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Haemostasis
Inflammation
200
Injury
Blood
vessel
Macrophage
Neutrophil
Migratory
epithelial cells
Fibroblast
Proliferation
Scar
Proliferating
fibroblasts
Figure13.2 Graphical illustration of wound healing in phases: haemostasis, inflammation, proliferation
and remodelling. Source: BioRender/https://app.biorender.com/biorender- templates2023/figures/all/
t- 5fa1b1622a60ac00a3d858ec- wound- healing/last accessed on 15 December, 2022.
tissue
Remodelling
Wound healing in skin and oral mucosa shares many common cellular and molecular processes,
as described above; however, there are also notable differences due to the distinct characteristics
and functions of these two tissue types.
A significant difference is the environment. Oral mucosal wounds benefit from a protective
mucus layer, which expedites healing and protects against further damage. The mucus layer also
aids in maintaining lubrication in the oral cavity. It is known that for skin wound healing, a moist
environment results in faster reepithelialisation, angiogenesis and wound maturation(24, 25). In
oral mucosa, saliva does not only provide a natural moist environment, it also contains wound
healing stimulating growth factors, e.g. epidermal growth factor (EGF), VEGF, fibroblast growth
factor (FGF) and histamine(26, 27). Moreover, saliva contains many antimicrobial peptides that eliminate microorganisms, e.g. defensin, histatin, cathelicidin, lysosome, lactoferrin and lactoperoxidase
(23, 28). It has been shown that a healthy oral biofilm, with increased antimicrobial peptide expression,
improved barrier function in reconstructed human gingiva (29, 30). Furthermore, microbes
positively affect wound healing by activating macrophages, dendritic cells and T cells, resulting in stem
cell proliferation stimulating cytokines, e.g. TNF- α, IL- 6, IL- 10 and IL- 17(31, 32).
t.me/Dr_Mouayyad_AlbtousH
References
Another factor is the inflammation response during wound healing. In oral wounds, the baseline
immune status is higher, but the inflammation response was shown to be reduced and concluded
earlier than in skin wounds(33). The number of immune cells, e.g. neutrophils, macrophages and
T cells, and the levels of inflammation mediators, e.g. IL- 6, IL- 8, IL- 23, IL- 24, TNF- α and TGF- β, in
oral mucosa are reduced compared to skin(3, 34, 35).
An essential characteristic of the oral mucosa is that it contains more blood vessels than the skin,
which is essential regarding wound healing properties since blood vessels bring oxygen, nutrients
and immune cells to the injury site(12).
Regarding epithelial regeneration, i.e. reepithelialisation, where epithelial cells (keratinocytes)
cover the wound, the oral mucosal epithelial cells (keratinocytes) have a relatively faster proliferation rate and are less differentiated compared to the skin keratinocytes(11, 35). This contributes to
the quicker regeneration potential of oral mucosal wounds(7, 11).
The repair process in the skin involves the deposition of a significant amount of collagen by
fibroblasts. This results in the formation of fibrotic tissue, which can lead to noticeable scar formation. In oral mucosa, the fibroblasts show increased proliferation, migration and efficiency in
remodelling connective tissue(36, 37). Due to the rapid proliferation of fibroblasts and the minimal need for extensive collagen production, oral mucosal wound healing tends to result in less
noticeable scarring than skin wounds.
13.4 Summary
201
In summary, the presence of saliva, more efficient inflammation response, faster reepithelialisation (i.e. wound closure) and extracellular matrix remodelling all contribute to faster healing with
less scarring of oral mucosal wounds to cutaneous wounds.
References
1 Wallace HA, Basehore BM, Zito PM. Wound Healing Phases. StatPearls. Treasure Island (FL):
StatPearls Publishing Copyright © 2023, StatPearls Publishing LLC.; 2023.
2 Korkmaz HI, Flokstra G, Waasdorp M, Pijpe A, Papendorp SG, de Jong E, etal. The complexity of
the post- burn immune response: an overview of the associated local and systemic complications.
Cells. 2023;12(3):345.
3 Waasdorp M, Krom BP, Bikker FJ, van Zuijlen PPM, Niessen FB, Gibbs S. The bigger picture: why
oral mucosa heals better than skin. Biomolecules. 2021;11(8):1165.
4 Yousef H, Alhajj M, Sharma S. Anatomy, Skin (Integument), Epidermis. StatPearls. Treasure Island
(FL): StatPearls Publishing Copyright © 2023, StatPearls Publishing LLC.; 2023.
5 Presland RB, Jurevic RJ. Making sense of the epithelial barrier: what molecular biology and genetics
tell us about the functions of oral mucosal and epidermal tissues. J Dent Educ. 2002;66(4):564– 74.
6 Qin R, Steel A, Fazel N. Oral mucosa biology and salivary biomarkers. Clin Dermatol.
2017;35(5):477– 83.
7 Turabelidze A, Guo S, Chung AY, Chen L, Dai Y, Marucha PT, etal. Intrinsic differences between
oral and skin keratinocytes. PLoS One. 2014;9(9):e101480.
8 Gibbs S, Ponec M. Intrinsic regulation of differentiation markers in human epidermis, hard palate
and buccal mucosa. Arch Oral Biol. 2000;45(2):149– 58.
9 Agarwal S, Krishnamurthy K. Histology, Skin. StatPearls. Treasure Island (FL): StatPearls Publishing
Copyright © 2023, StatPearls Publishing LLC.; 2023.
t.me/Dr_Mouayyad_AlbtousH
202
10 Brizuela M, Winters R. Histology, Oral Mucosa. StatPearls. Treasure Island (FL): StatPearls
Publishing Copyright © 2023, StatPearls Publishing LLC.; 2023.
11 Glim JE, Everts V, Niessen FB, Ulrich MM, Beelen RH. Extracellular matrix components of oral
mucosa differ from skin and resemble that of foetal skin. Arch Oral Biol. 2014;59(10):1048– 55.
12 Szpaderska AM, Walsh CG, Steinberg MJ, DiPietro LA. Distinct patterns of angiogenesis in oral
and skin wounds. J Dent Res. 2005;84(4):309– 14.
13 Chen J, Ahmad R, Li W, Swain M, Li Q. Biomechanics of the oral mucosa. J R Soc Interface.
2015;12(109):20150325.
14 Castaño O, Pérez- Amodio S, Navarro- Requena C, Mateos- Timoneda M, Engel E. Instructive
microenvironments in skin wound healing: biomaterials as signal releasing platforms. Adv Drug
Deliv Rev. 2018;129:95– 117.
15 Gilaberte Y, Prieto- Torres L, Pastushenko I, Juarranz Á. Chapter1- Anatomy and function of the
skin. In: Hamblin MR, Avci P, Prow TW, editors. Nanoscience in Dermatology. Boston: Academic
Press; 2016, pp. 1– 14.
16 Fenner J, Clark RAF. Chapter1- Anatomy, physiology, histology, and immunohistochemistry of
human skin. In: Albanna MZ, Holmes Iv JH, editors. Skin Tissue Engineering and Regenerative
Medicine. Boston: Academic Press; 2016, pp. 1– 17.
17 Lu Y, Zhu WY, Tan C, Yu GH, Gu JX. Melanocytes are potential immunocompetent cells: evidence
from recognition of immunological characteristics of cultured human melanocytes. Pigment Cell
Res. 2002;15(6):454– 60.
18 Nilima S, Vandana KL. Melanin: a scavenger in gingival inflammation. Indian J Dent Res.
2011;22(1):38– 43.
19 Han S- K. Basics of wound healing. In: Han S- K, editor. Innovations and Advances in Wound
Healing. Berlin, Heidelberg: Springer Berlin Heidelberg; 2016, pp. 1– 37.
20 Wang JHC, Thampatty BP, Lin J- S, Im H- J. Mechanoregulation of gene expression in fibroblasts.
Gene. 2007;391(1):1– 15.
21 Caselli E, Fabbri C, D’Accolti M, Soffritti I, Bassi C, Mazzacane S, etal. Defining the oral
microbiome by whole- genome sequencing and resistome analysis: the complexity of the healthy
picture. BMC Microbiol. 2020;20(1):120.
22 Deo PN, Deshmukh R. Oral microbiome: unveiling the fundamentals. J Oral Maxillofac Pathol.
2019;23(1):122– 8.
23 van ‘t Hof W, Veerman EC, Nieuw Amerongen AV, Ligtenberg AJ. Antimicrobial defence systems
in saliva. Monogr Oral Sci. 2014;24:40– 51.
24 Junker JP, Kamel RA, Caterson EJ, Eriksson E. Clinical impact upon wound healing and
inflammation in moist, wet, and dry environments. Adv Wound Care (New Rochelle).
2013;2(7):348– 56.
25 Svensjö T, Pomahac B, Yao F, Slama J, Eriksson E. Accelerated healing of full- thickness skin
wounds in a wet environment. Plast Reconstr Surg. 2000;106(3):602– 12. discussion 13- 4.
26 Brand HS, Ligtenberg AJ, Veerman EC. Saliva and wound healing. Monogr Oral Sci.
2014;24:52– 60.
27 Lei X, Cheng L, Lin H, Pang M, Yao Z, Chen C, etal. Human salivary Histatin- 1 is more efficacious
in promoting acute skin wound healing than acellular dermal matrix paste. Front Bioeng
Biotechnol. 2020;8:999.
28 Marsh PD, Do T, Beighton D, Devine DA. Influence of saliva on the oral microbiota. Periodontol
2000. 2016;70(1):80– 92.
29 Laheij AM, de Soet JJ, Veerman EC, Bolscher JG, van Loveren C. The influence of oral bacteria on
epithelial cell migration invitro. Mediators Inflamm. 2013;2013:154532.
t.me/Dr_Mouayyad_AlbtousH
References
30 Shang L, Deng D, Buskermolen JK, Janus MM, Krom BP, Roffel S, etal. Multi- species oral biofilm
promotes reconstructed human gingiva epithelial barrier function. Sci Rep. 2018;8(1):16061.
31 Karin M, Clevers H. Reparative inflammation takes charge of tissue regeneration. Nature.
2016;529(7586):307– 15.
32 Zheng D, Liwinski T, Elinav E. Interaction between microbiota and immunity in health and
disease. Cell Res. 2020;30(6):492– 506.
33 Mak K, Manji A, Gallant- Behm C, Wiebe C, Hart DA, Larjava H, etal. Scarless healing of oral
mucosa is characterised by faster resolution of inflammation and control of myofibroblast action
compared to skin wounds in the red Duroc pig model. J Dermatol Sci. 2009;56(3):168– 80.
34 Glim JE, van Egmond M, Niessen FB, Everts V, Beelen RH. Detrimental dermal wound healing:
what can we learn from the oral mucosa? Wound Repair Regen. 2013;21(5):648– 60.
35 Szpaderska AM, Zuckerman JD, DiPietro LA. Differential injury responses in oral mucosal and
cutaneous wounds. J Dent Res. 2003;82(8):621– 6.
36 Boink MA, van den Broek LJ, Roffel S, Nazmi K, Bolscher JG, Gefen A, etal. Different wound
healing properties of the dermis, adipose, and gingiva mesenchymal stromal cells. Wound Repair
Regen. 2016;24(1):100– 9.
37 Isaac J, Nassif A, Asselin A, Taïhi I, Fohrer- Ting H, Klein C, etal. Involvement of neural crest and
paraxial mesoderm in oral mucosal development and healing. Biomaterials. 2018;172:41– 53.
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14
Healing ofthe Dental Pulp andPeriodontal Tissues, Extraction
Socket andBone Fracture
Sachin Sarode and Gargi Sarode
Department of Oral and Maxillofacial Pathology, Dr. D. Y. Patil Dental College and Hospital, Pune, India
14.1 Introduction
The replacement of injured tissue with healthy tissue to restore function is referred to as healing.
One of the most fascinating phenomena that distinguishes a living thing is the ability to heal
wounds. Damaged tissue’s innate capacity to heal itself is a reaction to life. Over the past few
decades, there has been progress in our comprehension of the mechanisms underlying oral wound
healing and how these understandings are applied to modern clinical treatment strategies. It is
thought that an organism will eventually perish from an unhealed wound. Consequently,
frombirth onward, wound healing needs to be regarded as one of the main survival strategies. It
should be abundantly evident that the healing process of a wound is a highly intricate sequence
of biological events rather than an isolated, solitary phenomenon.
Healing is not an event, but a process. It consists of wound contraction, which is at least partially
attributed to myofibroblasts, which are modified fibroblasts that have ultrastructural similarities to
smooth muscle cells. Due to the division and migration of nearby cells, this contraction results in
shrinkage in the wound size during the few initial weeks and the substitution of the lost tissue.
‘Regeneration’ is the process of replacing destroyed tissue with comparable type tissue; ‘repair’ is
the process of replacing lost tissue with granulation tissue, which leaves scars.
Tissue healing is commonly seen as a stage of the inflammatory response because it is inextricably linked to the vascular and cellular processes that precede an injury. Healing occurs quickly
when the wound’s edges are close together; this is termed as primary healing or healing by first
intention. When tissue is lost and the wound’s borders cannot be closed, the wound shrinks,
granulation tissue fills it, and the surface of the wound becomes epithelialised. We refer to this as
secondary intention healing. Granulation tissue has a distinctively bright pink colour and is mostly
made up of fibroblasts and proliferating capillaries.
An array of growth factors (GFs) along with cytokines (CKs) is important in the process of
healing. The epithelium around the injured area produces an epidermal growth factor (EGF) that
aids in the repair of the epithelial tissue. Fibroblast growth factor (FGF), which is released by
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram,
Omar Kujan and Merva Soluk Tekkesin.
© 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
t.me/Dr_Mouayyad_AlbtousH
macrophages, mediates fibroblast activity in addition to transforming growth factor- α (TGF- α).
Blood vessel development is triggered by EGF. All tissues heal following injury in essentially the
same way, while there are several external and intrinsic variables that can alter this process.
Oral injuries are frequent; some are unintentional (such as jaw fractures), and others are
iatrogenic (such as extraction, biopsy, etc.), and some are the result of a disease process
(e.g. various mouth ulcers). The unique anatomical features of the mouth cavity, including the
teeth’s protrusion from the bone, the gingival tissues’ ongoing inflammation, and the myriad
microorganisms present in saliva’s warm, moist medium, all influence how different wounds heal.
This chapter focuses on the healing of dental pulp, periodontal tissues, extraction socket and
bone fractures. The functions of these oral structures, their healing processes, factors affecting the
healing and complications involved are also discussed.
14.2 Healing ofDental Pulp
Structured strata of cells that multiply and differentiate to finish root development make up normal pulp tissue(1). The pulp is a mesenchymal soft tissue that encompasses the central chamber
till the tip of the tooth root. It comes from the neural crest(2).
The prepositioned inflammatory process, pulp tissue repair and self- renewal are the functions
carried out by the pulp cells(3). The degree of bacterial invasion has important role to play in the
repair process.
Hertwig’s epithelial root sheath (HERS) forms a diaphragm that controls the number, form and
dimensions of the roots(4, 5). The papilla at the apical area stores undifferentiated mesenchymal
stem cells as a reservoir for further root dentin formation(6). In addition to the HERS, follicular
tissue and stem cells from the apical papilla (SCAP) are involved in the development of apical
complex cells that are responsible for the formation of root and periodontium(7, 8).
Nevertheless, following infection exposure, there are notable histopathologic changes at the
pulp– dentin interface, which include the displacement of tissue that resembles the periodontal
ligament, osteoblasts, and cementum, and the absence of cells(5, 9, 10). The damaged root canal
wall has no odontoblasts and is healed by the deposition of periodontal tissue. There is absence
of dentinal tubules and odontoblast processes. Apical papilla show significantly decreased
cellularity with a discontinuous or nonexistent HERS as the pulp tissue enters the necrotic
phase(5, 10).
The tooth is made up of the mineralised enamel and dentin, the interior soft tissue, pulp and a
one- way neurovascular supply. Because calcified tissue confines the dental pulp, the inflammatory
response raises the intra- pulp canal pressure. This pressure then travels down the root canal into
the root apex, resulting in periapical abscess(5, 11, 12). If the abscess is not treated, it may lead to
loss of bone anchorage and extrusion of tooth. The untreated condition can lead to resorption ofroots
and disruption of periodontium affecting the periodontal ligament space and alveolar bone(12). In
order to reduce intra- canal pressure causing pain, endodontic therapy comes into picture. The
treatment is also called root canal therapy (RCT) that includes removal of infected pulpal tissue
(9,11). The age as per the status of the root apex and the depth of the inflammation penetration
determine the pulp treatment mode, which can be determined by pulp capping (direct or indirect),
pulpectomy (partial or complete), apexification or apexogenesis(9). Pulp, dentin and periodontium
tissue will react to the pathogenic stressors by utilising chemical signalling and cell– cell communication to initiate a biological defence mechanism. These mechanisms may serve as the healing
foci of repair and regeneration.
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Differentiation of odontoblasts
n
Pulp wound healing
206
14.2.1 Healing Process
14.2.1.1 Pulp Wound Healing: Necrotic Layer andIts Function
Similar to other wounds, pulpal wounds almost usually develop a layer of necrotic tissue at their
surface. The presence of this layer has occasionally been viewed as a negative side effect, and the
high pH of calcium hydroxide has led to concerns about its suitability for pulp capping, for
example. However, the growth of reparative dentine beneath the exposed site may be facilitated in
part by the necrotic layer. Following pulp exposure, the creation of reparative dentine or healing
with a hard tissue requires some sort of surface on which the newly formed odontoblasts or cells
resembling odontoblasts can adhere. The basal membrane between ameloblasts and odontoblasts
functions as a structural meshwork helping in cell immobilisation during odontoblastic differentiation. GFs, tenascin and fibronectin are examples of basement membrane components that
support odontoblast development and polarisation(13– 15). The GFs along with TGF- β superfam-
ily control odontoblastic differentiation and the synthesis of extracellular matrix (ECM) during the
early stages of odontogenesis. Basement membrane constituents also function as ligands for cell
adhesion(13).
The necrotic layer functions as an attachment surface for substances promoting odontoblast- like
cell differentiation during pulpal wound healing, perhaps imitating some of the functions of the
basement membrane(16, 17). The trials showing that Teflon, an inert pulp- capping substance,
solely causes soft tissue reorganisation and does not cause the creation of hard tissue lend credence
to this assumption(18, 19). It would also explain, at least in part, the positive outcomes of the clinical
work and experimentation conducted with Ca(OH) despite − or perhaps precisely because of − its
caustic consequences.
Fibronectin has been mentioned as a major contender in the replacement- odontoblast differentiation and as one of the elements that may contribute to the preodontoblast polarisation and their
terminal development(17, 20).
Yoshiba etal. (20) investigated fibronectin expression in human teeth pulp capping during
experimental Ca(OH) treatment. According to the study, fibronectin connected to the first calcified
layer may have a role in the replacement- odontoblasts’ differentiation and organisation following
pulp capping(20). The tertiary dentine with few tubules had formed 28days after pulp capping,
and the dentine– pulp complex resembled that of a normal tissue(20) (Figure14.1).
14.2.1.2 Pulp Vasculature
Smaller arteries may reach the pulp through lateral canals, while arterioles with a diameter of
0.1 mm/less enter through the apical foramen. The capillary plexus that forms underneath the
odontoblast cell layer in the root canal comprises branches of the arterioles. The arterioles split off
to form a dense sub- odontoblastic terminal capillary plexus(21) in pulpal tissue. Particularly in the
Necrotic layer formation
Reparative dentin formation
Figure14.1 Pulpal wound healing: The function of the
necrotic layer.
Fibronecti
TGF-β I
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pulp, coronal pulp has twice the capillary blood flow than that of the radicular pulpal tissue(22).
Capillaries may infiltrate the odontoblast layer in younger teeth during dentogenesis in its rapid
phase to supply nutrients to the active cells(21).
Larger venules, possibly twice as massive as the arterioles, are still being formed by the postcapillary venules. It is believed that the venules’ incredibly thin walls make it easier for fluid to
enter and exit the vessels(23).
The dentine– pulp complex cells receive their nourishment and oxygen from the pulp vascular
system, which also removes harmful materials and heat generated during procedures like tooth
preparation. A local inflammatory response evoked is typified by decreased blood flow resistance
and dilatation of the arteries. Serum proteins and fluid enter into the tissue because of subsequent
increase in intravascular pressure and capillary blood flow followed by extravasation of leukocytes(24). Within four hours of the cavity being prepared, increased vascular permeability(24)
leading to entry of inflammatory cells ensures removal of bacterial toxins and metabolic waste
products. Tissue pressure rises because of cell extravasation, protein and fluid filtration resulting
in oedema. The pulp tissue is constrained by the low compliance environment created by the
surrounding dentine and enamel. However, the tissue pressure may rise to the point where it
surpasses the venular pressure compressing the venules. This obstruction of venous drainage
decreases the blood flow, which further worsens due to blood cell aggregation and increased blood
viscosity as a result of slower flow. The subsequent local hypoxia, rise in carbon dioxide and metabolic waste products and fall in pH cause vasodilatation of pulp vasculature leading to spread of
inflammation(25).
Measures must be taken to contain pulp necrosis within a region to prevent total necrosis. Studies
have demonstrated that under cavities/restorations, there are localised areas of inflammation
surrounded by healthy pulp. Pulp vasculature helps in stopping the spread of inflammation. The
macromolecules may be forced into the venules of the healthy site by tissue pressure(25) leading
to improved blood flow, oxygen delivery and elimination of harmful substances and metabolic
waste products by lowering the venule resistance (Figure14.2).
207
14.2.1.3 Nerves’ Involvement inControlling Pulp Inflammation
Along with the blood arteries, the nerve fibres enter the pulpal tissue to form a neurovascular bundle.
A vital plexus is evident in the coronal pulp and is called sub- odontoblastic plexus of Raschkow(21).
The pulpal tissue contains myelinated as well as unmyelinated sensory afferent and sympathetic
nerves. A- delta fibres make up most myelinated fibres, whereas C- fibres make up the bulk of
unmyelinated fibres. A- delta fibre terminals, which cause a sharp, prickling pain sensation, are
primarily found near the dentine– pulp junction. This is also where they typically shed their myelin
sheath. Sensing dull discomfort, C- fibres are more likely dispersed throughout the pulp (23).
Additionally, some A- beta mechanoreceptors that are vibration- sensitive exist(26).
Studies indicate that pulp nerves have a role in controlling defensive responses in the dentine–
pulp complex. Apart from the distinct nociceptive fibres, many A- delta and C- fibres are part of the
polymodal receptor system. Numerous characteristics of these receptors are not often associated
with nerve fibres, such as vasodilatation, pulp cell activity, dentinal fluid outflow and the control
of inflammatory responses (26). Rodd and Boissonade(27) suggested that the regulation of the
dentine– pulp complex defensive reaction might be the primary function of the nerves. Endogenous
inflammatory mediators (prostaglandins, histamine, bradykinin and interleukin- I [IL- I]) induce
vasodilatation resulting in vascular leakage directly through vascular receptors(28). Only an external stimulus on the tooth itself triggers the release of neuropeptides from afferent neurons, including substance P and calcitonin gene- related peptide (CGRP). Neuropeptides start a pro- inflammatory
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208
Local irritation causing local
inflammatory response
Extravasation of leukocytes
into pulp
Local hypoxia, ↑ carbon
dioxide and metabolic waste
products and fall in pH
resulting in vasodilatation of
pulp vasculature, causing
spread of inflammation
Figure14.2 Role of pulp vasculature in pulpal inflammation.
Decreased blood flow
resistance and arterial
dilatation
↑ tissue pressure because of
cell extravasation, protein
and fluid filtration,
and oedema
↑ intravascular pressure and
capillary blood flow
↑ tissue pressure causes
obstruction in venules leading
to ↑ flow resistance and
a corresponding decreased
blood flow
vascular reaction(26, 28). Furthermore, chemicals released by sympathetic and parasympathetic
nerve fibres play a role in the regulation of pulpal vascular reactivity(26).
Byers and Taylor(29) found that the sensory denervation of a rat tooth leads to pulpal necrosis,
while the healthy control tooth (same animal) sprouted a strong CGRP- positive response indicating a strong nervous system reaction to the exposure and infection(29) (Figure14.3).
14.2.2 Pulp Healing by Dental Procedures
Direct pulp capping (DPC)
DPC covers the exposed pulp directly with a dental biomaterial to facilitate pulpal healing and
create a mineralised tissue barrier (Figure14.4).
Mechanism of action of DPC
DPC biomaterials placed directly over exposed pulp tissue result in superficial necrosis. In addition
to inducing mineralisation, the DPC biomaterial has antibacterial qualities(30). A thin necrotic
layer is formed between the DPC agent and the essential pulp tissue because of the release of
hydroxyl ions from DPC biomaterials, which increase the pH of the underlying tissue(31). The
cells underneath this necrotic zone are shielded from the material’s alkaline pH(32) resulting in
pulpal regeneration and repair(33). By denaturing proinflammatory CKs and activating IL- 10, the
elevated pH may also have an anti- inflammatory effect(34– 37).
Protective liner
A protective liner serves as a barrier between the pulp and the restoration and is made of calcium
hydroxide, mineral trioxide aggregate (MTA), trisilicate cement or another biocompatible substance to encourage pulp tissue recovery(38– 40).
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Pulpitis
209
External
stimulus
A-delta fibres
C-delta fibres
Release of
neuropeptides
SP and CGRP
Control of defensive responses in the
dentine–pulp complex and transmission of
Stimulation of afferent nerve endings
sensory information
transmitting pain
Pulp
necrosis
Sensory denervation
(cutting the inferior
alveolar nerve)
Figure14.3 Involvement of nerves in controlling pulp inflammation.
Vascular system
Release of
PG, histamine,
BK and IL-I
Pulpal
wound
healing
Direct pulp
capping
Regenerative
endodonties
Pulp healing by
dental procedures
Complete
pulpotomy
Partial
pulpotomy
for traumatic
exposures
(Cvek
pulpotomy)
Partial
pulpotomy
for carious
exposures
Figure14.4 Pulp healing by dental procedures.
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Protective
liner
Indirect pulp
treatment
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