mal,or bacterial? How long has the irritant been
applied? How deep was the lesion? How much surface
area was involved? What is the status of the pulp at the
time of response? A second defensive reaction,in ?am-
mation within the pulp at the site of injury,should not
be ignored.This phenomenon will be explored in more
detail in chapter 4.
INDUCTION AND DEVELOPMENT OF
DENTIN AND CEMENTUM
Human tooth development spans an extremely long
period of time,starting with the induction of the pri-
mary dentition during the second month of embryoge-
nesis until completion of the permanent dentition
toward the end of adolescence.The primary dentition
is induced during the ?fth week of gestation,and bio-
mineralization begins during the fourteenth week of
gestation.In tandem,the ?rst permanent teeth have
reached the bud stage,and they begin biomineraliza-
tion just prior to birth.The ?rst primary teeth begin to
erupt in children at 6 months of age,and the ?rst per-
manent teeth erupt at 5 to 6 years of age.The third
molars are the last teeth to be formed,and their crown
development is completed between 12 and 16 years of
age.Therefore,the induction and development of the
human dentition persists during embryonic,fetal,
neonatal,and postnatal childhood stages of develop-
ment.Detailed descriptions of the histology and timing
of human tooth development can be readily found in a
number of excellent textbooks.4
Inductive tissue interactions,speci ?cally epitheli-
um-mesenchyme interactions,have been extensively
investigated and characterized throughout the various
stages of tooth crown and root morphogenesis.5–8The
developing tooth system has become a well-character-
ized model for de ?ning the molecular mechanisms
required for reciprocal signaling during epithelium-
mesenchyme interactions in crown and root morpho-
genesis and cytodifferentiation.9–13
It is now evident that the initial inductive signals for
tooth formation are synthesized and secreted from spe-
ci ?c sites de ?ned as odontogenic placodes within the
oral ectoderm that cover the maxillary and mandibular
processes.13The oral ectodermally derived inductive
signals are received by multiple cognate receptors locat-
ed on the cell surfaces of a speci ?c subpopulation of
cranial neural crest –derived ectomesenchymal cells
during the initial induction process and the subsequent
dental lamina,bud,and stages of tooth develop-
ment 8–13 (Figure 2-1).
During the transition from bud to cap stages,the
ectomesenchyme provides several cell lineages,including 26Endodontics one that becomes dental papilla mesenchyme and others that become progenitor cells for the subsequent devel-
opment of the periodontium.8,14,15At this time,multiple and reciprocal signals are secreted by the dental papilla mesenchyme,and these signals bind to the extracellular matrix and transmembrane cell receptors along the adja-cent enamel organ epithelium.A discrete structure with-in the enamel organ,termed the “enamel knot,”synthe-sizes and secretes a number of additional signals that also participate in the determination for the patterns of morphogenesis within the maxillary and mandibular dentitions:incisiform,caninform,and molariform.12,13Figure 2-1Early dental pulp,or dental papilla,exhibiting a cellu-lar mass at the center of this tooth bud in the early bell stage.Nerve ?ber bundles are evident in cross-section as dark bodies apical to dental papilla yet are absent in the papilla itself.Human fetus,19weeks.Palmgren nerve stain.Reproduced with permission from Arwil T,H ?ggstr ?ms I.Innervation of the teeth.Transactions Royal
School of Dentistry (Stockholm),3:1958.
Histology and Physiology of the Dental Pulp
27
The human genome was basically completed by the
year 200016;essentially all of the 100,000 regulatory
and structural genes within the human lexicon have
been identi ?ed,sequenced,and mapped to speci ?c
chromosomal locations.Further,combinations of
genes encoded within the human genomic deoxyri-
bonucleic acid (DNA) are now known to be expressed
during development that controls morphogenesis.A
number of these genes have been identi ?ed and char-
acterized as being expressed in the odontogenic pla-
code,dental lamina,and the bud,cap,bell,and crown
stages of tooth development in either the epithelial or
mesenchymal cells or both.Signi ?cantly,these genes
are expressed in various combinations during induc-
tion processes associated with many developing epider-
mal organ systems including the salivary gland,seba-
ceous glands,mammary glands,tooth,hair,and skin
morphogenesis.5
The speci ?city of induction re ?ects the particular
combinations of signaling molecules,their cognate cell
surface receptors,various intracellular signal pathways,
and a large number of transcriptional factors that reg-
ulate gene expression.These combinations further are
modi ?ed according to temporal and spatial informa-
tion during development;the combination used to
induce the dental lamina is different than that required for cap stage development and subsequent odontoblast cytodifferentiation.The hierarchy of these molecular mechanisms associated with the initiation and subse-quent early stages of tooth development is shown in Figure 2-2.Speci ?c mutations or alternations in one or more of these molecules result in clinical phenotypes including cleft lip and/or palate and a range of dental abnormali-ties with enamel,dentin,cementum,periodontal liga-ment,or alveolar bone disorders;for example,hypodontia or missing teeth as seen in X-linked anhy-drotic ectodermal dysplasia,which is caused by a muta-tion in the gene EDA ;familial tooth agenesis,which is caused by a mutation in the gene MSX1;and X-linked amelogenesis imperfecta,which is caused by a mutation in the gene amelogenin.17,18Recently,a mutation in the gene CBF-alpha1,a transcription factor,was found to cause cleidocranial dysplasia with hyperdontia.19The development of dentin is intriguing for several reasons.First,signals within the inner enamel epithelia of the enamel organ induce adjacent cranial neural crest –derived ectomesenchymal cells to become pro-genitor odontoblasts.Mutations in either the signaling molecules,cognate receptors,intracellular signal path-ways,transcription factors,or extracellular matrix mol-ecules can result in severe dental anomalies including Figure 2-2Molecular controls for the initiation and early stages of tooth morphogenesis.The initiation or site selection for tooth develop-ment is controlled by oral ectoderm-derived epithelial ?broblast growth factor (FGF) and bone morphogenetic protein (BMP)through their signaling pathways.The actions of these signaling pathways or circuits are dependent on the stage and position of development and the com-bination of transcription factors that are either induced (→) or repressed (_).This establishes the odontogenic placode.Thereafter,epithe-lium regulates the adjacent mesenchyme during the bud stage and the mesenchyme then promotes differentiation and in ?uences the adja-cent inner enamel epithelium through feedback loops in the cap,bell,and crown stages of tooth development.The reader is encouraged to see the following references for detailed analyses of these morphoregulatory molecules.2,7–10,14,16
tooth agenesis ,hypodontia ,and oligodontia and defects
in dentin deposition or biomineralization,termed
dentinogenesis imp erfecta.Several dentin extracellular
matrix proteins —dentin sialoprotein,dentin matrix
protein,and dentin phosphoprotein —are produced by
alternative splicing from one single gene product.
Mutations in any one of these encoded sequences,or in
type I collagen,result in dentinogenesis imp erfecta.
Mutations that are limited to type I collagen produce
osteogenesis imp erfecta with a form of dentinogenesis
imperfecta .
Following crown morphogenesis,cells from the cer-
vical loop give rise to Hertwig ’s epithelial root sheath
(HERS) cells,which,in turn,induce adjacent dental
papilla mesenchymal cells to engage in root forma-
tion.6–8Progressive cell proliferation and migrations
eventually outline the shape and size of the forming
roots.In this developmental process,two interpreta-
tions are currently being considered.First,evidence is
available to support the hypothesis that HERS cells
transdifferentiate into cementoblasts and secrete acel-
lular cementum matrix.8Second,evidence is also avail-
able to support the hypothesis that peripheral ectomes-
enchymal cells penetrate through the HERS and
become cementoblasts and secrete acellular cemen-
tum.6,7Of course,both processes may take place at dif-
ferent times and positions of cementogenesis.
The understanding of the induction and develop-
ment of cementum has also progressed in recent years.
Hertwig ’s epithelial root sheath cells provide signals
that induce the differentiation of odontoblasts and the
formation of the ?rst peripheral layer of dentin.It has
been known for almost 100 years that a small percent-
age of the human population expresses enamel pearls
along the root surfaces of permanent teeth.These
enamel-like aberrations in cementogenesis are intrigu-
ing and could offer new insights and strategies to
regenerate acellular cementum.
Recent advances have indicated that molecules pre-
sumed to be uniquely restricted to inner enamel
epithelium and ameloblasts associated with enamel
formation are also expressed in HERS.6–8Speci ?cally,
ameloblastin has recently been identi ?ed in both ameloblasts and HERS.20This association between
enamel and cementum has been previously discussed
with respect to coronal cementum.21These and other
studies have suggested that enamel matrix contains
molecular constitutents,presumably with growth fac-
tor bioactivities,that can induce acellular regeneration
when active on denuded human dentin root surfaces.
Recently,an enamel matrix preparation has been demonstrated to induce acellular cementum regenera-28Endodontics
tion on root surfaces associated with advanced peri-odontitis.22The available evidence strongly supports the hypothesis that enamel organ epithelium-derived cell phenotypes control coronal enamel deposition and the initiation of acellular cementum formation.23,24ANATOMY The living pulp,as we have seen,creates and shapes its own locale in the center of the tooth.The pulp,under normal conditions,tends to form dentin evenly,faci-olingually and mesiodistally.25The pulp therefore tends to lie in the center of the tooth and shapes itself to a miniaturization of the tooth.This residence of the pulp is called the pulp cavity,and one speaks of its two main parts as the pulp chamber and the root canal.The clin-ical implications of pulp form and variation are exten-sively covered in chapter 10.Indeed,the key word in understanding the gross anatomy of the pulp is “varia-tion.”Equally evident in any study of the pulp is the reduction in size of the chamber and canals with age.Such reduction in size thus becomes a new variation.In addition to changes in pulp size and shape with aging,external stimuli also exert an effect.Caries,attri-tion,abrasion,erosion,impact trauma,and clinical procedures are some of the major irritants that may cause formation of irritation dentin.The clinician must appreciate the resultant alterations in internal anatomy that accompany disease and damage of the pulp and dentin.Pulp Chamber At the time of eruption,the pulp chamber of a tooth re ?ects the external form of the enamel.1Anatomy is less sharply de ?ned,but the cusp form is present.Often the pulp suggests its original perimeter (and threatens its future) by leaving a ?lament of itself,the pulp horn,within the coronal dentin.A speci ?c stimulus such as caries leads to the formation of irritation dentin on the roof or wall of the chamber adjacent to the stimulus.Of course,with time,the chamber undergoes steady reduction in size as secondary,and irritation dentin is produced on all surfaces (Figure 2-3).Root Canal An unbroken train of connective tissue passes from the periodontal ligament through the apical root canal(s) to the pulp chamber.Each root is served by at least one such pulp corridor.Actually,the root canal is subject to the same pulp-induced changes as the chamber.Its diameter becomes narrowed,rapidly at ?rst as the foramen takes shape in the posteruptive months but with increasing slowness once the apex is de ?ned.The canal diameter
Histology and Physiology of the Dental Pulp29
tends to decrease slightly with age;irritants such as peri-
odontal disease may cause further constriction.
According to Orban,the shape of the canal,“to a large
degree,conforms to the shape of the root.A few canals
are round and tapering,but many are elliptical,broad
and thin.”26A curve at the end of the root means almost
invariably that the canal follows this curve.Meyer stated
that “roots that are round and cone-shaped usually con-
tain only one canal,but roots that are elliptical and have
?at or concave surfaces more frequently have more
canals than one”27(Figure 2-4).
The foramen can change in shape and location
because of functional in?uences on the tooth28(eg,
tongue pressure,occlusal pressure,mesial drift).The
pattern that develops is the reverse of the changes in the
alveolar bone around the tooth.Cementum resorption
occurs on the wall of the foramen farthest from the
force and apposition on the wall nearest.The net result
is a deviation of the foramen away from the true apex
(Figure 2-5).
Figure 2-3Schematic diagram of a mandibular molar showing
hard tissue apposition with time and/or irritation.Black arrows
indicate physiologic secondary cementum and dentin apposition;
white arrows indicate formation of dentin in response to irritants.
Pulp space undergoes continual reduction in size and volume.Note
that the ?oor of the chamber is a region of maximum secondary
dentin formation.
Figure 2-4Canal size and shape are a re?ection of the external
root surface.The upper diagrams show the possible canal con?g-
urations within each shaped root.The maxillary molar root sec-
tions illustrate that all sizes and shapes of canals may be seen in a
single tooth.
Figure 2-5Features often noted in normal yet aging tooth:devia-
tion of apical foramen as a result of mesial migration of the tooth
(top arrow).Selective resorption and apposition of cementum have
changed the position of the apex,causing narrowing of the apical
third of the root canal by increments of secondary dentin and ?ar-
ing of apical foramen from its smallest diameter at the dentinoce-
mental junction(bottom arrow)to its greatest diameter at the
cemental surface.Note the abundance of collagen ?bers in the
radicular pulp.Reproduced with permission from Matsumiya S.
Atlas of oral pathology.Tokyo Dental College Press;1955.
Foramina
The anatomy of the root apex is partially determined
by the number and location of apical blood vessels
present at the time of formation of the apex.When the
tooth is young and just erupting,the foramen is open.
Islands of dentin may appear within the mainstream of
connective tissue when the root sheath has induced
them,but these islands are widely separated.
Progressively,the main channel narrows.The primary
vessels and nerves,though never directly threatened
with strangulation,have a restricted passage.
Increments of cementum apposition contribute to this
continuous modeling.The possibilities of vascular
branching are so varied at the apex that prediction of
the number of foramina in a given tooth becomes
impossible (Figure 2-6).
It is known that the incidence of multiple foramina is high.29,30The majority of single-rooted teeth have a
single canal that terminates in a single foramen.Less
often,they possess an apical delta,which terminates in
a major channel and one or more collateral exits.
Occasionally,the delta has several channels of equal
magnitude.Root canals of the multirooted teeth,on
the other hand,tend to have a more complex apical
anatomy.Multiple foramina are the rule rather than the
exception.When accessory foramina are found in one
root of a multirooted tooth,the other roots usually
30Endodontics
have a similar condition.29Moreover,because the indi-vidual roots of such teeth often contain two or even three canals,a new factor is introduced.These canals can merge,but they need not and often do not merge before making their exit.Indeed,each may leave the root independently.Branching of the emergent canals within the apical area is a common ?nding because the preexisting vessels are linked.30It is also important to recall that cementum forms in abundance at the root apex.Because of the apposition of new layers of cementum,in response to eruption,the foramen anatomy is by no means constant.As stated above,the center of the foramen tends to deviate increasingly from the apical center.31Also,many root canals have two apical diameters.The minor diameter at the level of the dentinocemental junction can be as small as one half that of the major diameter at the external surface of the root.Cementum deposition tends to produce an apical funnel of increasing diver-gence.Contributing to this is secondary dentin forma-tion that narrows the dentinal ori ?ces of the canal (see Figure 2-5).Stereomicroscopic analysis of some 700 posterior root apices showed that at least half of the major foramina take eccentric positions that deviate as far as 2 mm from the apex.29Accessory foramina,on average,were found to be located twice the distance of the major foramina from the vertex (Figure 2-7).29Accessory Canals Communication of pulp and periodontal ligament is not limited to the apical region.Accessory canals are found at every level.Vascular perfusion studies have demon-strated vividly how numerous and persistent these trib-utaries are.32Many,in time,become sealed off by cementum and/or dentin;however,many remain viable.The majority appear to be encountered in the apical half of the root.These generally pass directly from the root canal to the periodontal ligament (Figure 2-8).A common area in which accessory canals appear is the furcation area of molar teeth (Figure 2-9).Burch and Hulen 33and Vertucci and Anthony 34found that molars frequently presented openings in the furcation areas.However,the studies did not determine how many of these represented patent (continuous) acces-sory canals all the way from the pulp to the periodon-tal ligament.Morphologic and scanning electron microscopic studies consistently show the presence of patent accessory canals or depressions that were assumed to be the openings to such canals.34–37In other studies,dyes were injected or drawn by vacuum into the furcation of molars.Approximately one half of
Figure 2-6Diverse rami ?cations of apical pulp space anatomy.
These models were made by drawing pulps from serial histologic
sections and “stacking ”the drawings.Many regions are obviously
inaccessible to conventional d ébridement methods.Adapted with
permission from Meyer W.Dtsch Zahnaerztl Z 1970;25:1064.
Histology and Physiology of the Dental Pulp 31
the teeth studied demonstrate patent accessory canals
from pulp space to furcation.38
HISTOLOGY
Regions
Classically,the pulp is described as having two de ?ned
regions,central and peripheral.39Typically,however,
studying sections of pulp under the microscope reveals
that the classic description is not consistent;levels of
activity dictate regional morphology.However,it is helpful to know the textbook description before study-
ing the variations.
The pulp is in intimate contact with the dentin and
survives only through the protection of its hard outer
covering.As the price of this protection,the pulp con-tributes to a close symbiosis.The way in which the nor-mal pulp relates to its immediate environment can be best explained by a review of its own morphology and that of the tissues with which it is con ?uent,namely,the dentin and the periodontal ligament.In general,the pulp demonstrates a homogeneity in its blend of cells,inter-cellular substance,?ber elements,vessels,and nerves.Peripheral Pulp Zone.On the periphery of the pulp,adjacent to the calci ?ed dentin,structural layers are apparent.These are usually evident in a medium-power photomicrograph (Figure 2-10).Next to the predentin lies the palisade of columnar odonto-blast cells.Central to the odontoblasts is the subodon-toblastic layer,termed the cell-free zone of Weil .40Figure 2-7Accessory foramen (arrow)in mandibular anterior
tooth.Accessory foramina are usually located within the apical 2 to
3 mm of root.(Orban collection.) Reproduced with permission
from Sicher H.Oral histology and embryology.5th ed.St.Louis:CV
Mosby;1962.
Figure 2-8A ,Necrotic pulp in maxillary second premolar in which irritants egress through lateral canals to the periodontium,creating in ?ammatory lesions (arrows).Although often invisible on pretreatment radiographs,the presence of lateral canals may be con ?rmed following obturation.B ,Bony lesions healed several months following root canal treatment.Accessory canals are impor-tant,not so much for the irritants they contain but because of their
communication to the PDL.(Courtesy of Dr.Manuel I.Weisman.)
A B
Plexuses of capillaries and small nerve ?bers ramify in
this subodontoblastic layer.Deep to the odontoblastic
layer is the cell-rich zone ,which blends in turn with the
dominant stroma of the pulp.The cell-rich zone con-
tains ?broblasts and undifferentiated cells,which sus-
tain the population of odontoblasts by proliferation
and differentiation.41
These zones vary in their prominence from tooth to
tooth and from area to area in the pulp of the same
tooth.The cell-free and cell-rich zones are usually
indistinct or absent in the embryonic pulp and usually
appear when dentin formation is active.The zones tend
to become increasingly prominent as the pulp ages.
Both of these zones are less constant and less promi-
nent near the root apex.
Central Pulp Zone.The main body of the pulp
occupies the area circumscribed by cell-rich zones.It
contains the principal support system for the periph-
eral pulp,which includes the large vessels and nerves
(Figure 2-11) from which branches extend to supply
the critical outer pulp layers.The principal cells are
?broblasts;the principal extracellular components are
ground substance and collagen.The environment of
the pulp is unique in that it is surrounded by an
unyielding tissue and fed and drained by vessels that
pass in and out at a distant site.However,it is classi-
?ed as an areolar,?brous connective tissue,contain-
ing cellular and extracellular elements that are found
in other similar tissues.These elements will be dis-cussed in more detail.32Endodontics
Structural Elements,Cellular Reserve Cells.The pulp contains a pool of reserve cells,descendants of undifferentiated cells in the primi-tive dental papilla.These multipotential cells are likely a ?broblast type that retains the capability of dedifferen-tiating and then redifferentiating on demand into many of the mature cell types.Beneath the odontoblasts,in the cell-rich zone,are concentrations of such cells.However,Frank demonstrated by radioautography that these cells produce little collagen,which is circumstan-tial evidence that they are not mature ?broblasts.42Baume has reviewed ultrastructural studies that sug-gest cytoplasmic connections between the odontoblasts and these subjacent mesenchymal cells.43Through such connections,on odontoblast injury or death,sig-nals may be provided to these less differentiated cells that may cause them to divide and differentiate into odontoblasts or odontoblast-like cells,as required.43Also important are the reserve cells scattered throughout the pulp,usually in juxtaposition to blood vessels.These retain the capacity,on stimulation,to divide and differentiate into other mature cell types.For example,mast cells and odontoclasts (tooth resor-bers) arise in the presence of in ?ammation.Signi ?cant are the unique cells that differentiate to form the calci ?ed tissue that develops under a pulp cap or pulpotomy when calcium hydroxide is placed in direct contact with the pulp.These unique cells are also frequently observed along the calci ?ed tissue forming at the base of tubules involved with caries,restorations,attrition,or abrasion.This calci ?ed tissue is not a true
Figure 2-9Inset demonstrates method of sectioning molars for viewing furcations.A ,Foramina of accessory canal indicated by arrow (×20original magni ?cation).B ,Foramen seen in A ,magni ?ed ×1,000.Canal is about 35 microns across,?aring to 60 microns at surface.Note two peripheral foramina on the rim.Reproduced with permission from Koenigs JG,Brilliant JD,Foreman DW.Oral Surg 1974;38:773.A B
Histology and Physiology of the Dental Pulp33
A B
D
E
C
Figure 2-10A,Medium-power photomicrograph from human pulp specimen showing dentin (D),predentin (P),odontoblast layer (O), cell-free zone (CF),cell-rich zone (CR),and central pulp (CP).B,Region similar to area bracketed in A.Cell-free zone contains large num-bers of small nerves and capillaries not visible at this magni?cation.Underlying CR does not have high concentration of cells but contains more cells than does central pulp.(A and B courtesy of Drs.Dennis Weber and Michael Gaynor.)C,Diagram of peripheral pulp and its prin-cipal elements.D,Scanning electron micrograph of dentin-pulp junction.Note corkscrew ?bers between odontoblasts(arrow).Reproduced with permission from Jean A,Kerebel JB,Kerebel LM.Oral Surg 1986;61:592.E,Scanning electron micrograph of pulpal surface of odonto-blast layer.Thread-like structures are probably terminal raveling of nerves.(Courtesy of Drs.R.White and M.Goldman.)
dentin,just as the cells that produce it are not true
odontoblasts.However,like the odontoblast,these cells
trace their origins to undifferentiated cells.
Fibroblasts.Most of the cells of the pulp are
?broblasts.These cells exhibit wide variation in their
degree of differentiation.44
Baume refers to them as mesenchymal cells,pulpoblasts,or pulpocytes in their
progressive levels of maturation.43These distinctions
are made,in part,because of the ability of these cells to
form calci ?ed tissues,something regular connective tis-
sue ?broblasts apparently cannot accomplish.
Pulpal ?broblasts are spindle-shaped cells with
ovoid nuclei (Figure 2-12).They synthesize and secrete
the bulk of the extracellular components,that is,colla-
gen and ground substance.The classic autoradiograph-
ic studies of Weinstock and Leblond,using 3H-proline,34Endodontics
demonstrated the process of collagen synthesis and secretion by the ?broblast.45Not only are ?broblasts the principal producers of collagen,they also eliminate excess collagen or partici-pate in collagen turnover in the pulp by resorption of collagen ?bers.This has been demonstrated to occur intracellularly by the action of lysosomal enzymes,which literally digest the collagen components.46Defense Cells.Histiocytes and Macrop hages.Undifferentiated mesenchymal cells (see Figure 2-12) around blood ves-sels (pericytes) can differentiate into ?xed or wander-ing histiocytes under appropriate stimulation.47Wandering histiocytes (macrophages) may also arise from monocytes that have migrated from vessels.These cells are highly phagocytic and can remove bacteria,foreign bodies (endodontic paste,zinc oxide,etc),dead cells,or other debris.48Pulpal macrophages and den-dritic cells thought to function like Langerhans ’cells have been identi ?ed in normal rat pulp.49These cells seem to be associated with pulpal immunosurveillance.Polymorphonuclear Leukocytes.The most common form of leukocyte in pulpal in ?ammation is the neu-trophil,although eosinophils and basophils are occa-sionally detected.It is important to know that although neutrophils are not normally present in intact healthy pulps,with injury and cell death they rapidly migrate into the areas from nearby capillaries and venules.50They are the major cell type in microabscess formation and are very effective at destroying and phagocytizing bacteria or dead cells.Unfortunately,their participa-tion often injures adjacent cells and may contribute to the development of wider zones of in ?ammation.Figure 2-11Cross-section from the central pulp showing major
support systems,including arterioles (A) with a muscular wall,
thin-walled lymphatics (L),venules (V),and nerve bundles (NB)
containing myelinated and unmyelinated nerves.Reproduced with
permission from Walton R,Leonard L,Sharawy M,Gangarosa L.
Oral Surg 1979;48:545.
Figure 2-12Pulpal ?broblasts showing spindle-shaped cyto-plasm.Plump nuclei (dark arrow)usually indicate active collagen formation.Condensed nucleus is in a “quiet ”cell,often termed a ?brocyte (open arrow).Pericytes (P) lie in close apposition to ves-
sels and differentiate into other typical pulp cell types on demand.
Histology and Physiology of the Dental Pulp35
Lymphocytes and Plasma Cells.These in?ammato-ry cell types generally appear following invasion into the area of injury by neutrophils.These cells are not normally present in healthy pulp tissue but are associ-ated with injury and resultant immune responses—attempts to destroy,damage,or neutralize foreign sub-stance(s).Their presence would therefore indicate the presence of a persistent irritant.
Mast Cells.Interestingly,mast cells are seldom in large numbers in normal,healthy pulps51but are com-monly found in in?amed pulps.52,53The granules of these cells contain histamine,a potent in?ammatory mediator,and heparin.These cells release these gran-ules or degranulate into the surrounding tissue ?uid during in?ammation.52
Since these cells are generally found near blood ves-sels,degranulation of mast cells releases histamine close to vascular smooth muscle,causing vasodilation. This increases vessel permeability,allowing ?uids and leukocytes to escape.
Odontoblasts.The principal cell of the dentin-forming layer,the odontoblast,is the ?rst cell type encountered as the pulp is approached from the dentin (Figure 2-13).These cells arise from peripheral mes-enchymal cells of the dental papilla during tooth devel-opment (see Structural Elements) and differentiate by acquiring the characteristic morphology of glycopro-tein synthesis and secretion54(Figure 2-14). Glycoprotein forms the predentin matrix,which is ren-dered mineralizable by the odontoblast,a unique cell producing a unique tissue,dentin.Synthesizing and secretory activities render the odontoblast highly polar-ized,with synthesis occurring in the cell body and secre-tion from the odontoblastic process.
The cell body contains organelles that represent dif-ferent stages of secretion of collagen,glycoproteins,and calcium salts.55Matrix secretion precedes mineraliza-tion with these two events separated in time and space by the predentin.As happens in bone,the initial miner-al seeding of predentin at the dentinoenamel junction is by formation of“matrix vesicles.”56,57 Classic studies by Weinstock and colleagues,45,58,59using an autoradi-ographic technique,have demonstrated the functional sequence of matrix production and secretion.This material has recently been reviewed by Holland.60
In histologic sections viewed under a light micro-scope,odontoblasts appear to vary from tall,pseudos-trati?ed columnar cells in the coronal pulp (see Figure 2-10) to a single row of cuboidal cells in radicular pulp to a ?attened,almost squamous shape near the apex.61,62These squamous cells often form an irregular, atubular dentin.
Scanning electron microscopy has provided a better view of the external morphology of the odontoblasts (see Figure 2-10,C and D).The large nucleus is located in the base of the cell,giving it a pear-shaped appear-ance.63 From an exquisite scanning electron micro-scopic study,French dental scientists have demonstrat-ed that odontoblast cell bodies “appear tightly packed in the pulp horn and successively pear shaped,spindle shaped,club shaped,or globular from the crown to the apex”64(Figure 2-15).
During dentin formation in the crown,the odonto-blasts are pushed inward to form the periphery of a pulp chamber,the circumference of which is increas-ingly smaller than the original circumference at the dentinoenamel junction.This explains why the cells are packed and palisaded into a pseudostrati?ed appear-Figure 2-13Pseudostrati?ed appearance of odontoblasts.Dark horizontal line (arrow)delineates cell body from the odontoblastic processes and predentin and was once termed “pulpodentinal membrane.”Ultrastructural examination has shown this to be a terminal cell web that forms a support and attachment area between adjoining cells.Reproduced with permission from Walton R,Leonard L,Sharawy M,Gangarosa L.Oral Surg 1979;48:545.
ance of coronal odontoblasts.Conversely,because the
space is not so compressed in the radicular pulp,the
odontoblasts maintain a columnar,cuboidal,or (in the
apical region) squamous shape.Also,the resulting cell
and tubule density is much higher in the pulp chamber
than in the root pulp.65This increased tubule density in 36Endodontics the chamber may explain the greater sensitivity and permeability of the dentin of the crown.The cell body manufactures the matrix material;the material is transported to and secreted from the odon-toblastic process.Classically,the odontoblastic process has been described as extending from the cell body to the dentinoenamel junction,a distance of 2 to 3 mm (ie,2,000 to 3,000 μm).This concept was based on the observations of many light microscopists using a vari-ety of special procedures and stains.66When dentin was examined by electron microscopy,the odontoblas-tic process was determined to be limited to the inner third of dentin,with the outer two-thirds of the tubule devoid of processes or of nerves but ?lled with extra-cellular ?uid.67–70More recent investigations indicate that odontoblastic processes may indeed extend to the dentinoenamel junction.71,72However,tubular struc-tures in dentinal tubules are not necessarily odonto-blastic processes.73,74Unequivocal identi?cation can be done only by identifying a trilaminar plasma mem-brane around the putative process using transmission electron microscopy.75,76The extent of the odontoblas-tic process remains controversial.77Therefore,modern interpretations of pulpal injury following conservative cavity preparation may not be attributable to amputation of odontoblastic processes but to desiccation,heat,and osmotic effects.Further,dentin sensitivity may not be related to direct stimula-tion of either odontoblastic processes or nerves in peripheral dentin since the tubules may be devoid of such structures in the periphery of dentin.After initial dentin formation,the odontoblast,via its process,can still modify dentin structure by produc-ing peritubular dentin.This is a hypermineralized cuff with little organic matrix within the tubule,decreasing the diameter of the tubule.78–80When irritated,the odontoblast can accelerate peritubular dentin forma-
Figure 2-14Odontoblasts,as viewed under the electron micro-
scope,show organelles essential for protein synthesis,a plump
nucleus ?lled with euchromatin,and cytoplasm rich with rough
endoplasmic reticulum (R) and a well-developed Golgi apparatus
(G).(Courtesy of Dr.Dale Eisenmann.)
Figure 2-15Diagram summarizing shape variation of odonto-blast cell bodies.A ,Pulp horn (pear shaped);B ,coronal midpulp level (spindle shape);C ,coronal midroot level (elongated club shape);D ,mid-third of root (short club shape);E ,apical third of root (globules).Reproduced with permission from Marion D,et al.Oral Surg 1991;72:473.A B C D E
Histology and Physiology of the Dental Pulp 37
tion to the point of complete occlusion of the tubule (Figure 2-16).81–83When tubule occlusions extend over
a large area,this is referred to as sclerotic dentin,com-
monly found in teeth with cervical erosion.44
Alternatively,irritated odontoblasts can secrete col-lagen,84amorphous material,or large crystals into the
tubule lumen;these occlusions result in decreases in
dentin permeability to irritating substances.
81–83
Although these secretions have been described as a
defensive reaction by the odontoblast to protect itself
and the underlying pulp,this “protection ”has never
been proved.
Extracellular.The dental pulp has most of its vol-
ume primarily composed of ?bers and ground substance.
These form the body and integrity of the pulp organ.
Fibers.The morphology of collagen ?bers,a
principal constituent in the pulp,has been described
at the level of both light and electron microscopy.At
the ultrastructural level,typical 640 angstrom band-
ing or electron-dense periodicity provides positive
proof of collagen ?ber identity.85These ?bers form a
loose,reticular network to support other structural
elements of the pulp.Collagen is synthesized and
secreted by odontoblasts and ?broblasts.However,the
type of collagen secreted by odontoblasts to subse-
quently mineralize differs from the collagen produced
by pulpal ?broblasts,which normally does not calcify.
They also differ not in basic structure but in the
degree of cross-linking,and in slight variation in hydroxylysine content.
86Tropocollagen is immature collagen ?bers that remain thin and stain black with silver nitrate,described in light microscopy as argyrophilic or reticu-lar ?brils.If tropocollagen molecules aggregate into larger ?bers,they no longer stain with silver and are generally termed “collagen ?bers.”If several collagen ?bers aggregate (cross-link) and grow more dense,they are termed “collagen bundles.”Collagen generally becomes more coarse (ie,develops more bundles) as the patient ages.Age also seems to permit ectopic calci-?cation of pulp connective tissue,ranging from the development of random calci ?cations to diffuse calci ?-cations 87to denticle (pulp stone) formation.Elastin,the only other ?brous connective tissue protein,is found only in the walls of pulp arterioles.Collagen has been described as having a unique arrangement in the peripheral pulp;these bundles of collagen are termed von Korff ’s ?bers.Most textbooks describe von Korff ’s ?bers as being corkscrew-like and originating between odontoblasts to pass into the dentin matrix (Figure 2-17).The tight packing of odontoblasts,predentin,capillaries,and nerves pro-duces very narrow spaces between and around odonto-blasts that can retain heavy metal stain (precipitates).Ten Cate ’s electron microscopic studies of the distribu-tion of these precipitates demonstrated their presence in narrow intracellular tissue spaces.88He claimed that they represented artifactual “stains ”that were not attached to collagen ?bers.88However,more recent scanning electron microscopic studies (see Figure 2-10,Figure 2-16Mineralization of dentinal tubules in an aging
human tooth.Electron micrograph of transparent root dentin from
a 45-year-old person.The more densely mineralized peritubular
dentin is white and the tubule itself is black.Two tubules are visible
in cross-section.The tubule on the left is almost completely occlud-
ed.The progressive nature of mineralization is evident in the tubule
on the right.(Courtesy of Dr.John Nalbandian.)Figure 2-17Peripheral pulp.The corkscrew-like structures (von Korff ’s ?bers) reportedly are collagen ?bers that originate in the pulp,pass between odontoblasts,and are incorporated into pre-dentin.That these are collagen ?bers is disputed.Reproduced with permission from Bernick S.155
D) of the predentin-pulpal border demonstrating
screw-like ?brous material have stimulated new specu-
lation that von Korff ’s ?bers are real structures.63
Ground Substance.This structureless mass,
gel-like in consistency,makes up the bulk of the pulp
organ.It occupies the space between formed elements.
The ground substance resembles that of other areolar,
?brous connective tissues,consisting primarily of com-
plexes of proteins and carbohydrates and water.More
speci ?cally,these complexes are composed of combina-
tions of glycosaminoglycans,that is,hyaluronic acid,
chondroitin sulfate,and other glycoproteins.89,90The
ground substance surrounds and supports structures
and is the medium through which metabolites and
waste products are transported to and from cells and
vessels.Aging of the pulp alters the ground substance,91
although there is no substantive proof that these alter-
ations signi ?cantly inhibit pulp functions.
Supportive Elements.
Pulpal Blood Supply.Numerous investigators have
described the blood supply of the dental pulp.92–95
Because the pulp itself is small,pulp blood vessels do
not reach a large size.At the apex and extending
through the central pulp,one or more arterioles branch
into smaller terminal arterioles or metarterioles that are
directed peripherally (Figure 2-18,A).Before the arte-
rioles break up into capillary beds,arteriovenous anas-
tomoses often arise to connect the arteriole directly to
a venule.96These arteriole-venule shunts are identi ?ed
by the presence of irregularly oriented myoepitheli-
um-like cells surrounding them and by the cuboidal
nature of the cells lining their lumen.97The classic
description of microcirculatory beds includes capillar-
ies that branch off arterioles at right angles (Figure
2-18,B).Unfortunately,no such structures have been
found in human pulps.Instead,arterioles branch into
terminal arterioles,which,in turn,give rise to capillar-
ies (Figure 2-19).
Capillary density is highest in the subodontoblastic
region with loops passing between odontoblasts
(Figure 2-20).98–100In the subodontoblastic region,
capillaries with fenestrations occur frequently and reg-
ularly in both primary and permanent teeth (Figure 2-
21).The fenestrae (“windows ”) are spanned by a thin
diaphragm of plasma membrane.The frequency of
fenestration falls off rapidly when examining central
capillaries,being as low as 4% in the coronal pulp.98,101
Capillaries empty into small venules that connect
with fewer and successively larger venules.At the apex,
multiple venules exit the pulp.These venules connect
with vessels that drain the periodontal ligament or
adjacent alveolar bone.The vessels of the pulp have 38Endodontics
Figure 2-18A ,Perfused pulp of dog premolar showing the size and location of vessels.L arger central vessels are arterioles and venules.Peripherally directed are smaller metarterioles that branch into the rich network of looping capillaries of peripheral pulp.B ,Schematic diagram of classic microcirculatory vascular bed that would represent a region of central and peripheral vessels as seen in A .Arterioles are invested by a continuous layer of smooth muscle cells.Metarterioles have discontinuous clusters of smooth muscle with capillaries branching directly off metarterioles.Precapillary smooth muscle sphincters are strategically located to control capil-lary blood ?ow.True capillaries lack smooth muscle.Arteriovenous shunts represent direct connections between arterioles and venules.Their muscles are innervated by sympathetic nerve ?bers.A repro-duced with permission from Seltzer S,Bender IB.The dental pulp.2nd ed.Philadelphia:JB Lippincott;1975.p.106.
A B
Histology and Physiology of the Dental Pulp39
thinner muscular walls (tunica media) than vessels of comparable diameter in other parts of the body. Undoubtedly,this is an adaptation to the surrounding protective and unyielding walls.102Kim and his associ-ates have obtained evidence that suggests that most vasodilating agents induce only a transient,brief increase in pulpal blood ?ow followed by a decrease in blood ?ow owing to collapse of local venules.103 Apparently,the vasodilation either directly impinges on venules or permits transudation of?uid across cap-illaries that indirectly compresses the thin-walled venules in the low-compliance system of the pulp chamber.
The above-described general vascular architecture is found in each tooth root.Alternate blood supply is available to multicanaled teeth,with the resulting rich anastomoses in the chamber.The occasional vessels that communicate via accessory canals have not been Figure 2-19Corrosion resin casts of the pulp vessels of a dog pre-molar.A,Higher magni?cation of the region enclosed by the square labeled A in C demonstrates many hairpin capillary loops within the pulp horn (×300 original magni?cation).B,Higher magni?ca-tion of the area enclosed by the square labeled B in C.Arterioles (a) arborize from artery to form a capillary (c) network on the surface of the radicular pulp.Venule (V) is about 50 micrometers in diam-eter.Arterioles are about 10 micrometers in diameter.Super?cial capillary network demonstrates cross-fence shape.C,Montage of the entire pulp made from multiple,overlapping scanning electron micrographs (×50 original magni?cation).The three projections in the coronal region represent three pulp horns,apical foramen (af). (Courtesy of Drs.K.Takahashi,Y.Kishi,and S.Kim.)
C
A B
demonstrated to contribute signi ?cantly as a source of
collateral circulation.
Lymphatics.The presence of pulpal lymphatics is disputed.104,105However,lymphatics have been identi-?ed in the pulp at the ultrastructural 98and histologic
levels by the absence of red blood cells in their lumina,
the lack of overlapping of endothelial margins,and the absence of a basal lamina.87,98,106–108They arise as lym-
phatic capillaries in the peripheral pulp zone (Figure 2-
22) and join other lymph capillaries to form collecting
vessels.87These vessels unite with progressively larger
lymphatic channels that pass through the apex with the
other vasculature.Numerous authors,using both histo-
logic and functional methods,have described extensive
anastomoses between lymph vessels of the pulp,peri-odontal ligament,and alveolar bone.108–
114Functional Implications.The presence of arteriove-nous shunts 32,96in the pulp provides the opportunity
for blood to shunt 115,116past capillary beds since these
arteriole-venule connections are “upstream ”from the
capillaries.Alternatively,the arteriole-venule shunts
could remain nearly closed (in a constricted state),and
most of the blood would pass peripherally in the pulp
to perfuse capillaries and the cells that they support.115
It has been suggested that the distribution of blood
?ow might change during pulp in ?ammation.117
Increased dilation of arteriole-venule shunts may pro-
duce “hyperemia,”in which more blood vessels than
normal are open and ?lled with blood cells;this may
indicate more rapid blood ?ow or represent partial sta-
sis.Further,this dilation of arteriole-venule shunts may
“steal ”blood from capillary beds,causing accumula-
tion of waste products.40Endodontics
Capillary fenestration may indicate that these capil-laries are more permeable to large molecules or that they allow more rapid ?uid movement across the endothelium.118However,studies on pulp capillaries
Figure 2-20Electron micrograph of subodontoblastic capillary
looping between odontoblasts.Portions of several red blood cells are
seen within the lumen.Reproduced with permission from Avery J.100
Figure 2-21A ,Electron micrograph of cross-section of the capil-lary loop passing between and closely surrounded by odontoblasts.Inset shows higher magni ?cation of a portion of endothelial wall of the capillary demonstrating fenestrations (arrow).B ,Subodonto-blastic capillary with large nucleus of endothelial cell impinging on lumen.Plasticity of red blood cell (black)allows it to adapt to irreg-ular contours of lumen.Prominent basement membrane encircles the periphery of the cell.(A courtesy of Dr.K.Josephsen,Denmark;B courtesy of Dr.Robert Rapp.)A B
Histology and Physiology of the Dental Pulp 41
suggest a lower than normal permeability to large mol-
ecules.On the other hand,a higher rate of ?uid move-
ment has not been ruled out.Increased transudation of
plasma and polymorphonuclear neutrophil leukocytes
from the circulation occurs most often in venules 50
rather than capillaries.
The structural identi?cation of lymph capillar-ies 87,98,107complements the functional studies of
Walton and Langeland,108who demonstrated that sub-
stances placed in the pulp chamber can be found in
regional lymph nodes.The open endothelial margins
and incomplete basal lamina permit entry of large mol-
ecules and even bacteria.The fact that materials placed
on pulps can migrate to lymph nodes 119indicates the
possibility of immunologic reactions to substances that
enter the pulp.120Bernick described the appearance of
lymphatics in the in?amed pulp and surmised that
their function is to remove the excess ?uid and debris
that accompanies in?ammation.87
Unfortunately for the pulp,the lymphatics may col-
lapse as pulp pressure rises,thus inhibiting removal of irritants and ?uid.Clearly,more investigation is required before one can understand how lymphatic function is disturbed in pulp in?ammatory conditions.The anastomoses of pulpal,periodontal,and alveolar lymphatics may be important routes for the spread of pulpal in?ammation into adjacent tissues during the removal of irritants and ?uid from the pulp.These structural interrelationships have not received the attention they deserve.Finally,the extent and degree of anastomoses of apical venules with those of the peri-odontal ligament and alveolar bone need investiga-tion.92Vessels may provide a route for local anesthetic movement during intraosseous or periodontal liga-ment injections 121rather than the ?uid “dissecting”through perivascular tissue spaces.122These same path-ways have been implicated as routes of spread of in?ammation from pulp to periodontal ligament and/or bone and vice versa.Nerves.Several nerve bundles,each containing numerous unmyelinated and myelinated nerves,pass into each root via the apical foramen.The majority are unmyelinated nerves,123–125most of which are part of the sympathetic division of the autonomic nervous sys-tem;these have been shown to cause reductions in pulp blood ?ow when stimulated.126,127The remaining nerves are myelinated sensory nerves of the trigeminal system (Figure 2-23).The myelinated nerve ?bers branch extensively beneath the cell-rich zone to form the so-called plexus of Raschkow (Figure 2-24).From here,many ?bers lose their myelin sheath and pass through the cell-free zone to terminate as receptors or as free nerve endings near odontoblasts (Figure 2-25);others pass between odon-toblasts to travel a short distance up the dentinal tubules adjacent to odontoblastic processes.128 The nerve end-ings terminate far short of the dentinoenamel junction;rather,endings are found only in tubules of the inner dentin and predentin,on or between odontoblasts.129Byers has found that intradental nerves pass approxi-mately 100 μm into the tubules,regardless of the dentin thickness,in a wide variety of animal species.130Perhaps nerve ?bers cannot be nourished beyond a 100 μm dif-fusion distance.Some sensory axons exhibit terminal aborizations that innervate up to 100 dentinal tubules.130Signi ?cantly,sensory nerves of the pulp respond to noxious stimuli with pain sensation only,regardless of the stimulus.This pain is produced whether the stimulus is applied to dentin or the pulp.Cavity preparation in the unanesthetized tooth is painful at any depth of dentin.How can this occur if there are no sensory nerves in the outer two-thirds of
dentin? The answer probably lies in the hydrodynamic
Figure 2-22Lymphatic capillary arising and collecting from with-
in the odontoblast-subodontoblast region of a human pulp.Arrows
delineate margins of the vessel,draining toward the central pulp.
Reproduced with permission from Bernick S.87
42
Endodontics
Figure 2-23Schematic drawing showing sensory nerve location in pulp and dentin.Percentage of innervated tubules at regions A through D is indicated (left).Px = plexus of Raschkow;cfz = cell-free zone;O = odontoblasts;p = predentin.Reproduced with permission from Byers M.144 Figure 2-24Branching of nerve bundles as they approach the
subodontoblastic region (plexus of Raschkow).(Courtesy of Dr.
James Avery.)
Figure 2-25Nerve terminal (arrow)located between adjacent
odontoblasts near calcifying https://www.doczj.com/doc/e612713710.html,rge number of vesicles is
characteristic of nerve terminal.Terminal is closely applied to the
adjacent odontoblastic process;this does not,however,represent a
synapse.(Courtesy of Dr.James Avery.)
Histology and Physiology of the Dental Pulp43 theory in which ?uid movement within tubules stimu-
lates distant sensory nerve endings (see Byers et al and
Avery128–131for reviews).
Highly organized junctions have been demonstrated
between some nerve ?bers and odontoblasts.132–136
Although they do not appear to be typical synaptic
junctions,their existence must be functional.t is
unclear whether the activity is sensory or motor.
An additional function of sympathetic nerves is the
possible regulation of the rate of tooth eruption.
Sympathetic nerve activity in?uences local blood ?ow
and tissue pressure by opening or closing arteriovenous
shunts as well as arteriolar blood ?ow;this may sec-
ondarily affect eruptive pressure.137Activation of sym-
pathetic ?bers not only reduces pulpal blood ?ow138
but also decreases the excitability of intradental
nerves.139Thus,there is a very intimate relationship
between pulpal nerves and their excitability and local
blood ?ow.140
Numbers and concentrations of nerves vary with
the stage of tooth development and also with location.
Fearnhead and others have reported that very few
nerves appear in the human pulp prior to tooth erup-
tion.41,141,142After eruption,the highest number of
nerves is found in the pulp horns (about 40% of the
tubules are “innervated”).The number of nerves per
tubule drops off to about 4.8% in the more lateral
parts of the coronal dentin to less than 1% in the cer-
vical region (see Figure 2-23),with only an occasional nerve in radicular dentin.143Patterns of branching nerves seen with the light microscope would con?rm numbers of nerves at different levels.There is little branching off the main nerve bundles until the coro-nal pulp.Regions of sensitivity also correlate in that coronal pulp and dentin are more painful to stimuli than are radicular pulp and dentin.The same stimuli applied to dentin were described as “sharp”when applied to coronal dentin but “dull”when applied to radicular dentin.144Restorative procedures in rat teeth cause sprouting of pulpal and intradental nerves that may modify both dentin sensitivity145and local in?ammatory reactions.146
Interestingly,removal of the pulp by extraction of the tooth or by pulpectomy and,presumably,pulpotomy results in the successive degeneration of the cell bodies located in the spinal nucleus of the trigeminal nerve,the main sensory ganglion,and the peripheral nerve lead-ing to the tooth in the socket.147Bernick observed the effects of caries and restorations on underlying nerves in the pulp.148He found a degeneration of the sub-odontoblastic plexus of nerves associated with the pro-duction of irritation dentin.He concluded that “the ter-
minal nerves in the injured pulp are sensitive to the noxious products of caries and the restorative proce-dures.An apparent decrease in sensitivity results in restored teeth.”The lack of sensitivity that accompanies the caries process may be attributable,at least partially, to degeneration of underlying nerves.
Calci?cations.Basically,there are two distinct types of pulpal calci?cations:formed structures com-monly known as pulp stones (denticles) and tiny crys-talline masses generally termed diffuse (linear) calci?-cations (Figure 2-26).Pulp stones seem to be found predominantly in the coronal pulp,whereas the calci?-cations found in radicular pulp seem to be of the dif-fuse variety.149
Calci?cations are common in the dental pulp,with a tendency to increase with age and irritation.It has been speculated that these calci?cations may aggravate or even incite in?ammation of pulp or may elicit pain by pressing on structures;however,these speculations have not been proved and are improbable.Although these calci?cations are not pathologic,their presence under certain conditions may be an aid in diagnosis of pulpal disease.Moreover,their bulk and position may interfere with endodontic treatment.
Pulp Stones.These discrete calci?c masses appear with frequency in mature teeth.150Although there is increased incidence with age,they are not uncommon Figure 2-26Unin?amed pulp.Typical pattern of calci?cations. Larger pulp stones in the chamber blend into linear diffuse calci?ca-tions in the canal.Reproduced with permission from Bernick S.155
in young teeth.It has also been demonstrated that their
occurrence and size often increase with external irrita-
tion.151Pulp stones also may arise spontaneously;their
presence has been identi ?ed on radiographs (Figure 2-
27) and,on histologic examination,even in impacted teeth.152Interestingly,there appears to be a predisposi-
tion for pulp stone formation in certain individuals,possibly a familial trait.Pulp stones have been classi ?ed as two types,true or
false.However,recent careful histologic examination
has discounted the true pulp stone.Supposedly,true
pulp stones are islands of dentin,demonstrating
tubules and formative odontoblasts on their surface.
However,serial sectioning has shown that these are not
islands but peninsulas —extrusions from dentin
walls.152,153Therefore,the term “denticle,”which
would imply dentin structure,is a misnomer.The term
“pulp stone ”is more correct,particularly because the
“false ”pulp stone so closely resembles gallstones and
kidney or ureter stones.
Pulp stones,like other types of stones,are formed
from clearly concentric or diffuse layers of calci ?ed tis-
sue on a matrix that seems to consist primarily of col-lagen.154Their structure may help explain their origin;
it has been shown that potential nidi of pulp stones
may occur in the sheaths associated with blood vessels
(Figure 2-28) and nerves.155Other potential nidi are
calci ?cations of thrombi in vessels or calci ?cation of clumps of necrotic cells.153Whatever the nidus,growth
is by incremental layering of a matrix that quickly
acquires mineral salts.
44Endodontics
Pulp stones are also classi ?ed according to location.“Free ”stones are those that are islands,“attached ”stones are free pulp stones that have become fused with the continuously growing dentin,and “embedded ”stones are formerly attached stones that have now become surrounded by dentin.Pulp stones may be important to the clinician who attempts access preparation or to negotiate canals.Either free or attached denticles may attain large size and occupy considerable volume of the coronal pulp (Figure 2-29).Their presence may alter the internal anatomy and confuse the operator by obscuring,but not totally blocking,the ori ?ce of the canal.Attached denticles may de ?ect or engage the tip of exploring instruments in the canals,thus preventing their easy passage down the canal.156Pulp stones of sufficient size are readily visible on radiographs,although the majority are too small to be seen except on histologic examination.The large,dis-crete masses,occasionally appearing to nearly ?ll the chamber (Figure 2-30),are likely to be those of natural occurrence.The chamber that appears to have a diffuse and obscure outline may represent a pulp that has been subjected to a persistent irritant and has responded by forming large numbers of irregular pulp stones.This ?nding is a diagnostic aid and indicates a pulp exposed to a persistent chronic irritant.Diffuse Calci ?cations.Also known as linear calci-?cations because of their longitudinal orientation,
Figure 2-27Second molar demonstrates chamber nearly ?lled
with pulp stones (arrow).Stones may have arisen spontaneously,
or their presence may indicate chronic irritation and in ?amma-
tion from caries and/or deep restoration.(Courtesy of Dr.G.
Norman Smith.)Figure 2-28Calci ?cation of the sheath surrounding this small vessel may form a nidus for growth of a larger calci ?ed structure,a pulp stone.Reproduced with permission from Bernick S.J Dent Res 1967;46:544.
牙体牙髓病学实验教学方法的探索 陈敏 1 徐江 1 梁君2 （1石河子大学医学院一附院口腔科，新疆石河子，832008；2新疆军区69006部队，新疆乌鲁木齐，830000） 【摘要】牙体牙髓病学是一门操作技能性很强的临床学科，在牙体牙髓实验课的教学中开展以针对培养学生临床思维能力和临床操作技能为主的教学方法，可有效提高牙体牙髓病学实验的教学质量，促进学生对牙体牙髓病学理论知识的掌握和运用程度。 【关键词】牙体牙髓病学实验；教学方法改进；临床操作技能 牙体牙髓病学是一门操作技能性很强的口腔临床学科，也是口腔内科学教学中所占课时比重最大，临床服务对象最多的一门学科。因此，在口腔医学学生的培养中除了强调理论知识的教学外，更应强调实践能力的培养。牙体牙髓实验课是巩固理论知识，拓宽临床视野，训练和掌握牙体牙髓病学基本操作能力的最佳平台。临床带教中发现，经过系统理论学习的口腔医学学生在进入临床实习时，无法对就诊病人全身情况和口腔问题形成一个系统的认识，从而无法确立正确的诊断开展有效的治疗程序。针对上述问题，我口腔内科教研组在牙体牙髓实验课的教学中进行了以针对培养学生的临床思维能力和临床操作技能为主的教学尝试，有效地提高了学生对牙体牙髓病学理论知识的掌握程度，提高了牙体牙髓病学实验的教学质量，并缩小了医学生由基础理论向临床实践过渡的落差感［1］。 1 转变教学观念，强化以人为本的实验教学意识 1.1由直接灌输式的教学方式向主动操作型的教学方式的转变。 传统的实验课通常是由教师列举实验的目的、内容、方法和步骤，学生按要求动手完成相关的操作。实验报告的撰写也是以此为基础的一种简单概括或理论知识的总结。虽然也有许多图片、模型介绍，但学生只是被动的接受知识，缺乏自主学习的能力。由于缺少学生自己的体验和分析，实验课学到的知识很难被其自身消化吸收，成为自身知识体系的有机组成成分；在今后的临床工作中遇到实际问题就会缺乏自主判断能力，无法将学到的知识运用于解决临床实际问题的实践中。因此，我们从过去那种“直接灌输式”转变为以解决临床问题为中心，把培养学生的动手能力作为教学的核心内容，诱导学生从书本知识向临床操作过渡
牙体牙髓病学练习题 一、A1 1、对固位钉的描述不正确的是 A、固位钉的钉道应大于钉的直径 B、固位钉的数目应根据牙体缺损情况而定 C、摩擦固位钉的钉道大于钉的直径 D、自攻螺纹钉遇到一定阻力即于颈部折断 E、黏固钉的固位力相对不强 2、下列哪种材料对牙髓刺激小并可促进牙本质形成 A、磷酸锌水门汀 B、聚羧酸水门汀 C、玻璃离子水门汀 D、氢氧化钙糊剂 E、银汞合金 3、玻璃离子充填时，洞形要求错误的是 A、洞有一定的深度 B、洞缘去除无基釉 C、洞缘可做洞斜面 D、可降低固位形要求 E、洞底可呈弧形 4、制备倒凹是为了 A、获得良好的抗力形 B、便于垫底 C、便于充填 D、获得良好的固位形 E、便于放置盖髓剂 5、大面积龋损修复时，固位钉在修复体与牙本质中长度一般应为 A、小于2mm B、大于2mm C、1.5~2mm D、1~1.5mm E、1mm 6、增强窝洞抗力的方法不包括 A、去除无基釉 B、去除薄壁弱尖 C、保留承力区的薄壁弱尖 D、洞缘线设计为圆钝曲线 E、洞形成箱状 7、下列不属于复合树脂嵌体的特点的是 A、固化不受光照的影响
B、可减少微渗漏 C、较树脂充填修复抗压能力强，且耐磨 D、主要适用于Ⅱ、Ⅲ类洞 E、解剖外形恢复较好 8、过小牙常见于 A、上颌切牙 B、下颌切牙 C、上颌侧切牙 D、下颌侧切牙 E、上颌尖牙 9、牙体形态异常不包括 A、融合牙 B、釉质发育不全 C、牙中牙 D、过小牙 E、畸形中央尖 10、牙齿发育异常不包括 A、结构异常 B、牙列异常 C、形态异常 D、数目异常 E、萌出异常 11、Hutchinson牙是指 A、遗传性乳光牙本质 B、结合牙 C、先天性梅毒的半月形切牙 D、畸形舌侧沟 E、牙本质过敏 12、有关先天性梅毒牙描述正确的是 A、多见于恒牙，乳牙少见 B、一般是在胚胎早期遭受受梅毒严重侵犯导致 C、梅毒螺旋体可通过胎盘作用于胎儿 D、患者可表现为半月形的磨牙 E、桑葚状磨牙与间质性角膜炎以及神经性耳聋称为哈钦森三征 13、先天性梅毒牙常见牙位为 A、11、12、16、21、22、26、31、32、36、41、42、46 B、11、16、21、26、31、32、36、41、42、46 C、11、16、21、26、31、35、36、41、45、46 D、11、12、16、21、22、26 E、31、32、36、41、42、46
《牙体牙髓病学实验》课程教学大纲 教案 口腔医学院牙体牙髓病学教研室
前言 口腔临床基本技能实验教学内容以学生为中心，注重引导学生以疾病为主线，根据对疾病的认知过程，在同一层次从多个角度共同认识疾病的发生发展规律和治疗方法，扎实培养学生掌握“三基”(基础实验知识、基本实验操作技能与基本实验方法)。通过本课程学习，要求学生熟悉龋病、牙体病、牙髓根尖周病的检查、诊断和基本治疗方法，并着重培养学生分析问题、解决问题的能力，掌握确定口腔疾病诊疗计划的临床思路，为后期进入临床实习打下良好的基础。 本课程为口腔医学专业的必修课，总学时数为80学时。
参考书目 1.《仿真人头模实验室实验指导》，重庆医科大学附属口腔医学院自编教材，2007,3 2.《牙体牙髓病学》第二版，主编：樊明文出版社：人民卫生出版社 3.《口腔医学实验教程》第二版，主编：王嘉德出版社：人民卫生出版社 4.《口腔医学实验教程附册》第二版，主编：王嘉德出版社：人民卫生出版社 5.《Fundamentals of Operative Dentistry》Second Edition. James B. Summary Bylj.
目录 实验一仿真人头模的使用，口腔医师的术式、支点（与钻针切割硬物练习） -----------------------------------------1 实验二牙体牙髓病治疗常用器械及其使用 -------------1 实验三牙体牙髓病口腔检查与病历书写-----------------2 实验四龋病损害及窝洞结构认识和分类，石膏牙Ⅰ类洞的制备 ---------------------------------------------------2 实验五石膏牙Ⅱ、Ⅲ、Ⅴ类洞的制备 -----------------3 实验六离体下颌磨牙Ⅰ、Ⅴ类洞的制备 --------------3 实验七离体下颌第一双尖牙Ⅱ、Ⅴ类洞制备 ----------4 实验八仿头模上上颌磨牙Ⅰ、Ⅴ类洞制备 ------------4 实验九仿头模上下颌磨牙Ⅱ类洞的制备 --------------5 实验十仿头模上下颌双尖牙Ⅱ、Ⅴ类洞的制备 --------5 实验十一盖髓术，常用粘固粉的调制应用，窝洞垫底，银汞合金充填术 ---------------------------------------------6 实验十二仿头模前牙IV类洞的制备及钉固位、树脂粘接修复术 ---------------------------------------------------6 实验十三髓腔解剖、开髓法、离体牙开髓术，干髓术 --7 实验十四离体前牙、前磨牙根管预备 ----------------7 实验十五离体磨牙根管预备 -----------------------8 实验十六离体牙根管充填 -------------------------8 实验十七牙体牙髓常见病临床病例展示----------------9
第一部分龋病 第二部分牙发育异常 第三部分牙急性损伤 第四部分牙慢性损伤 第五部分牙髓病 第六部分根尖周病 第一部分龋病 病因 分类 治疗 龋病是在以细菌为主的多种因素作用下，牙齿硬组织发生的慢性、进行性破坏 的一种疾病。致龋的多种因素，主要包括细菌和牙菌斑、食物以及牙齿所处的环境 等。牙菌斑中的致龋细菌是龋的主要病原菌。 龋病时，牙齿硬组织的病理改变涉及牙釉质、牙本质和牙骨质，基本变化是无机物脱矿和有机物分解。 病因——牙菌斑 牙菌斑的形成最初阶段是获得性膜的形成。通过获得性膜使大量细菌黏附于牙面；首先是球菌，以后是杆菌：丝状菌等。从获得性膜形成到一定量的细菌黏附和聚集在牙面，经过2天牙菌斑初步成形。此时菌斑质地松散，其中以链球菌为主。一般5-7天菌斑成熟，细菌数量、种类都趋稳定。 致龋细菌 1.变形链球菌 是口腔天然菌群中占比例最大的链球菌属中的一种。该菌与人类龋病密切相关 。变形链球菌有强的致龋性主要取决于其产酸性和耐酸性。在菌斑中生存的变形链 球菌可使局部pH下降至5.5以下。变形链球菌耐酸性强，在pH4.5时仍能继续生活并 产酸。从而造成局部硬组织脱矿，龋病病变过程开始。 变形链球菌能以蔗糖为底物合成胞外葡聚糖、果聚糖及胞内多糖。葡聚糖介导 细菌的黏附，促进菌斑的形成，是变链球菌重要的致龋毒力因子。 变形链球菌不仅是冠部龋病的主要致病菌，也是根部龋的主要致病菌。 2.乳杆菌属 乳杆菌是口腔的正常菌群，为革兰阳性兼性厌氧或专性厌氧杆菌。 乳杆菌对人类的致龋作用较弱，且更多涉及牙本质龋，在牙本质龋损、根面龋 损中有较多的乳杆菌存在。乳杆菌可能不是龋病发生的初始致病菌，但参与龋病的 发展。乳杆菌数量增加不是导致龋病开始的原因，而是龋病进展的结果。
牙体牙髓病学大纲.txt11生命是盛开的花朵，它绽放得美丽，舒展，绚丽多资；生命是精美的小诗，清新流畅，意蕴悠长；生命是优美的乐曲，音律和谐，宛转悠扬；生命是流淌的江河，奔流不息，滚滚向前牙体牙髓病学绪论 了解：牙体牙髓病学的主要内容、特点及发展简史。 第一篇龋病 第一章概述 第一节龋病的概念 掌握：龋病的定义；龋病的特征。 了解：龋病的直接危害和间接危害；龋病的历史，龋病学的研究内容。 第二节龋病流行病学 掌握：龋病的好发部位。 熟悉：龋病流行病学的评价方法。 了解：目前龋病的流行情况，龋病的流行趋势。 本章思考题： 1、龋病的概念、临床特征？ 2、龋病的好发部位？ 第二章龋病病因及发病过程 第一节牙菌斑 掌握：牙菌斑的三层结构特点；获得性膜的概念及其功能，微生物致龋的证据，三大主要的致龋微生物菌属；牙菌斑与龋病的关系。 了解：不同牙面菌斑的组成，牙菌斑的形成和发育，细菌的附着和聚积，菌斑微生物学，牙菌斑的物质代谢，糖的分解代谢和合成代谢。 第二节饮食因素 掌握：蔗糖与龋病的关系及其机制，氟的抗龋机理。
了解：蔗糖和其他碳水化合物，了解蛋白质、脂肪和其他物质与龋病的关系。 第三节宿主 掌握：牙对龋病敏感性的差异及其原因，唾液与龋病的关系。 了解：唾液的基本组成，唾液的几种主要蛋白质的功能，龋病与免疫的关系。 第四节影响龋病发生发展的其他因素 了解：龋病与年龄、种族、性别和遗传的关系。 第五节病因学说 掌握：龋病病因的四联因素理论。 熟悉：内源性理论、外源性学说、蛋白溶解学说、蛋白溶解－鳌合学说，Miller化学细菌学说（先进性与局限性）。 本章思考题： 1、牙菌班的形成过程？ 2、影响龋病发生和发展的其他因素？ 3、龋病病因四联因素理论？ 第三章龋病临床特征和诊断 第一节龋病的临床病理过程 熟悉：釉质龋、牙本质龋、牙骨质龋的临床病理学特征。 了解：脱矿和再矿化。 第二节龋病的临床表现及分类 掌握：龋病的好发部位及其规律，好发牙，好发牙面，牙面好发部位，常用的临床检查方法，浅、中、深龋的临床表现和诊断、鉴别诊断。 熟悉：龋病的临床分类，龋病的检查方法，早期龋的检查方法。 本章思考题：
实验实习指导 前言 口腔临床医学是实践性极强的一门学科，实验室课程设置是口腔临床医学教育的重 要环节。结合我院办学定位和实验条件，建设了 “口腔形态学与机能学实验室”、“口腔技能实验室”、“口腔仿真人头模实验室”三个实验室，并将各分支学科的相应内容以实验室为单位进行设置，以期达到实 验室的高效率利用和管理，同时培养学生以口腔为单位，综合利用各分支学科知识 的思维模式。本实习指导为口腔仿真人头模实习指导，内容涵盖本院开设的牙体牙 髓病学、牙周病学、口腔修复学和口腔颌面外科学实验项目中需要在仿真人头模上 完成的实习内容。 口腔仿真人头模实验室守则 1、实验前必须认真预习实验讲义或实验指导书，掌握实验的原理、方法、 步骤；了解有关仪器的性能、配置；熟悉其操作规程及安全注意事项。综合开放性 实验项目，必须在实验教师的指导下拟定出正确的实验方案。 2、不迟到，不早退，不无故缺席，有事必须向指导老师请假。 3、尊重实验室老师，服从相关工作人员的安排和指导。必须在教师指导下，严格 按操作规程进行，如违反操作规程而发生事故当追究责任。 4、遵守课堂纪律，保持室内安静，严禁高声喧哗。专心实验，不许窜教室，不说 与实验无关的话，不做与实验无关的事。上课时应关闭手机、小灵通等通讯工具， 以免影响教学秩序。 5、节约用水、电。根据实验需要领取适当适量所需材料，避免浪费。 6、严格遵守基础实验教学中心安全管理条例和仪器设备操作规程,不准违规操作；保持基础实验教学中心整洁、规范、文明、有序的工作环境。爱护公共财务 ，公用器械由学生组长负责领取，于当天实验完成后立即清洁归还。个人器械发给 本人保管，期末清洁归还，如有损坏或遗失，按《重医大口腔系关于损坏、遗失实 验器材实行赔偿的暂行办法的通知》照价赔偿。 7、学生不得单独进入实验室。如遇学生因故补做实验，或在非实验教学时间情况 下要求进入实验室进行实验的，应由指导老师批准，通知实验室，安排教师到场指导。 8、保持实验室及楼道清洁。实验时，学生须穿白色工作服，衣帽整齐，书包不得 放在实验桌上，不得在实验室内吃东西，不随地吐痰和乱丢纸屑，严禁吸烟。 9、下课前15分钟清理归还公用物资，清洁桌面后学生方可离开实验室。组长安排 值日生完成实验室清洁，灯、椅摆放整齐，关好门窗水电。 10、所有学生必须遵守《实验室守则》，有关表现要作为实验评分的考查内容。 实 习 指 导
龋病 龋病：以细菌为主的多种因素影响下牙体硬组织发生慢性进行性破坏的一种疾病。 患病率：表示病程长的慢性病如龋病存在或流行的频率，具体指调查或检查时点，一定人群中的患病情况。 发病率：表示在某一特定观察时期内，可能发生某病如龋病的一定人群新发生龋病的频率。 DMF：decayed-missing-filled的缩写，即龋齿数、因龋失牙数、因龋补牙数的总和，称龋失补指数。 DMFT：反应患者口腔中罹患龋病的牙数，包括龋齿数、因龋失牙数、因龋补牙数的总和。 DMFS：代表受龋病累及的牙面数。 牙菌斑dental plaque：牙面菌斑的总称，软而粘的未矿化细菌性沉积物，牢固粘附牙面和修复体表面，由粘性基质和嵌入细菌组成。是细菌生长发育繁殖的微生态环境，代谢产物可造成活体牙周组织破坏。 获得性膜：是由唾液蛋白货糖蛋白吸附至牙面所形成的生物膜，由蛋白质、碳水化合物和脂肪组成，功能包括修复货保护釉质表面，为釉质提供有选择的渗透性，影响特异性口腔微生物对牙面的附着，作为菌斑微生物的底物和营养。 脱矿：在酸的作用下，牙中的矿物质发生溶解，钙和磷酸盐等无机离子由牙中出。 再矿化：使钙、磷和其他矿物离子沉积于正常货部分脱矿的釉质中或釉质表面的过程。 猛性龋rampant caries：急性龋的一种类型，其病程进展很快，多数牙在短期内同时患龋，常见于颌面及颈部接受放射治疗的患者，也称放射性龋。 静止龋arrested caries：由于病变环境发生变化，隐蔽部位变得开放，原有致病条件发生了变化，龋病不再继续进行，但损害仍保持原状，也是一种慢性龋。继发龋：龋病治疗后，由于充填物边缘或窝洞周围牙体组织破裂，形成菌斑滞留区，或修复材料与牙体组织不密合，留有小的缝隙，这些都可能称为致病条件，产生龋病，称为继发龋。 线性釉质龋：非典型龋病损害，主要发生于上颌前牙唇面的新生线。 隐匿性龋：牙釉质脱矿常从表面下层开始，有时可能在看似完整的牙釉质下方，具有隐匿性，临床易漏诊。
1．Resistance form 抗力形：是使修复体和余留牙结构构成足够抗力，在承受咬合力时，不折裂的形状。 2.Secondary caries 继发龋，龋病治疗后由于充填物边缘或窝洞周围的牙体组织破裂形成菌斑滞留区或修复材料与牙体组织不密合，留有小的缝隙，这些都可能成为致病条件产生龋病，称为继发龋。 3.Retrograde pulpitis 逆行性牙髓炎，袋内的细菌及毒素通过根尖孔或侧副根管逆行进入牙髓，引起根部牙髓的慢性炎症，也可由局限的慢性牙髓炎急性发作。 4．Dentine hypersensitivity 牙本质过敏症：又称过敏性牙本质，是牙在受到外界刺激，如温度（冷、热）、化学物质（酸、甜）以及机械作用（摩擦或咬硬物）等所引起的酸痛症状。5．Root canal therapy 根管治疗：是治疗牙髓病及根尖周病首选的方法，它是彻底清理根管内炎症和坏死物质、扩大成形根管，并对根管进行适当消毒、最后严密充填根管，以除去根管内感染性内容物对根尖周组织的不良刺激，防止根尖周病的发生或促进根尖周病的愈合。 1. Biological width 生物学宽度（1）：龈沟底与牙槽嵴顶之间的恒定距离（2），包括结合上皮和牙槽嵴顶上方的结缔组织（1），约2mm（1）。 2. 非附着性龈下菌斑 位于附着性龈下菌斑表面（1），直接与龈沟上皮或袋内上皮接触（1.5），是
牙周炎的“前沿地带”(1.5)，主要由Gn厌氧菌、螺旋体组成(1) 窝洞：采用牙体外科手术的方法去除龋坏组织，并按要求备成的洞型，窝洞具有一定的形状，能容纳和支持填充材料，达到恢复牙齿外形和功能的目的。 残髓炎：属于慢性牙髓炎，临床特点常表现为自发性钝痛、放散性痛、温度刺激痛。发生在经牙髓治疗后的患牙，由于残留了少量炎症根髓或者多根牙遗漏了未作处理的根管。 主尖锉：在根管预备中，选用合适根管粗细，既能深入牙本质牙骨质界又有摩擦感的锉叫初尖锉，根管预备一般预备到到比初尖锉大三个号，叫主尖锉。 牙本质过敏症：又称过敏性牙本质，是牙在受到外界刺激，如温度、化学、机械刺激所引起的酸痛症状。其特点是发作迅速、疼痛尖锐、时间短暂。牙本质过敏不是一种独立的疾病，而是各种牙体疾病所共有的症状，发病高峰在40岁左右。继发龋：龋病治疗后，由于充填物边缘或窝洞周围牙体组织破裂，形成菌斑滞留区，或修复材料与牙体组织不密和，留有小的缝隙或存在微渗漏，或原有的病变组织未去净就进行了充填，形成致病条件再发生的龋病。 Wedge-shaped defect：楔状缺损：牙齿唇、颊侧颈部硬组织发生缓慢磨耗所致的楔壮的缺损。 Smear layer：污染层：切削牙体组织产生的热是有机质变性，变形的有机质和切削下来的牙本质粉末，牙本质小管溢出液、唾液和细菌等混合，在钻磨压力下吸附于洞壁而形成。 逆行性牙髓炎：牙周病时深牙周袋中的细菌通过根尖孔或侧支根管进入牙髓引发炎症，这种经亚洲途径发生的逆行感染称逆行性牙髓炎。 抗力形：抗力形是使充填体和余留的牙体组织获得足够的抗力，在承受咬合力时
牙体牙髓病学练习题及答案 来源：本站原创更新日期：2013年05月17日 1.意外穿髓，穿髓孔直径<0.5mm的恒牙最好选用的治疗方法 A 间接盖髓 B直接盖髓. C安抚治疗 D双层垫底E牙髓失活术 2.温度刺激出现迟缓且不严重的疼痛，表明可能是 A牙髓正常 B.牙髓坏死 C 可复性牙髓炎 D急性牙髓炎 E慢性牙髓炎 3.关于牙本质过敏症不正确的是 A 是一种临床常见症状 B 龋病的常见症状C磨耗的常见症状 D牙折的常见症状 E独立的常见疾病 4.急性牙髓炎最有效的应急处理是 A 局部麻醉 B 开髓引流 C服用止疼药 D消炎止疼药 E针灸镇痛 5.急性不可复性牙髓的疼痛性质中，最具诊断特点的是 A 自发性痛，阵发性加重B冷刺激引起疼痛C热刺激引起疼痛 D疼痛向颌面部放射E持续性胀痛 6.慢性闭锁性牙髓炎的临床表现为，除外 A不定时的自发痛 B热测引起迟缓性疼痛 C 洞内探及穿髓孔 D可有自发性疼痛史 E 叩诊多有不适感 7.意外穿髓临床上常用的盖髓剂是 A氢氧化钙 B抗生素+激素 C玻璃离子黏固粉 D聚羧酸锌黏固剂 E氧化锌丁香油糊剂 8.随着年龄的增大，后牙咬牙合面有磨耗，根尖部牙骨质沉积使牙根增长，若做根管治疗其根管工作长度 A 变长. B 变短 C 没变化 D 因人而异. E 以上都不对 9.年轻恒牙活髓切断术的主要目的为 A保护牙髓活力，牙根继续发育B维持牙列完整行使功能C不刺激根尖周组织 D牙髓活力正常有利于颌骨及颅面的发育E减少患者就诊次数 10.牙髓温度测验的注意事项如下，除外 A先测对侧同名牙 B 隔离唾液C冷测可用小冰棒 D热测可用热牙胶E置于牙齿咬牙合面上
一、名词解释 1继发龋：龋病治疗后，由于充填物边缘或窝洞周围牙体组织破裂，形成菌斑滞留区，或修复材料与牙体组织不密合，留有小的缝隙，这些都可能成为致病条件，产生龋病，成继发龋。 2根管治疗术：是治疗牙髓病及根尖周病首选的方法，它是彻底清理根管内炎症牙髓和坏死物质、扩大成形根管，并对根管进行适当消毒、最后严密充填根管，以去除根管内感染性内容物对根尖周组织的不良刺激，防止根尖周病的发生或促进根尖病变愈合。 3.残髓炎：属于慢性牙髓炎，临床特点常表现为自发性钝痛、放散性痛、温度刺激痛。发生在经牙髓治疗后的患牙，由于残留了少量炎症根髓或多根牙遗漏了未作处理的根管。 5．retrograde pulpitis 逆行性牙髓炎：逆行性牙髓炎的感染来源于患牙牙周病所致的深牙周袋。袋内的细菌及毒素通过根尖孔或侧、副根管逆行进入牙髓，引起根部牙髓的慢性炎症，也可由局限的慢性牙髓炎急性发作。此型牙髓炎的感染走向与通常由冠部牙髓开始，逐渐向根部牙髓进展的牙髓炎方向相反，故名为逆行性牙髓炎。 4.窝沟封闭：是窝沟龋的有效预防方法。封闭剂作为一屏障，使窝沟与口腔环境隔绝，阻止细菌、食物残渣及其酸性产物等致龋因子进入窝沟。含氟封闭剂有屏障和持续释放氟，促进再矿化的双重作用。 5.牙本质过敏症：又称过敏性牙本质，是牙在受到外界刺激，如温度、化学物质以及机械作用等所引起的酸痛症状。其特点为发作迅速、疼痛尖锐、时间短暂。牙本质过敏不是一种独立的疾病，而是各种牙体疾病共有的症状，发病的高峰年龄在40岁左右。 6根尖诱导成形术：牙根尚未发育完成期间，牙髓已经感染、坏死、分解或已有根尖周病变，则牙根停止发育，采取促使根尖的形成或封闭的治疗方法。 7再矿化治疗：用人工的方法使已经脱矿、变软的釉质发生再矿化，恢复硬度，使早期釉质龋终止或消除的方法。 8牙髓切断术：是指切除炎症牙髓组织，以盖髓剂覆盖于牙髓断面，保留正常牙髓组织的治疗方法。 9 逐步后退法：选用能深入根管达牙本质牙骨质界的初尖锉，确定工作长度，由初尖锉逐步扩大到主尖锉（比初尖锉大三号），由预备根 管尖段，到预备根管中段及冠段，最后通畅整个根管的预备方法称逐步后退法。适用于直根管和轻中度弯曲根管。 10鸠尾固位：固位形的外形似斑鸠的尾部，由鸠尾峡和膨大的尾部组成，借助于峡部的扣锁作用防治充填体从洞底呈水平方向脱位，一般鸠尾峡后牙为颊舌径的1/4—1/3，前牙为邻面洞舌方宽度的1/3—1/2。 11 获得性膜acquired pellicle：唾液中的糖蛋白以及其他成分黏附在牙齿表面形成的一层均质无细胞的生物膜。 磨牙症：睡眠时有习惯性磨牙或白昼也有无意识磨牙习惯者。 楔状缺损wedge-shaped defect：是牙齿唇颊侧颈部硬组织发生缓慢消耗所致的缺损，常呈楔形。 釉质发育不全enamel hypoplasia:在牙发育期间,由于全身疾患,营养障碍或严重的乳牙根尖周感染导致的釉质结构异常.分釉质发育不全和釉质矿化不全两种类型. 二、简答题 获得性膜的作用： 1)、修复或保护釉质表面2)、为釉质提供有选择的渗透性 3)、影响特异性口腔微生物对牙面的附着4)、作为菌斑微生物的底物和营养。 简述龋病的诊断方法 ①视诊：观察牙齿的色泽改变②探诊：探察有无缺损、龋洞，受损组织质地软硬程度③温度诊检查 ④X线照相检查：咬翼片和根尖片，以确定不易探察到的龋损，如邻面龋和隐匿龋 充填后疼痛的原因及处理原则？（5分） 1、牙髓性疼痛 ①激发痛冷热痛：钻磨过程产热或酸蚀剂刺激致牙髓充血的表现。咬合痛：可能与过高充填、金属电流作用有关。 ②自发痛原因同上或诊断有误。 处理牙髓充血者，应去除充填体，进行安抚治疗，待症状消失后再行充填；由电流作用引起者，去除银汞合金充填体，更换非金属材料充填；如对颌牙修复体不良，则更换对颌牙修复体。患牙出现自发痛，应进行牙髓治疗，但治疗前应排除同侧有无其他牙髓炎的患牙。 2、牙周性疼痛 ①咀嚼痛：原因：充填物过高、粘结修复时酸蚀液刺激牙颈部。处理：磨除高点，颈部用氟化钠糊剂脱敏，用塞治剂保护。 ②持续性自发钝痛：原因：充填物悬突压迫牙间乳头，邻面接触区恢复的凸度不理想。处理：去除悬突、修整邻面或重新充填。 充填物折裂、松脱 1.原因（1）窝洞预备：没有足够的抗力形固位形， （2）充填材料调制不当：充填修复材料调制各组分的比例不当，材料被污染、调制时间过长 （3）填充方法不当：未严格隔湿，充填压力不够 （4）过早承担合力：材料未固化完全，过早受力，易折断。 2.处理：去除充填物修整洞形，重新按照正规操作完成洞的修复。 牙隐裂的治疗方法： 1调牙合,排除牙合干扰,减低牙尖斜度以减小劈裂力量 2 均衡全口牙合力负担,治疗和(或)拔除全口其他患牙,修复缺失牙 3 隐裂牙的处理：隐裂仅达釉牙本质界,着色浅,无继发龋者,酸蚀,釉质粘接剂光固化处理. 有继发龋或裂纹着色深,已达牙本质浅层,中层者,沿裂纹备洞,氢氧化钙糊剂盖髓,氧化锌丁香油粘固剂暂封,2-4周后无症状则换光固化复合树脂.已有牙髓病变者,牙髓治疗,调牙合加冠修复.
《牙体牙髓病学》教学大纲 课程编码：08430010 课程名称：牙体牙髓病学 学分：4 总学时：60学时 理论学时：30学时 实验学时：30学时 先修课程要求：口腔解剖生理学、口腔组织病理学、口腔生物学、口腔颌面医学影像学 适应专业：口腔医学 教材： 《牙体牙髓病学》，樊明文主编，第三版，人民卫生出版社 一、课程在培养方案中的地位、目的和任务 牙体牙髓病学是研究牙体硬组织疾病发病机制、病理变化、病理生理、临床表现、治疗及转归的一门学科。 牙体牙髓病学应使学生掌握牙体硬组织常见病、多发病的病因、发病机制、临床表现、诊断、防治的理论知识和技能，把学过的医学基础、医学理论、口腔医学基础和口腔医学的知识运用到牙体牙髓病学当中。为毕业后独立从事口腔医学临床工作和继续提高奠定基础，并且培养良好的工作和服务态度。 二、课程基本要求 1.基本理论和基本知识： 基础理论和基本知识：掌握龋病、牙体硬组织常见非龋疾病、牙髓病、根尖周病的病因、发病机制、临床病理、临床表现、诊断、鉴别诊断、预后、治疗和预防方面的基本理论和基本知识。 2.基本技能： (1)结合临床诊断和治疗，在老师指导下学生运用所学知识，通过自已动手，完成规定的各项诊治工作，提高独立诊治能力和初步的临床科研能力。基本了解诊室管理和各类工作人员的合作关系。 (2)熟悉常用的牙体牙髓病学英文单词及阅读有关英文参考资料。可能条件下将部分或全部使用英语原版教材。
四、考核 考核方式：理论考试笔试，实验课采用考核及评估方式评定成绩。 成绩构成：理论考试70%，实验和平时成绩30%。 五、课程基本内容 绪论 [目的要求] 了解牙体牙髓病学的定义、内容、任务和意义。 [讲课时数] 2学时 [教学内容] 1.牙体牙髓病学的概念。 2.牙体牙髓病学发展简史。 [教学方法] 讲授法 [教学手段] 多媒体教学 第一章龋病的概念与流行病学 [目的要求] 1.掌握龋病的定义和特征和龋病的好发部位。 2.熟悉龋病的历史、龋病学的研究内容、现代人龋病流行情况、龋病流行趋势；
牙体牙髓病学 A1 型题 1、导致龋病发生的因素为 A、细菌因素 B、宿主因素 C、食物因素 D、时间因素 E、四联因素 2、牙骨质龋属于 A、慢性龋 B、浅龋 C、中龋 D、深龋 E、继发龋 3、深龋患牙的临床表现 A、仅有食酸甜食物不痛 B、食物嵌入洞内痛 C、偶在夜间陷痛 D、温度测验一过性敏感 E、牙髓电活力测验迟钝 4、检查邻面龋常用的最有效的方法是 A、视诊 B、叩诊 C、探诊 D、透照 E、咬合翼片 5、窝洞预备的原则不包括 A、去净腐质 B、保护牙髓 C、点线角锐利 D、制备固位形 E、制备抗力形 6、用玻璃离子水门汀充填的洞形不要求 A、洞有一定深度 B、洞缘可留无基釉 C、洞缘需做小斜面 D、可不要求固位形 E、洞底可呈圆弧形 7、复合树脂与牙本质表面的粘接方式是 A、固位洞形 B、化学性粘接 C、粘接齐粘合 D、机械性锁合粘接 E、机械性与化学性粘接 8、急性龋临床表现之一是 A、中老年人多见 B、龋坏组织色深 C、龋腐质地湿软 D、早期出现酸痛症状 E、多伴有釉质发育异常 9、龋齿缺损的治疗方法 A、自行修复 B、药物治疗 C、充填治疗 D、离子导入 E、再矿化疗法 10、口腔扪诊不能了解病变的 A、位置、大小和轮廓 B、性质、组成和结构 C、波动、搏动和压动 D、表面特征、温度和硬度 E、移动度及其与邻近组织的关系 11、对釉质发育不全的处理如下，除外： A、口服钙片 B、贴面修复 C、充填缺损 D、桩冠修复 E、全冠修复 12人体氟摄入量高的主要来源是 A、粮食中氟含量高 B、素菜中氟含量高 C、饮水中氟含量高 D、燃料中氟含量高 E、空气中氟含量高 13、畸形中央尖的临床表现不包括 A、位于前磨牙舌尖三角嵴上 B、尖呈圆锥形或钝圆状突起 C、其基底直径约为2mm D、X线片见尖内纤细髓角突入 E、中央尖折断可致牙髓感染 14牙外伤本质暴露时，对其进行修复的时间至少应在 A、即刻 B、2周后 C、4周后 D、6-8周后 E、3个月后 15、不适合用于充填前牙楔状缺损的材料是 A、复合体 B、银汞合金 C、流动树脂 D、玻璃离子粘固粉 E、光固化复合树脂
《牙体牙髓病学》课程教学大纲 一、课程性质和教学目标 牙体牙髓病学是口腔医学的重要骨干学科之一，它是研究牙体硬组织和牙髓组织疾病发病机制、病理变化、病理生理、临床表现、治疗及转归的一门学科。本课程通过对牙体牙髓疾病基本和扩展性教学内容的讲授，结合相应的教学实践，加深对于牙体牙髓病学基本理论和临床防治的基本知识和技能的理解和掌握，为今后从事临床工作以及毕业后继续教育奠定坚实的基础。 二、教学基本要求 在本课程中，教师应具备严肃的态度、严格的作风，重视讲授理论与教学实践的相结合，利用多媒体、网络等各种教学手段，通过教学实践与课堂讨论使学生对基本理论的认识更深入，并可结合科研适当介绍本学科国内外的发展动态与学术前沿。体现学生的学习主体地位，教师通过启发、提问、引导等方法，以充分发挥学生的积极性和学习潜能。培养学生科学的临床思维方法-分析问题和解决问题的能力，树立高尚的职业道德。 牙体牙髓病教学应以牙体硬组织病、牙髓病、根尖周病为重点。通过系统学习，应达到以下基本要求： 1、掌握牙体硬组织病的病因、诊断和治疗原则； 2、掌握牙髓病、尖周病的病因、诊断和治疗原则； 3、了解老年牙病的发病特点和治疗原则； 4、掌握口腔检查方法、病历书写； 5、掌握牙体硬组织病、牙髓病、尖周病的常规治疗技术； 6、了解牙体病、牙髓病治疗常用设备、器械的使用和保养技术。 三、教学内容及要求 第一篇龋病 【绪论】 掌握：龋病的定义、特征和好发部位。 熟悉：龋病的评价方法（患病率、发病率和龋均数）。 了解：龋病的历史，龋病学的研究内容龋病的研究内容，龋病的发病情况和流行趋势。【病因和发病过程】 （1）牙菌斑 掌握：牙菌斑的三层结构特点，获得性膜的概念及其功能，微生物致龋的证据，三大主要的致龋微生物菌属，致龋性牙菌斑在龋病发生过程中的作用。 了解：牙菌斑的结构、牙菌斑的形成和发育及牙菌斑的物质代谢，细菌的附着和聚积，菌斑微生物学。
实验实习指导 前言 口腔临床医学是实践性极强的一门学科，实验室课程设置是口腔临床医学教育的重要环节。结合我院办学定位和实验条件，建设了“口腔形态学与机能学实验室”、“口腔技能实验室”、“口腔仿真人头模实验室”三个实验室，并将各分支学科的相应内容以实验室为单位进行设置，以期达到实验室的高效率利用和管理，同时培养学生以口腔为单位，综合利用各分支学科知识的思维模式。本实习指导为口腔仿真人头模实习指导，内容涵盖本院开设的牙体牙髓病学、牙周病学、口腔修复学和口腔颌面外科学实验项目中需要在仿真人头模上完成的实习内容。 口腔仿真人头模实验室守则 1、实验前必须认真预习实验讲义或实验指导书，掌握实验的原理、方法、步骤；了解有关仪器的性能、配置；熟悉其操作规程及安全注意事项。综合开放性实验项目，必须在实验教师的指导下拟定出正确的实验方案。 2、不迟到，不早退，不无故缺席，有事必须向指导老师请假。 3、尊重实验室老师，服从相关工作人员的安排和指导。必须在教师指导下，严格按操作规程进行，如违反操作规程而发生事故当追究责任。 4、遵守课堂纪律，保持室内安静，严禁高声喧哗。专心实验，不许窜教室，不说与实验无关的话，不做与实验无关的事。上课时应关闭手机、小灵通等通讯工具，以免影响教学秩序。 5、节约用水、电。根据实验需要领取适当适量所需材料，避免浪费。 6、严格遵守基础实验教学中心安全管理条例和仪器设备操作规程,不准违规操作；保持基础实验教学中心整洁、规范、文明、有序的工作环境。爱护公共财务，公用器械由学生组长负责领取，于当天实验完成后立即清洁归还。个人器械发给本人保管，期末清洁归还，如有损坏或遗失，按《重医大口腔系关于损坏、遗失实验器材实行赔偿的暂行办法的通知》照价赔偿。 7、学生不得单独进入实验室。如遇学生因故补做实验，或在非实验教学时间情况下要求进入实验室进行实验的，应由指导老师批准，通知实验室，安排教师到场指导。 8、保持实验室及楼道清洁。实验时，学生须穿白色工作服，衣帽整齐，书包不得放在实验桌上，不得在实验室内吃东西，不随地吐痰和乱丢纸屑，严禁吸烟。 9、下课前15分钟清理归还公用物资，清洁桌面后学生方可离开实验室。组长安排值日生完成实验室清洁，灯、椅摆放整齐，关好门窗水电。 10、所有学生必须遵守《实验室守则》，有关表现要作为实验评分的考查内容。实习指导 实习一仿真人头模的使用 [目的和要求]
牙体牙髓病学试题(答案) 1．影响龋病发生的因素有： A 细菌 B 易感牙面 C 食物 D 一定的时间 E 以上因素都有 2．浅龋的最常使用的常规诊断方法是() A X线片检查B探诊C显微放射摄影法 D氩离子激光照射E冷热诊 3. 隐裂发生最多的牙齿是() A 前磨牙B第一磨牙C上颌第一磨牙 D上颌第二磨牙E下颌第二磨牙 4．X线检查一般不使用于() A He面龋B深龋C牙折 D慢性根尖周炎E牙髓疼痛 5．最适宜作直接盖髓剂的药物是() A EOE B氢氧化钙糊剂C 抗菌素糊剂 D抗菌素加激素糊剂E 1-2%聚甲醛 6．额外牙最多发生的部位是() A 下颌两中切牙之间B上颌两中切牙中间 C上颌两双尖牙之间D 上颌第二磨牙远中侧 E下颌第三磨牙远中侧 7．急性牙髓炎应急镇痛治疗的最好方法是（） A药物消炎，镇痛 B 局部麻醉下开髓引流，辅以药物镇痛 C直接或间接盖髓D拔除牙髓E拔除牙齿 8 .牙髓坏死后牙齿变色的原因（） A失去血液供应 B血红蛋白分解产物进入牙本质小管 C脓液进入牙本质小管 D细菌分解产物进入牙本质小管
E胆固醇结晶进入牙本质小管 9 .诊断牙本质过敏症的主要方法为（） A问诊B探诊C摄X线片D 扣诊E望诊 10. 恒牙列中患龋的频率最高的是（） A下颌第一前磨牙B下颌第二前磨牙 C上颌第一前磨牙D上颌第二前磨牙 E以上都不是 11. 临床记录中，舌面为（） A Ｌa B L C M D D EO 12. 青少年畸形中央尖所致牙髓坏死首先用（） A根尖诱导成形术B牙髓塑化治疗 C拔除 D 根管治疗E根管外科 13. 对于牙本质过敏首选的治疗方法有（） A药物脱敏B 牙髓治疗C 牙周洁治 D 垫底充填E树脂充填 14 .目前认为菌斑中最主要的致龋菌是（） A乳酸杆菌B血链球菌C大肠杆菌 D葡萄球菌E变形链球菌 15 釉珠附着在（） A根尖牙骨质表面 B 髓腔内壁 C近颈部牙骨质表面D 根管内壁E牙冠表面 16. 畸形中央尖最好发于（） A下颌第一磨牙B下颌第二磨牙 C下颌第三磨牙D下颌第二前磨牙 E下颌第一前磨牙 17 制备倒凹是为了（） A 获得良好的抗力形 B 便于垫底 C 便于充填 D 获得良好的固位形 E 便于放置盖髓剂、 18. 浅表有隐裂.无明显症状，但牙髓活力正常者。其治疗应首选（）
第一单元龋病 一、A1 1、获得性膜是指 A.牙萌出时牙面上胚胎来源的有机物 B.牙面上积累的食物残渣沉积物 C.吸附至牙面的唾液蛋白或糖蛋白 D.均匀分布于牙面上的微生物层 E.在菌斑作用下由菌斑微生物所分泌的蛋白膜 【正确答案】：C 【答案解析】：获得性膜是唾液的糖蛋白及其他一些成分选择性黏附在牙表面形成的无细胞、均质状的生物膜。 2、用复合树脂充填时，垫底材料不能用 A.磷酸锌黏固粉 B.聚羧酸锌黏固粉 C.玻璃离子黏固粉 D.氧化锌丁香油黏固粉 E.氢氧化钙制剂 【正确答案】：D 【答案解析】：由于粘固粉中的丁香油酚对聚合物有阻聚作用，甚至对已经聚合者，也可有某种程度的解聚作用。因此，与自凝塑料、树脂类材料、聚羧酸锌粘固粉和玻璃离子粘固粉均不能直接接触。 【该题针对“牙体牙髓病学第一单元龋齿单元测试”知识点进行考核】 3、随着龋病的发生，牙菌斑内哪些细菌数量下降 A.变形链球菌 B.血链球菌 C.乳杆菌 D.放线菌 E.酵母菌 【正确答案】：B 【答案解析】：在龋病发病期间变形链球菌、放线菌、乳杆菌和酵母菌数量增加时，而血链球菌和韦永菌数量减少。 【该题针对“牙体牙髓病学第一单元龋齿单元测试”知识点进行考核】 4、根面龋中最常分离到的细菌是 A.乳杆菌 B.血链球菌 C.变形链球菌 放线菌D. E.牙龈卟啉单胞菌 【正确答案】：D
【答案解析】：在龈下菌群和人类根面龋的牙菌斑中最常分离到的微生物是放线菌。 【该题针对“牙体牙髓病学第一单元龋齿单元测试”知识点进行考核】 5、激光防龋的主要功能不包括 A.促使釉质形成抗酸性强的玻璃样物质 B.减少脱钙量 C.抑制变形链球菌的生长 D.通过解吸附作用使菌斑脱落 E.与氟化物结合，可促进牙本质小管钙化 【正确答案】：D 【答案解析】：激光防龋经激光照射后的釉质，可形成抗酸性强的玻璃样物质，减少牙脱钙。与氟化物应用相结合，或促使氟透过牙骨质、牙本质小管，促进钙化。经激光照射后的变形链球菌生长受到抑制。目前，激光防龋还处于实验室研究阶段，距实际应用还有一定的距离。 【该题针对“牙体牙髓病学第一单元龋齿单元测试”知识点进行考核】 6、含有氟并具有一定防龋作用的材料是 A.聚羧酸锌黏固粉 B.复合树脂 C.玻璃离子聚合黏固粉 D.磷酸锌黏固粉 E.氧化锌丁香油黏固粉 【正确答案】：C 【答案解析】：玻璃离子聚合粘固粉：是一种对牙髓刺激轻，对牙体硬组织有粘结性，但强度较银汞合金低的多用途材料。适用于Ⅲ类、Ⅴ类洞，用于乳牙充填，作窝洞封闭剂以预防龋病。一般不永久。 【该题针对“第一章单元测试”知识点进行考核】 7、冠部浅龋的龋坏程度仅限于 A.牙釉质内 B.牙骨质内 C.牙釉质或牙骨质内 D.牙本质内 E.牙骨质或牙本质内 【正确答案】：A 【答案解析】：浅龋位于牙冠部时，一般均为釉质龋，但若发生于牙颈部时，则是牙骨质龋。【该题针对“牙体牙髓病学第一单元龋齿单元测试”知识点进行考核】 8、代谢蔗糖能力最强的细菌是 A.轻链球菌 B.唾液链球菌 C.乳杆菌 D.变形链球菌 E.放线菌 【正确答案】：D
牙体牙髓病学试题(答案) 1．影响龋病发生的因素有： A 细菌 B 易感牙面 C 食物 D 一定的时间 E 以上因素都有 2．浅龋的最常使用的常规诊断方法是() A X线片检查B探诊C显微放射摄影法 D氩离子激光照射E冷热诊 3. 隐裂发生最多的牙齿是() A 前磨牙B第一磨牙C上颌第一磨牙 D上颌第二磨牙E下颌第二磨牙 4．X线检查一般不使用于() A He面龋B深龋C牙折 D慢性根尖周炎E牙髓疼痛 5．最适宜作直接盖髓剂的药物是() A EOE B氢氧化钙糊剂C 抗菌素糊剂 D抗菌素加激素糊剂E 1-2%聚甲醛 6．额外牙最多发生的部位是() A 下颌两中切牙之间B上颌两中切牙中间 C上颌两双尖牙之间D 上颌第二磨牙远中侧 E下颌第三磨牙远中侧 7．急性牙髓炎应急镇痛治疗的最好方法是（）
1 / 35 A药物消炎，镇痛 B 局部麻醉下开髓引流，辅以药物镇痛 C直接或间接盖髓D拔除牙髓E拔除牙齿 8 .牙髓坏死后牙齿变色的原因（） A失去血液供应 B血红蛋白分解产物进入牙本质小管 C脓液进入牙本质小管 D细菌分解产物进入牙本质小管 E胆固醇结晶进入牙本质小管 9 .诊断牙本质过敏症的主要方法为（） A问诊B探诊C摄X线片D 扣诊E望诊 10. 恒牙列中患龋的频率最高的是（） A下颌第一前磨牙B下颌第二前磨牙 C上颌第一前磨牙D上颌第二前磨牙 E以上都不是 11. 临床记录中，舌面为（） A Ｌa B L C M D D EO 12. 青少年畸形中央尖所致牙髓坏死首先用（）A根尖诱导成形术B牙髓塑化治疗 C拔除 D 根管治疗E根管外科
13. 对于牙本质过敏首选的治疗方法有（） 2 / 35 A药物脱敏B 牙髓治疗C 牙周洁治 D 垫底充填E树脂充填 14 .目前认为菌斑中最主要的致龋菌是（） A乳酸杆菌B血链球菌C大肠杆菌 D葡萄球菌E变形链球菌 15 釉珠附着在（） A根尖牙骨质表面 B 髓腔内壁 C近颈部牙骨质表面D 根管内壁E牙冠表面 16. 畸形中央尖最好发于（） A下颌第一磨牙B下颌第二磨牙 C下颌第三磨牙D下颌第二前磨牙 E下颌第一前磨牙 17 制备倒凹是为了（） A 获得良好的抗力形 B 便于垫底 C 便于充填 D 获得良好的固位形 E 便于放置盖髓剂、 18. 浅表有隐裂.无明显症状，但牙髓活力正常者。其治疗应首选（）备洞充填C B 全冠修复 A 开髓失活 E拔除患牙调颌治疗D
2020年口腔助理医师《牙体牙髓病学》试题及答案（卷一） 1、根管治疗过程中由于医源性原因使髓腔和牙齿外表面意外穿通，称为 A、器械分离 B、髓腔穿孔 C、根管穿孔 D、软组织化学损伤 E、牙根折裂 2、预防器械断离的关键是 A、准确判断X线片中的根管形态 B、充分的根管冲洗 C、牙髓一定要拔除干净 D、髓腔通路入口一定尽量扩大 E、掌握正确使用器械的方法 3、若器械分离时所有方法均不能去除根管内的器械，则最后可使用保留牙齿的方案是 A、拔除 B、根尖手术 C、根管冲洗 D、开放根管 E、全冠修复术 4、以下哪项是器械断离的常见原因
A、术前没有观察X线片 B、开髓时磨牙髓室底穿通 C、使用方法不当，给器械过度施力 D、根尖预备到根尖孔之外 E、器械过度预备导致根管侧穿 5、原本畅通的根管在预备过程中突然工作长度丧失，原有操作器械尖端丧失，即应考虑 A、器械断离 B、根管侧穿 C、髓底穿通 D、牙根折断 E、软组织化学损伤 6、以下药物中作为根管倒充填材料时渗透最小，根尖封闭性显著优于其他封闭剂的是 A、氢氧化钙 B、树脂类 C、氧化锌丁香油类 D、玻璃离子类 E、硅酮类 7、关于氢氧化钙类根管封闭剂的优点没有 A、具有强碱性 B、超强的X线阻射性能
C、促进根尖周组织愈合 D、诱导硬组织形成 E、较好的抗菌效果 8、对于氧化锌丁香油类根管封闭剂的优点说法错误的是 A、具有一定的稠度 B、较好的封闭性能 C、无明显收缩性 D、对根尖周组织的刺激性较小 E、无X线阻射性 9、K型根管器械的横截面是 A、圆形 B、三角形 C、水滴形 D、椭圆形 E、不规则形 10、下列锉针手柄的颜色与25号根管锉针相对应的是 A、紫 B、红 C、白 D、蓝 E、黑 正确答案及答案解析