molecules on endothelial and epithelial cells with ___ on neutrophils facilitates neutrophil migration?
1- ICAM-1 and LFA-32- Beta 2 integrins
286
The distribution of leukocytes in periodontal disease is not even. ____ predominate in the connective tissue and ______ in the sulcus
1- mononuclear cells2- Neutrophils
287
The clinical ebb and flow of periodontal disease is a reflection of fluctuations in ?
Adaptive immunity
288
What are antigen presenting cells?
Cells that take up microbes and their antigens, then migrate to lymph nodes and interact with T cells to present antigen; They include B cells, macrophages, and at least 2 types of dendritic cells (langerhans, dermal)They express MHC class II molecules ncessary for antigen presentation (MHC expression might be induced in other cells of the periodontium as well)
289
What is the predominant phenotype of T cells in the stable periodontal lesion?And what happens as the lesion worsens?
CD4+ helperMay lead to a progression towards a destructive, B cell dominated lesion
290
Antibodies1- What produces them?
2- Which antibodies are found most common in perio?
3- Are they helpful/hurtful
1- B cells. These antibodies seem to have high titer but low biologic activity. High levels of plasma cells also are seen with high levels of antibodies2- IgG (few IgM and IgA)
3- Unknown. Sometimes can lead to production of autoantibodies which may contribute to destruction?
291
What aspect of immunity potentially can explain the fluctuations noted in periodontal disease?
The interaction between T helper cells (Th1 and Th2)Definitive evidence for this is lacking
292
What are the major inorganic components of calculus?
Calcium phosphate, calcium carbonate, magnesium phosphate
293
What two types of crystals are also typically found in calculus
Hydroxyapetite, octacalcium phosphate
294
What does the organic component of calculus consist of?
Protein-polysacchardie complexes, desquamated epithelial cells, leukocytes, and various micro-organisms
295
what are the differences between supra and subgingival plaque?
Ratio of calcium to phosphate is higher subgingivallySodium content increases with pocket depth
296
What is the main source of minerals for supragingival vs subgingival calculus?
Supra- salivaSub- GCF
297
which is potentially more important in calculus formation, phosphorus or calcium?
Phosphorous
298
Dental plaque is composed primarily of ?
Microorganisms
299
In supragingival plaque, what bacteria predominate at the tooth surface vs. the outer surface of the plaque mass?
Gram-positive cocci and short rods (surface)
| Gram-negative rods and filaments (spriochetes), outer surface
300
Three phases of plaque formation?
1- pellicle formation, organic material, acquired, happens within 1 minute of cleaning, bacteria attach to this, not to the tooth directly
2- adhesion of bacteria
3- colonization and plaque maturation
301
What determines if bacteria will adhere to a pellicle?
specific interactions b/w microbial cell surface "adhesin" molecules and receptors in the salivary pellicle (only a small proportion of oral bacteria will fit this)
302
What is coadhesion? What does this lead to?
Primary colonizers adhered to the tooth surface provide new receptors for attachment by other bacteriaMicrocolonies and eventually to a mature biofilm
303
Is bacterial growth faster in old or new plaque?
Faster in new, nutrients become limited as the plaque biomass grows
304
How much more resistant are organisms in a biofilm than in their planktonic state?
1000 to 1500 times
305
What is the ecologic plaque hypothesis?
total amount of dental plaque and the specific microbial composition of plaque may contribute to health and disease (mix of specific plaque hypothesis and nonspecific...)
306
Periodontitis is considered a mixed infection; treatment with antibiotics?
Difficult because not all periodontopathogens are equally susceptible to the same antibiotic
307
recent microbiologic tests indicated that the presence of periodontopathogens alone is not sufficient for the development of periodontitis; several of these pathogens have been identified in disease free patients
So the specificity (presence of a pathogen means periodontitis) of microbial detection is very low; so the understanding of etiology is complicated; threshold level between health and disease is unknown and different between different individuals
308
Does periodontitis fit into Koch's postulates? (bacteria routinely isolated from diseased individuals; grown in pure culture in the lab; produces a similar disease when put into others; be recovered from the same disease in lab animals)
No, primary problems being the inability to culture all the organisms that have been associated with the disease, the lack of a good animal model to study periodontitis, and the difficulties inherent in defining and culturing sites of active disease
309
Allogenic vs autogenic succession? (change in bacterial community)
Allogenic- change in the composition of a bacterial community as the result of external, nonmicrobial factors (ex: smoking)Autogenic- interbacterial and viral-bacterial interactions are involved
310
The current concept concerning the etiology of periodontal disease considers 3 groups of factors that determine whether active periodontal destruction will occur in a subject: what are they?
1- susceptible host2- presence of pathogenic spp.
| 3- absence/small proportion of so-called beneficial bacteria
311
Comparing the microbiota b/w health, gingivitis, and periodontitis, what microbial shifts can be identified as health progressed to periodontitis?
1- From facultative anaerobes to obligate anaerobes2- From nonmotile to motile
3- From cocci to rods
4- From gram-positive to gram-negative
5- from fermenting to proteolytic species
312
What are gingipains?
enzymes responsible for at least 85% of the total host protein degradation activity (They are tissue destructive enzymes released by bacteria)
313
What is direct recognition of microbes by the host mediated by?
By the recognition of MAMPs by Pattern-recognition receptors (PRRs)
314
How long does it take for adative immunity to have an adequate cellular or humoral response?
7 to 10 days
315
What are critical for recognition of microbes by the innate immune system and for bridging innate and adaptive immune responses?
TLRs (these are PRRs)
316
What IL is likely involved in the tolerance of commensal bacteria?
IL-8 (not released in response to commensals)
317
Are epithelial cells equipped with PRRs?
YES, they respond to MAMPs by secreting various cytokines and chemokines (IL-8, antimicrobial peptides)
318
Expression of Th1-type cytokines has been associated with _____, whereas Th2 cytokines were found in higher levels in _______-affected tissues
1- gingivitis
| 2- Periodontitis
319
RANKL, produced by? (involved in osteoclast differentiation, survival, activation)
fibroblasts, osteoblasts, chondrocytes, mesenchymal cells, T and B cells
320
OPG- decoy receptor of RANKL- secreted by?
osteoblastic cells, bone marrow stromal cells, fibroblasts
321
Patients with periodontal disease have higher levels of?
RANKL, lower levels of OPG
322
The increased susceptibility of diabetic patients to infection has been hypothesized as being due to?
PMN deficiencies
323
How do systemically administered steroids hinder healing?
depressing inflammatory reaction, inhibits growth of fibroblasts and the production of collagen, and the formation of endothelial cells
