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Oral Histology > L8 > Flashcards

L8 Flashcards

1
Q

The Dental Pulp

A

Soft connective tissue that supports dentin
Unique as tooth tissue
vascular
not calcified

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2
Q

The Dental Pulp: Embryonic origin

A

ectoderm- neural crest ectomesenchyme-dental papilla

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3
Q

The Dental Pulp: Constituents:

A

cells & cellular elements
blood and lymphatic vessels
extracellular matrix

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4
Q

Like dentin, pulp has an

A

extracellular matrix and contains parts of cells (nerve fibers). Unlike dentin, pulp has blood vessels & whole cells.

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5
Q

Functions in Development: 2. “formative” function:

A

DENTINOGENESIS

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6
Q

ODONTOBLASTS:

secrete

A

organic matrix of dentin

collagen is major component; provides scaffold for mineralization

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7
Q

Odontoblasts: participate in

A

mineralization
transport Ca++ ions that comprise the HAP crystal
secrete proteins important in controlling mineralization
dentin phosphoprotein (from DSPP gene)

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8
Q

Dentin Phosphoprotein

A 
Relatively Specific to dentin 
  (< amts., transient in bone, cementum, or enamel)
Prominent dentinal protein (> 50% NCP’s)
Binding sites for collagen
Highly phosphorylated
High in serine/aspartic acid
Acidic/anionic
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9
Q

DPP: Binds to

A

collagen in forming dentin matrix

Attracts Ca++ ions to INITIATE MINERALIZATION

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10
Q

Dentinogenesis (crown) begins during the

A

“BELL STAGE”

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11
Q

Just prior to dentinogenesis

A

Tissue layers of dental organ present
Crown outline present
No odontoblasts or ameloblasts

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12
Q

Late Bell Stage

A

Inner enamel epithelial cells… Ameloblasts
Undifferentiated mesenchymal cells (dental papilla)… Odontoblasts
Dentin secreted
Enamel secreted

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13
Q

Dentinogenesis:

A

cusp tips to cervix

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14
Q

Dentinogenesis:

A

periphery to pulp center

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15
Q

Odontoblast differentiation begins when cells in the

A

outer layer of the papilla stop dividing. Following the last mitosis, cells closest to the future DEJ proceed through dramatic changes that modify their shape and transform their function. First, the undifferentiated papilla cells began to elongate into a columnar shape & nuclei migrate to basal part of the cell. They subsequently grow processes that extend toward the future DEJ and begin to secrete dentin. The organic matrix of dentin is secreted 1st & subsequently the matrix is mineralized. When dentin secretion begins, the cells are considered ODBs and the dental papilla becomes the dental pulp. Dentin is laid down over a period of time. During this time, ODBs migrate toward the pulp center and one major ODB process becomes dominant and elongates.

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16
Q

WHAT KICKS OFF (INDUCES) odontoblast differentiation?

A

Inductive signal for odontoblast differentiation: secreted molecules from enamel organ- most likely the enamel knot (epithelial-mesenchymal interaction)
multiple molecules:
several families of signaling/growth factors implicated
2 prominent & best documented:
BMP’s (bone morphogenetic protein)
Wnt’s *(pronounced “went”)

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17
Q

Evidence for a role of Wnt10a in odontoblast differentiation

A

Technique:
At multiple time points:
Stained for Wnt10a using “in situ hybridization” (detects mRNA for Wnt10a)
Stained for dentin sialophosphoprotein (DSPP, a sign of odontoblast differentiation)

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18
Q

Wnt10a

A

1st expressed in enamel knot(s)
Then pre-odontoblasts at the cusp tip
Then successively more cervical parts of teeth

In other words, Wnt10a expression immediately precedes the “wave” of odontoblast differentiation

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19
Q

Wnt Signaling is Also Important in the Adult Pulp

A

In adult, Wnt is released by pulp cells after injury
Modifying the Wnt receptor complex to amplify effects of Wnt binding increases production of reparative dentin & dentin proteins in animal models

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20
Q

Pulp in the crown is the

A

“pulp chamber” or “coronal pulp”. Coronal pulp includes extensions into each cusp called ‘pulp horns’. Pulp in the roots constitutes the “root canal”/“radicular pulp”. The root canal is continuous with periodontium at the apical foramen, a very small opening (.3-.4mm) normally at the base of the tooth.

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21
Q

Pulp is not “normally” calcified, but ectopic* calcifications are common… 2 types:

A

Pulp stones

Diffuse calcifications

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22
Q

The cause of pulp stones and diffuse calcifications is

A

unknown and the degree to which they indicate pathology is not clear. However, they can be found in teeth which appear perfectly healthy. A relationship with age is often claimed, but the empirical evidence is variable. It has been difficult to assess whether these ectopic calcifications harm pulp. However, they can complicate endodontic therapy.

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23
Q

Pulp core=

A

is located central to the odontogenic zone & contains fibroblasts & trunks of larger branches of both nerves & blood vessels.

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24
Q

Odontoblasts –

A

bodies in pulp, process in dentin.

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25
Q

Fibroblasts –

A

pulp only, secrete ECM for pulp only.

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26
Q

Dendritic cells usually in

A

periphery in cell – usually around cell free/cell rich area.

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27
Q

Odontoblasts

Fibroblasts

A

confined to pulp

secrete ECM

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28
Q

Resident immune cells

A

macrophage
lymphocytes
eosinophils
dendritic cells

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29
Q

inflammation

A

plasma cells
mast cells
pmn’s

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30
Q

PG’s & Associates (the GAGs)

A

smaller: decorin, byglycan (most prevalent)
larger: versican, syndecan
GAGs: dermatan, chondroitin, heparin sulfate
Functions:
matrix for diffusion
collagen fibrillogenesis
water retention ( pressurizes pulp resist compressive forces)

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31
Q

Glycoproteins

A

e.g., fibronectin

Function: role in cell adhesion to ECM

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32
Q

Collagen (I & III)

A

both fibrillar collagens

Function: tensile strength

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33
Q

Similarities & differences compared to dentin:

A

Dentin has type I collagen but little or no Type III (consistent with the fact it’s a hard connective tissue)

(Mature) pulp does not contain DSPP!

34
Q

STEM CELLS

A

high capacity for self-renewal
“plastic”: can generate multiple cell types*

PLENTIFUL DURING DEVELOMPENT BUT ALSO PRESENT IN ADULTS

35
Q

Dental pulp stem cells can be

A

induced to form a number of cell types, not only odontoblasts & also adipocyte- and glial-like cells in vitro…

36
Q

Stem Cell Niches Probably Present

A

in

Multiple Locations of Mature Pulp

37
Q

Precise roles of different stem cell populations in the pulp are just being

A

worked out, but they probably play a role in response to injury

A role for pericytes (perivascular cells) in the response to pulp injury was recently studied….

38
Q

Transgenic mice can be

A

used to track the role of different stem cell populations after injury

39
Q

Pericytes (and ONLY pericytes) are

A

marked in this transgenic mouse

40
Q

The staining can be controlled so that it

A

“turns on” at a defined point in time

41
Q

This experiment tracked

A

pericytes after injuring the original odontoblasts

The results demonstrated that pericytes transform into new odontoblasts

However, not all new odontoblasts came from pericytes suggesting that other types of stem cells also contribute

42
Q

Successes with dental stem cells

A

Creating tooth buds or repairing tooth structure in animal models
Treating other conditions like multiple sclerosis (MS) or spinal cord injury

43
Q

Limitations with dental stem cells

A

Size and shape of engineered teeth poorly controlled
How to integrate an engineered tooth into the jaw?
Human teeth take months-years to form

44
Q

Due to limitations, a more practical use for DPSC’s is likely to be

A

repair

E.g., regenerating pulp tissue lost to caries

Much research is currently focusing on the optimizing such procedures in preclinical models

45
Q

Canine Model of Total Pulp Regeneration

A

Isolated stem cells from maxillary canines for autologous implants
Removed pulp tissue from incisors
Implanted stem cells, G-CSF (granulocyte colony stimulating factor) in combination or separately using a biocompatible, degradable collagen matrix
Performed functional tests (e.g. blood flow), removed repaired teeth, analyzed histology.
Good repair took place

46
Q

Combination of stem cells and G-CSF was important

A

G-CSF*: named for its function in transforming leukocyte precursors into granulocytes (neutrophils)

Produced by many tissues

Variety of functions
Chemotactic for many types of stem cells, including DPSCs
Promotes neurogenesis & angiogenesis
Anti-apoptotic

47
Q

Hypothesized Mechanisms: DPSCs are

A

multipotent, providing raw material for new pulp tissues
BUT, they have other important functions:
Anti-inflammatory
Secrete trophic factors promoting angiogenesis & neurogenesis

48
Q

G-CSF promotes these processes :

A

Keeps DPSC’s in the area, because DPSC’s have G-CSF receptors
Attracts other stem cells from surrounding tissues
Anti-apoptotic & proliferative effects

49
Q

Odontoblasts

A

unique to pulp2nd most numerous cell type in pulp

50
Q

Odontoblasts: Functions:

A 
Dentinogenesis
Nutrients to dentin (provides water)
Immune support potentially.
Cell bodies &amp; processes
(extent- still an open?)
Cell body dimensions:
Crown: 25-50uX5-7u
Root: more cuboid
Processes thinner
51
Q

Junctions Between Odontoblasts

A

Desmosomes & Adherens junctions: “sticky”, maintain position and polarity

Gap Junctions: channels between cells; coordinate dentiogenesis

52
Q

Tight: apical“weld” membranes

A

Depending on the exact form of the proteins & their extent , tight junctions can form an inter-cellular barrier

53
Q

Functional assays suggest that although some smaller molecular weight substances can pass between adjacent odontoblasts,

A

TIGHT JUNCTIONS inhibit the passage of larger molecules and probably bacteria

54
Q

Pulp is:

A

highly vascularized
also has a lymphatic system
presence of blood & lymphatic vessels distinguish it from other tooth tissues

55
Q

Blood flow in pulp under neural control…

A

Sympathetic: CONSTRICTS!
Alpha-adrenergic receptors
Parasympathetic (? But doubtful)
Sensory!

56
Q

The nervous system controls

A

pulpal blood flow. The autonomic component of this control is mainly sympathetic, via norepinephrine and alpha adrenergic receptors. Parasympathetic control is doubtful. However, importantly, sensory nerves also affect pulp blood flow (see below).

57
Q

Don’t’ get confused! It’s true that sympathetic activation usually causes

A

skeletal vasculature to dilate. However, it causes vasculature to the GI tract and skin, as well as the dental pulp to constrict.

58
Q

Lymphatic Vessels in Pulp

Note similarity to vascular pattern

A

Importance in Healing:

Drain proteins accumulated during inflammation

59
Q

The tooth interior (pulp & dentin) is

A

highly innervated

Small Adelta & C fibers

A delta– sensory pain fibers
C- some are sensory pain fibers, others are sympathetic

Also Abeta

Sensory pain fibers

Previously thought that innervation was nearly exclusively by small diameter nerve fibers but a contribution of Abeta fibers is now recognized

!! Main sensation arising from activating nerve fibers innervating the pulp (& surrounding dentin) is PAIN

60
Q

Pulp innervation begins at

A

Bell stage

61
Q

density of innervation increases until

A

eruption & more slowly until a few years afterward

62
Q

innervation probably

A

decreases with aging

63
Q

both primary & secondary dentition is

A

innervated

64
Q

nerves enter through the

A

apical foramen & terminate in pulp-dentin border zone and dentin

65
Q

mature teeth, odontoblasts do not

A

extend all the way to the DEJ.

66
Q

However, remember: early in dentinogenesis, odontoblasts processes reach

A

outer dentin

Later, they seem to retract*

*However, note that the issue of the extent of the odontoblast process is still controversial

67
Q

Nerve Fibers Also

A

Profusely Innervate the Pulp-Dentin Border Zone

68
Q

Hydrodynamic
Theory
of Dentinal Pain

A

If nerve fibers do not extend all the way to the DEJ, what accounts for the fact that a patient will feel pain as soon as a drill passes from the enamel into the dentin; in other words, what accounts for the high pain sensitivity @ the DEJ? Also, once the dentin is exposed, it is clear that MANY stimuli can give rise to pain, including air drying, osmotic stimuli such as foods that contain a high concentration of sugar or cold stimulation.

Current thinking is that the most likely explanation for dentinal sensitivity is the HYDRODYNAMIC THEORY. Hydrodynamic theory proposes that all dentinal stimuli that cause pain–, have something in common: each of these stimuli cause fluid movement in dentinal tubules. This fluid movement in turn causes deformation of mechanically-sensitive nerve endings, close to and in the dentin.

Original evidence for the hydrodynamic mechanism came from experiments done on extracted human teeth. An investigator named Branstromm measured fluid flow thru dentin that resulted from various stimuli and was able to show a rough correlation with the ability of these stimuli to cause pain when applied to superficial dentin in a person.

69
Q

Mechanically-activated ion channels (“mechanoreceptors”) are

A

embedded in the membranes of nerve fiber endings of AΔ & Aβ fibers in the pulp/dentin border region

70
Q

When the nerve fiber endings are deformed:

A

Ion channels open
Na+ sodium flows into the nerve endings,
Depolarizing them & giving rise to action potentials

71
Q

However, the odontoblast most likely has some function in

A

dentinal sensitivity, at the very least, due to crowding & proximity in tubule, the odontoblast process affects fluid dynamics around nerve process.

72
Q

BOTTOM LINE: HYDRODYNAMIC MECHANISM CONSIDERED MOST IMPORTANT FOR DENTIN SENSITIVITY BUT ROLE OF ODONTOBLAST STILL

A

UNDER INVESTIGATION

73
Q

PAIN ALSO ARISES DIRECTLY FROM

A

STIMULI IN THE PULP

hydrodynamic fluid flow not required

74
Q

Other pulp nerve fiber endings, especially C fibers, have receptors for

A

inflammatory & thermal stimuli

Members of the TRP receptor family

TRP receptors are a family of transmembrane receptors for thermal & inflammatory pain in many regions of the body

75
Q

Multiple types of nerve fibers & receptors underlie pain from the

A

tooth interior (pulp & dentin)

76
Q

Pulpal (inflammatory) stimuli activate more C fibers, probably those that terminate

A

deeper, in subodontoblastic layer. This activation of different types of nerve fibers by different types of stimuli may account for why the quality of pain experienced is different for dentinal versus pulpal stimuli. Stimuli applied to dentin (A fibers) cause sharp, piercing pain; pulp inflammation (C fibers) is associated with pain described as dull & aching. The quality of pain can therefore be useful on a diagnostic basis. Of course, in many clinical situations, these types of pain are intermingled because integrity of dentin is disturbed, in conjunction w/pulpal inflammation.

77
Q

It is interesting and significant that pain nerve fibers in the tooth have functions that extend beyond the

A

sensory. Certainly, one role of these fibers is sensory: to inform the organism that the tooth is injured, and this in turn serves a protective role by limiting use. However, it is now appreciated that these fibers also have an important regulatory influence on the pulp itself. This is mediated largely by the release of a class of neuromodulators called neuropeptides. Tooth nerves contain a variety of neuropeptides: two prominent ones are substance P AND CGRP (calcitonin-gene related peptide).

78
Q

Peptides sythesized in cell body in trigeminal ganglion:

A

@ central endings: transmitter function
Peptides bind w/receptors on brain neurons  pain
@ peripheral endings: local regulatory function
Peptides bind w/receptors on vasculature/local cells  pro-inflammatory

79
Q

These substances are synthesized in the

A

cell bodies of these neurons (in the trigeminal ganglion). From there, they are transported to the central endings of the fibers in the central nervous system (the trigeminal nucleus of the brainstem) also to the peripheral endings in the tooth. When these fibers are activated by a painful stimulus, e.g., injury or inflammation, neuropeptides are released at both the central and peripheral ends. In the brain, they serve a neurotransmitter role. However in the pulp, they have effects on local cells with appropriate receptors.

80
Q

Vasodilation

A

(opposes sympathetic control)

81
Q

Interactions with immune cells

A

Stimulation of cytokine production by macrophages

Chemotactic effects on immune cell migration

Oral Histology (14 decks)

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