Pulp (2)

The Magnitude of Orthodontic Treatment
• An estimated 15,00,000 ( 1.5 million)
patients undergo orthodontic treatment
globally & is increasing.
• Therefore approximately 30 million teeth
are being moved about – some over very
short spans and some over considerable
spans.
www.indiandentalacademy.com

Are we doing it right ?
• The basic dictum is –
“Even if you do no good – do no harm”
• Iatrogenic damage incident to orthodontic
treatment is well recognised and written
about.
• Orthodontics as a specialty is over a 100
years old. The biologic sense is today more
dominant than the mechanical aspects that
bore sway half a century ago.www.indiandentalacademy.com

Historic Articles
• Marshall.J.A:A study of bone and tooth changes incident
to experimental tooth movement and its application to
orthodontic practice.
Int.J.orthod.19: 1-17, 1933
• Biologic Orthodontic Therapy and Reality
PROF. DR. ALBIN OPPENHEIM
Angle Orthodontist April, 1936
• Oppenheim A. Human tissue response to orthodontic
intervention of short and long duration.
AM J ORTHOD 1942; 28:263-301.www.indiandentalacademy.com

Periodic re-evaluation – Welcome !
• As technology and our understanding of the
physiology improve, it is mandatory that we
periodocally revise our precepts, theory and
practice.
• Seminars & workshops such as this offers
an unique oppurtunity – to reasses our
strengths & weaknesses.
• The topic of pulp is most appropriate.

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Pulpal response to Force
Orthodontic Orthopedic

67
Incident to Mechanotherapy
Etching
Bonding
Debonding
Clean-up of the enamel surface

Miscellaneous Factors
• Age
• Orthognathic surgery
• Trauma

Study Methods
• Histologic methods (Stenvik -70, Anstendig-72)
• Histomorphometry
• Pulp tissue respiration rate.
• Direct microscopic observation (Guevara – 80)
• Flourescent microsphere injection (Kvinnsland – 89)
• Laser Doppler flowmetry (Jones , Sano-2002)

Some facts to be remembered
Dental pulp is a specialized tissue, because of
where it is and how it functions.
Because pulpal tissue is located in a rigid dentinal
cover, its vitality depends on blood vessels
passing through the apical foramen.
Any alteration in pulpal blood flow or vascular tissue
pressure can endanger the health of the dental pulp.

Some facts to be remembered
Some authors have termed orthodontic tooth
movement a “controlled trauma” for the
dental tissues.
If this were the case, then it would be natural
after orthodontic tooth movement to
observe similar degeneration to what is seen
after traumatic injuries

Pulpal relation to other structures
There is also the root resorption effect of orthodontic
forces. After orthodontic forces are applied, some researchers
have stated that root resorption is seen more often in
pulpless teeth, whereas
Others state that intact teeth showed more root resorption.
The increase in the amount of root resorption in
intact teeth points to the importance of the close relationship
between dental pulp and the surrounding tissues.

Reaction to Intrusion (Stenvik & Mjor)
• Teeth were intruded with forces ranging from 35-
250.gms for 4 -35 days (with FA)
• Vacoulisation of the pulp increased proportionally
to the intrusive force
• Evidence of vascular stasis. More in teeth with
closed apical foramina. May act as nidus of
calcification.
• A reduction in the width of the predentin zone.

Reaction to Extrusion (Mostafa et al 1991)
• A comparison between the extruded and
nonextruded maxillary first premolars revealed
characteristic pulpal reactions resulting from the
orthodontic extrusion
• One of the earliest degenerative changes was the
presence of vacuoles in the pulp tissues as well as
in the odontoblastic layer
• Further, the odontoblastic vacuolization was more
pronounced coronally than apically.

Reaction to Extrusion (Mostafa et al 1991)
• Circulatory disturbances were manifested as
dilated and congested blood vessels The
odontoblastic degeneration was most probably due
to the compromised blood supply.
• The duration of these pathologic changes is
controversial. Oppenheim and Butcher and Taylor
obtained contradictory results, varying from
temporary reversible degeneration to permanent
irreversible degeneration and ultimate necrosis of
the dental pulp after orthodontic treatment.

• Fibrotic changes appeared 4 weeks after
activation . Stenvik et al were able to show
signs of healing and scar tissue formation in a
long-term intrusive study.
• It is known that the reparative properties of
the pulp are extensive.
• However, the limit of tolerance varies from
person to person. The ultimate fate of these
circulatory disturbances seems to be
resolution through reparative processes.

Normal pulp tissues in a control specimen. (Magnification, ´200.)
Pulpal reactions to extrusion - Mostafa, Iskander, and El-
Mangoury, AJO.1991

Coronal pulp of an extruded tooth at 1 week after activation. A and B, Note the marked
vacuolization and degeneration of the odontoblastic layer and congested blood vessels.
(Magnifications: A, ´100; B, ´200.) C, Note severe odontoblastic degeneration and pulp
vacuolization. Dilated and congested blood vessels are also seen. (Magnification, ´300.)www.indiandentalacademy.com

Coronal pulp of an extruded tooth at 4 weeks after activation. Note that the
pulp tissues show fibrosis (fibrous tissue reaction) and that the degree of
vacuolization and blood congestion has decreased. (Magnification, ´200.)

Orthodontic force application on the pulpal
tissue respiration rate
• This stasis of blood flow could depress respiration rate by a
combination of two mechanisms:
• (1) the actual decrease in available O2 present in the reduced blood
volume entering the tooth and (2) a phenomenon reported by
Oppenheim in which the alkalinity of the pulp tissue is neutralized by
the acid formed through decomposition of blood elements in the tissue
stroma.
• This change in pH could then alter the membrane permeability and the
involved enzyme systems' efficiency to utilize O2.

•This investigation demonstrated that the pulp tissue
respiration in seventeen subjects was depressed an average of
27 percent as a result of orthodontic force application of 6
ounces applied for 72 hrs
• A positive correlation between the age of the
participant and the amount of tissue respiratory
depression was also demonstrated.
• The greater occurrence of root resorption and pulpal pathosis
observed in the adult orthodontic patient may be related to this
greater depression in pulpal tissue respiration.
(The effect of orthodontic force application on the pulpal tissue respiration rate in the human
premolar - Hamersky AJO-DO Apr 1980 )www.indiandentalacademy.com

The effect of time on pulpal recovery
• The radiorespirometric method showed that the mean
respiration rates of experimental pulpal tissue compared
with control pulpal tissue remained depressed
approximately 33.2% after the 7-day rest period.
• One group returned to normal respiration rates and one
that did not within a 1-week rest period.
• Age and apical opening size correlated with the return of
the respiration rates to normal during the 1-week rest
period.
• Age was negatively correlated with respiration rate and
apical opening size correlated with the return of the
respiration rates to normal during the 1-week rest period.
(Response of human pulpal tissue after orthodontic force application -
Unsterseher, Nieberg, Weimer, and Dyer AJO-DO Sep 1987)www.indiandentalacademy.com

Effect of Age on Pulpal response
Pulpal response to orthodontic tooth movement –
Popp, Årtun, and Linge (AJO-DO ‘92)
Age group studied: 9-17 yrs 100 consecutive pts
• Concluded that routine orthodontic treatment
performed during adolescence causes minimal
damage to the pulp and periodontal ligament.
• The observed narrowing of the pulp canal may
be regarded as a normal aging process.

• The force magnitudes used under usual clinical
conditions do not exceed the physiologic limits of
healthy dental tissues.
• Accordingly, on the basis of this study, there is no
justification for classifying routine orthodontic
tooth movement in adolescents as pathologic.
discrepancies.
• Therefore the circulation changes demonstrated
histologically and the observed changes in pulpal
respiration incident to experimental tooth
movement may be of limited clinical significance.

Effect of forces on Pulpal Blood Flow (PBF)
• Laser Doppler flowmetry is a recent technique and can
measure repeatedly the PBF without damage.(Ramsay ’91,
McDonald.F ’94 , Buckley –’99)
• Sano et al (2002) studied the effects of continous intrusive
forces of 0.5 – 2.0N were applied for 6 days.
• PBP was significantly reduced during the period of force
application.
• Pulpal recovery indicates that upto 0.5N changes are
reversible. Also coincides with the recommendation of 40-
50.gms of force (Ricketts ‘79)

Pulpal response to Orthognathic Surgery
• Orthognathic surgery represents a potential risk of vascular
compromise to the disconnected segment.
• LeFort I osteotomy is associated with a particularly high
risk because the primary vascular supply to the buccal
alveolus, periodontium, and teeth is severed.
• If, in addition, the greater palatine arteries are severed,
experimental studies indicate a 90% drop in pulpal and
alveolar blood flow.
• No similar problem with BSSO

• The most frequently occurring sequela was pulp
canal obliteration. As many as 43% of the patients
treated with LeFort I osteotomy showed
radiographic signs of obliteration as opposed to
less than 6% in the nonoperated controls.
• As many as 21% of the patients treated with
LeFort I osteotomy showed pulp necrosis, as
opposed to 10% in the nonoperated group.
(Ellingsen & Artun:Pulpal response to orthognathic
surgery .AJO-DO.Apr.1993)

Pulpal Blood Flow Associated with
Orthognathic Surgery
• The Le Fort I osteotomy appears to result in an initial rise in blood
flow, as measured via the maxillary central incisor pulps, immediately
after surgery; this may constitute a form of hyperaemic inflammatory
response.
• Longitudinal series of readings, taken over a 6-month period on 15
patients, that the maxillary perfusion recorded at the central incisor
pulps may be permanently affected in many Le Fort I osteotomy
patients.
• For patients that already have prejudiced blood supply this could lead
to devitalization and discoloration of incisors.
(Buckley et al: An Evaluation of the Changes in Maxillary Pulpal Blood Flow Associated
with Orthognathic Surgery . J.Orthodontics, 1999 )

RPE produces orthopedic forces in the range of 7.54 – 15.8 kg
(Zimring & Isaacson 1965)
Vessel area and diameters were the parameters that
showed significant change during this study with dilatation of
vessels & was related to the duration of force application
There was slight increase of predentin width in the 3- month
group The observed vascular changes and the increase in
fibrous elements represent the increasing duration of
excessive force application or may occur as a result of
the beginning of tooth movement, with decreasing
orthopedic force levels.
Kayhan, Küçükkeles¸, and Demirel AJO_DO 473
Volume 117, Number 4

Pulpal reactions to orthodontic alignment
of palatally impacted canines
• Traction & alignment of canines increases the risk of
pulpal changes, with pulpal obliteration occurring in
more than 20% of the previously impacted canines.
15% of them tested non vital with electronic pulp
testing.
• However, the relationship between the magnitude of
vascular impairment and the onset of pulpal changes
remains undetermined.
• (Pulpal and periodontal reactions to orthodontic alignment of palatally impacted canines Heather
Woloshyn, Jon Årtun,... Angle Orthodontist 1994 No. 4, 257 – 264)

Temperature & the oral cavity
• The temperature range of ingested food in the oral
cavity may vary between 7º and 75º C and
temperature range at the tooth surface from 5º to
48º C.
Graf W. Von die thermische belastung der zahne
beim verzehr extrem heiber und kalter speisen.
Dtsch Zahnarztl Z 1960;15:30-4.

• Studies indicate, overall, that a temperature rise of 10°F
(approx. 6°C) can cause irreversible pulpal responses.
• Temperatures in excess of 20°F (approx. 11°C) may cause
necrosis of the pulp
• Lesions of the pulp tissue caused by thermal effects are
confined to that portion of the pulp underlying the inner ends
of cut dentinal tubules.

• If the insult to the pulp is great enough, burn lesions can
present as coagulation necrosis and often develop intra
pulpal abscesses which appears to occur quite early and
may remain indefinitely.
• Resolution of a large burn area can occur with the entire
area involved first filling in with granulation tissue. This
tissue then undergoes reorganization by stimulated
odontoblasts with resultant reparative dentin formation.
However, if healing is not successful, a large expanding
abscess will develop.
(J.A. von Fraunhofer, D.J. Allen. Angle Orthodontist, 1993 No. 4, 299 – 304 )www.indiandentalacademy.com

Thermal Debonding devices
• (1) devices that use an electrical heating
element, (Electro thermal debracketing –
ETD )
and
• (2) devices that use energy delivered by
lasers. (Laser debonding LD)

ETD
• ETD An alternative method to conventional
bracket removal that minimizes the potential for
ceramic bracket failure as well as trauma to the
enamel surface
• The brittle nature of ceramic brackets has resulted
in a higher incidence of bracket fracture during
conventional debonding, either with pliers or with
high speed rotary abrasion diamond burs.

Dentaurum
thermodebonding
unit inserted into
bracket slot.

Scheu-Dental ceramic
thermodebonding plier
with ceramic bracket
inserted. Through closing
the plier, the metal bars
above the bracket come
into contact and start the
induced current, which
heats the plier tips.

ETD
• Electrothermal debonding is the technique of removing
bonded brackets from enamel surfaces with a rechargeable
battery device that generates heat.
• The heating element is heated to approximately 450° F as
the unit is activated. The heat is transferred to the bracket
through a tip that is inserted into the bracket slot. When
heat is applied to the bracket, it deforms the adhesive-
bracket interface, and the bracket can then be gently
separated from the enamel surface.
• Thermal debonding has shown no evidence of overt
enamel fracture, and the failure site has shifted toward the
tooth-resin interfacewww.indiandentalacademy.com

ETD
• The drawback of using these devices is that there
is no quantitative control of the amount of thermal
energy delivered to the ceramic bracket, which in
turn may overheat the tooth during bracket
removal
• Heat conducted to the pulp through the dentin
would cause vasodilation, resulting in increased
blood flow to the pulp. If this blood inflow is
greater than the blood outflow, the situation
results in pulpal hyperemia and engorgement. This
situation is reversible, depending on the initial
status of the pulp and its ability to repair.

Pulpal effects of ETD
- A controversial area
• Takla & Shivapuja (1995) 24 hours after debonding
The effects seen at 24 hours after debonding were hyperemia,
engorgement, and the start of inflammation in some cases.
• 30 days after debonding
Teeth extracted 30 days after ETD showed varied responses. The
responses ranged from complete recovery in some cases to persistence
of inflammation and pulpal fibrosis. The presence of inflammation
could possibly be explained by inadequate healing time. Although the
internal pulpal temperature was not studied

Pulpal effects of ETD
• Kraut et al (’91) found no evidence of pulpal
necrosis or inflammation 2 weeks after ETD of
ceramic brackets.
• Jost Brinkman (’92) reported localised pulpal
damage on ETD of ceramic brackets when
more than one thermal cycle was used.
• Cummings et al have pointed out that
radiorespirometric methods and LDF methods
have shown depression of the pulpal ability to
recover and further thermal insults could
contribute to non-vitalitywww.indiandentalacademy.com

• Thermodebonding of metal brackets worked
properly and without any obvious pulp damage.
• There were problems related to the
thermodebonding of ceramic brackets:
– (1) if more than one heating cycle was necessary,
several teeth showed localized damage of the pulp with
slight infiltration of inflammatory cells,
– (2) bracket fractures occurred frequently, and enamel
damage could be shown, and
– (3) often with Transbond (Unitek/3M, Monrovia,
Calif.) as the adhesive, more than one heating cycle
was necessary for bracket removal, and thus patients
complained about pain.
(Thermodebonding of metal and ceramic brackets - Jost-
Brinkmann, Stein, Miethke, and Nakata- AJO-DO 1992
Nov 410 - 417):

Pulp tissue of tooth 24 hours after three heating cycles with
thermodebonding appliance showing extravascular erythrocytes.
The respective ceramic bracket was bonded with a high-melting
adhesive, Transbond. (Original magnification ´260.)

Mechanics of ETD
• To allow bracket debonding with ETD, the
composite adhesive softens above a critical
temperature of 300° to 392° F.
• Dentin, being a poor conductor of heat,
usually protects the pulp from this high
temperature

Zach and Cohen’s Work
• By using rhesus Macaca monkeys, performed an
experiment on the effects of externally applied heat on the
dental pulp. The increase in intrapulpal temperature ranged
from 4° to 30° F.
• Results from histologic sections of pulpal tissues showed
that an intrapulpal temperature increase of 4° F (1.8° C)
did not cause any pulpal damage in their Macaca sample.
However, an increase in pulpal temperature of 10° F (5.5°
C) caused pulpal necrosis in 15% of the teeth. They have
also found that for an increase in intrapulpal temperature
of 20° F (11.1° C), 60% of the teeth showed abscess
formation. A temperature elevation of 30° F (16.6° C),
pulpal necrosis occurred in all teeth

Zach and Cohen’s Work
• The distal end of the odontoblast processes toward
the dentinoenamel junction will experience a
higher temperature change than the cell nucleus in
the pulpal wall. However, the overall cellular
response of the odontoblast should be considered.
There may be transient unfavorable cellular
responses due to the high temperature exposure of
the odontoblast processes, but the overall pulpal
response seems to be favorable

Current Status of ETD
• Most studies had used thermocouples for evaluating
pulpal temperature rise.
• Thermal image analysis – gives accuracy of 0.1o
C
• Cummings et al (’99) with thermography reported that
for a 3 sec heating cycle the pulpal wall temperature
was 16.8o
C and when retained for 6 sec(when brackets
are not successfully debonded) the temperature rise
was 45.6o
C
• Hence the actual temp at the pulpal side is much more
than hitherto presumed. Thermocouples need a
conducting medium – enamel & dentin and hence the
error in assesment.

• A cooling cycle is indicated for applications of
ETd beyond 3 secs.
• Air & water is not indicated as coolants because of
the increased pain & sensitivity.
• Ceramic brackets – mono & polycrystalline differ
in their heat transfer properties, so also the
bonding resin – filled & highly filled also play a
significant role in the heat transfer.
• Length of time of heat contact with pulp is also a
critical factor. Teeth with thinner pulpal walls –
incisors vs molars will transmit more heat.

• Orthodontic applications of dental lasers, include
enamel etching and bracket/attachment
debonding especially ceramic brackets.
• A variety of lasers have been tried.
• CO2 –Normal & Super Pulse (allows cooling
between cycles)
• Nd-YAG Lasers

• Commercial Nd:YAG laser
• At power outputs of 1–3W temp rise exceed 6°C.
Consistent direct bonding of orthodontic
attachments required the dental enamel irradiation
at an output power 2W
(J.A. von Fraunhofer, D.J. Allen. Angle Orthodontist,
1993 No. 4, 299 – 304 )

• Nd: YAG laser Temperature changes are a
function of lasing powers and times. Lasing
times of less than 5 seconds would not increase
pulpal temperature more than 1°C.
(Laser-aided degradation of composite resin Brian W.
Thomas, Charles R. Hook, Robert A. Draughn - Angle
Orthodontist 1996 No. 4, 281 - 286 )

• CO2 Laser- Able to debond in 2.9 + 0.9 secs
at 2 watts setting with pulpal rise of only
1.4o
C and at 3 watts produced only 2.1o
C.
These are well within physiologic limits
• Resin type also mattered – 4 META resins
ere more easily debonded than BIS_GMA
resins.

Reduced torque for Laser Debonding
• Tocchio et al debonded monocrystalline and
polycrystallinebrackets that had been bonded with
Dynabond(3M Unitek).
• By using an externally applied stress of either 0 or 0.8
MPa, the brackets were debonded by irradiating their
labial surfaces at light power densities between 3 and 33
W/cm2 and with laser light at wavelengths of 248, 308,
and 1060 nanometers(nm).
• Light and scanning electron microscopy showed no enamel
or bracket damage in any sample in this study.

MECHANISM OF LASER DEBONDING
• Laser energy can degrade the adhesive resin by 3
methods:
thermal softening, thermal ablation, and photoablation.
• Thermal softening occurs when the laser heats the
bonding agent until it softens. Clinically, this results in
the bracket’s succumbing to gravity and sliding off the
tooth surface.
• Thermal ablation occurs when heating is fast enough to
raise the temperature of the resin into its vaporization
range before debonding by thermal softening occurs.www.indiandentalacademy.com

MECHANISM OF LASER DEBONDING
• Photoablation also results in the bracket’s being blown
off the tooth surface. It occurs when very high-energy
laser light interacts with the adhesive material and the
energy level of the bonds between the adhesive resin
atoms rapidly rises above their dissociation energy
levels, resulting in decomposition of the material.
• Thermal softening is a relatively slow process. This
means that it can lead to a large rise in both tooth and
bracket temperature.
• Thermal ablation and photoablation proceed rapidly,
and very little heat diffusion occurs; therefore, the
tooth and the bracket stay near physiologicwww.indiandentalacademy.com

General Recommendations:
1.The time spent to debond ceramic brackets is less when using
lasers.
2. Debonding forces are significantly reduced with lasers.
3. The risk of enamel damage and bracket fracture is significantly
reduced with lasers.
4. The CO2 super-pulse laser is superior to normal pulseCO2 and
YAG lasers.
5. MMA resins are recommended over Bis-GMA resins.
6. The use of monocrystalline brackets is suggested over
polycrystalline brackets.

General Recommendations:
7. Ceramic brackets should be irradiated and
debonded one by one immediately after laser
exposure.
8. The risk of pulpal damage is significantly reduced
if the following are used:
a. Super-pulse CO2 laser at 2 W for less than 4
seconds.
b. CO2 laser (10.6 m) for 3 seconds at 3 W.
c. CO2 laser (normal pulse) at 18 W for 2 seconds.

• CO2 Laser when used for etching at 3 watts
produced a pulpal increase of 3.5o
C.
However the clinical bond strengths were
adequate but much less than chemical
bonding.
• Laser etching is still in its infancy –
basically due to its high cost.

• The mechanism of pulpal mediation of pain is of
interest to all clinicians because of its clinical
relevance.
• Pain is universally reported by all patients at the
commencement of orthodontic treatment.
• Recently encephalins related to pain mediation has
been described in teeth undergoing orthodontic
tooth movement

• Walker ’97 reported the existence of an enkephalin,
methionine enkephalin (ME), in an extract of human tooth
pulp tissue and the effect of orthodontic force on ME
concentration.
• Orthodontic force caused a significant decrease in ME
concentrations in the group of experimental teeth
compared with controls.
• Orthodontic force mobilizes at least one neuropeptidergic
pathway in the human tooth pulp which implication in the
pharmacotheraputic management of pain.

• Intrapulpal axon response to orthodontic movement -
Bunner and Johnsen ’97.
• Answers the question whether there is degenerative pulpal
change during ortho trt.
• No significant changes were found in intrapulpal axons
(either qualitatively or quantitatively) of healthy premolars
undergoing conservative orthodontic treatment. At worst,
the percentage of a degenerating axon is small initially.
The process is not progressive. No inflammation was
evident in the pulps of treated teeth.

• The application of orthodontic forces used
with fixed appliances involves cellular
strain, direct tissue damage, inflammatory
changes, and wound healing. These
situations are likely to involve the release of
angiogenic growth factors in the pulp.

• Following orthodontic tooth movement,
• Substance P (SP) (Nicolay et al., 1990)
• Vasoactive intestinal polypeptide (VIP; Motakef et a!.,
1990) have been located in cat pulp,
• Calcitonin gene-related peptide (CGRP) (Kvinnsland and
Kvinnsland, 1990) has been located in rat pulp.
• A number of vaso active neuropeptides may play a part in
neovascularization; in investigation of CORP.
• VIP, neurokinin A (NKA) and neuropeptide Y (NPY),
only CGRP was found to stimulate proliferation of
endothelial cells (Haegerstrand et a!., 1990).

• A number of polypeptide growth factors have been
implicated in the initiation of the angiogenic response
and in regulating endothelial cell proliferation in
wound healing
• Fibroblast growth factor (bFGF); Terranova et al., 1987,
• Platelet-derived growth factor (PDGF),
• Insulin-derived growth factor (IGF-1),
• Epidermal growth factor (EGF),
• Transforming growth factors (TGF-a and TGF-13),
[Schultz and Grant, 1991]
• and in hypoxic and ischaemic conditions in the body
Endothelial cell growth factor (VEGF), Hank er aL, 1995].

Pulp may have a role in remodelling
• These factors may therefore participate in an
angiogenic response of the pulp to orthodontic
force application. Regulation of angiogenesis is by
a balance of factors which may be stimulators or
inhibitors.
• Angiogenic growth factors released from the pulp,
in response to orthodontic force, can induce
angiogenesis in other tissues.

Pulp (2)

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