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Indirect pulp treatment (IPT)
When the deepest carious dentin in a primary tooth is left unremoved to prevent pulp exposure, or
when the tooth has deep caries but no visible pulpitis, IPT is recommended(41, 42). The affected
dentin should be fully sealed off from the oral environment.
Partial pulpotomy for carious exposures
When a young permanent tooth has a carious pulp exposure and the pulp bleeding is under control, the technique is indicated. The aim is that the teeth with immature roots should continue
their regular apexogenesis and root growth(43, 44).
Partial pulpotomy in traumatic exposures
Cvek pulpotomy is indicated in a vital, traumatically exposed, young permanent tooth, especially
one with an incompletely formed apex to maintain pulp vitality(45, 46).
Complete pulpotomy
It is indicated to enable apexogenesis in immature permanent teeth with exposed pulp due to
caries(47, 48).
Regenerative endodontics
The term is used for biological techniques intended to restore damaged tooth anatomy, including
the pulp– dentin complex, dentin, and root tissues, physiologically(49, 50).
14.2.3 Factors Affecting Pulp Healing
Therapeutic factors ● Biochemical preparation
● Intracanal dressing
● RC filling
● Obturation: apical limit
● Apical foramen expansion
Systemic factors Chronic conditions
● Diabetes
● Hypertension
● Menopause/osteoporosis
Note. RC, Root canal.
14.2.4 Response ofPulp Healing
Favourable response Unfavourable response
Recovery and return to normal Inflammation
Tertiary dentine formation Necrobiosis
Pulp revascularisation Infection/no infection leading to necrosis
Pulp fibrosis Infection of RC
Pulp canal calcification Internal root resorption
Combinations of the abovementioned effects
Note. RC, Root canal.
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14.3 Healing ofPeriodontal Tissue
In comparison to epidermal wound healing, periodontal wound repair is a more complicated
process. Periodontium is an open system which is persistently contaminated. The interfaces
between its tissues and the non- vascular root surfaces present a challenge in restoring the tissue
integrity. The body’s capacity and the mechanisms governing healing determine how well the periodontal therapy works. It is critical to realise that a complex web of biological communications in
the target area determines the sequence in which events occur during wound healing following the
therapy. When a mucoperiosteal flap is placed on avascular root surfaces lacking the periodontal
connection, a complex event takes place (51). The periodontal surgical wound is an incision
characterised by clean edges resulting in profused bleeding but generally has a good healing
prognosis(52).
14.3.1 Factors Affecting Periodontal Healing
Local ● Plaque/calculus
● Excess manipulation of tissue
● Trauma
● Foreign bodies
● Repetitive procedures
● TFO
Systemic
Note. TFO, Trauma from occlusion.
● Age
● Infections
● Diabetes mellitus
● Nutritional deficiencies
● Hormonal imbalance
● Detrimental habits
● Stress
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14.3.2 The Role of GFs in Periodontal Wound Healing
GFs are naturally occurring cell products secreted and activated when the need for cell division
arises, such as during healing of wounds. GFs influence mitotic rate, cell cycle and tissue integrity
and promote the development of ECM components, proliferation and chemotaxis. They get attached
to the high- affinity cell membrane receptors to carry out various functions.
Inflammatory and endothelial cells, osteoblasts, periodontal ligament cells and binding proteins
through proteolysis all release GFs. For instance, PDGF (platelet- derived factors), insulin- like
growth factors (IGF- II), platelet- derived endothelial cell growth factor (PDECGF), TGF- B1 and
bone morphogenic proteins (BMPs). Following soft tissue and bone damage, the expression of
several growth differentiation factors may control the healing(53).
14.3.3 Complications ofHealing Process After Periodontal Surgery
After periodontal surgery, healing usually proceeds smoothly and effectively with the achievement
of treatment goals. Occasionally, issues following surgery develop that impede the healing process,
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encourage ongoing inflammation, cause necrotic or hyperplastic reactions, produce deformities
and tumour- like lesions or are connected to bleeding or exudation following surgery, among
other issues. Other complications include slow epithelisation, displacement of flaps, abscess
formation, etc(54).
14.3.4 Cell Lineage inWound Healing
The synthetic cells that support the periodontal tissues’ regular functions and turnover seem to be
part of a diverse cell population. In the steady state, the proliferation of the fibroblast lineage in the
periodontal ligament is counterbalanced by migration and mortality. Mammals have two types of
renewal cell systems: blood cells and the epithelial cells lining the small intestine. Stem cells are
the most basic cells in these systems; they can give rise to numerous specialised cell types within a
tissue and exhibit considerable self- renewal and response to regulatory cues. The sites of stem cells
are limited to a certain niche within the tissue. Periodontal ligament cell populations near blood
vessels have some characteristics of stem cells, but it’s unclear if these progenitors’ daughter cells
really migrate and add to the populations of periodontal ligament cells. The renewal system and
the presence of distinct and discrete rate functions in cell subpopulations. Variations in fibroblast
function have been linked to cellular origins in certain cases. Anatomically, the periodontium’s
connective tissue cell populations are divided into compartments called the gingival, periodontal
ligament, bone and cementum(55).
14.3.5 Concept ofPeriodontal Healing
The two main goals of periodontal therapy are the removal of bacterial plaque and the anatomical
abnormalities caused by periodontitis. Elimination of gingival inflammation, reduction of periodontal pockets’ depth due to gingival recession and the acquisition of clinical attachment can be
observed following the removal of bacterial plaque. The two main surgical methods used to remove
these anatomical abnormalities are resective and regenerative(56).
14.3.5.1 Histologic Patterns ofWound Healing
Wound healing after periodontal therapy can show one/more of six general histologic patterns(54),
which are as follows:
1) Absence of repair mechanism
2) Long junctional epithelium (JE) attachment to the root surface
3) Connective tissue attachment to the root surface
4) New bone separated from the root surface
5) New bone with root resorption and ankylosis to the root surface
6) New attachment apparatus
The cell type propagating the root surface decides the nature of the future attachment The root
surface is repopulated by four different cell types: which are as follows:
1) Epithelial Cells: If the epithelium reaches the root first, JE is formed.
2) Cells Derived from Connective Tissue (Gingiva): Fibres parallel to the tooth and remodelling of
alveolar bone.
3) Cells Derived from the Bone: Resorption of root and ankylosis.
4) Cells Derived from Periodontal Ligament: Formation of new cementum and periodontal ligament.
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14.3.6 Wound Healing Following Dental Treatments
The periodontium recovers by forming a long JE after non- surgical therapy(57).
14.3.6.1 Scaling andRoot Planing
Day One: Epithelial migration begins.
Day Two: Inflammation decreases and epithelialisation is enhanced.
Day Five: New epithelial attachment is gained and residual rete pegs involute(58).
14.3.6.2 Curettage
A blood clot fills the gingival sulcus right after curettage.
After two days: Decreased inflammation and vascularity and epithelium starts covering the gingiva.
After four days: Restoration of JE and sulcular epithelium.
After six days: Gingiva appears light red and oedema is markedly reduced.
After seven days: Tissue appears pink and shrunken and marginal gingiva appears smooth and glossy.
After two weeks: Well- adapted marginal gingiva(59).
14.3.6.3 Gingivectomy
A gingivectomy is the removal of the gingiva. On the surface, a clot forms after gingivectomy.
Thereis some necrosis and inflammation in the surgical incision. The first clot is replaced by
granulation tissue. Just beneath the surface layers of inflammation and necrosis, there is a rise in
new connective tissue cells in about a day, primarily angioblasts. On the third day, a large number
of juvenile fibroblasts are visible nearby. A new gingival border and sulcus are grown coronally by
the granulation tissue. In two weeks, capillaries from the periodontal ligament blood vessels move
into the granulation tissues and join the gingival blood vessels. After gingivectomy, epithelial cells at
the margins overlying granulation tissue within a day or more. The primary intention iswhat brings
about healing. Between 24 and 36 hours, the margins experience their peak in epithelial activity.
The newly formed epithelium over a fibrin layer near the wound, which subsequently gets
resorbed and is replaced by a connective tissue bed. The epithelium cells move forward by toppling,
with the help of new basal lamina and hemidesmosomes that attach the cells to the substrate. In
most cases, surface epithelisation is finished in 5– 14days.
Keratinisation is lower in the first four weeks following surgery than it was before. It takes
roughly a month to complete epithelisation. After the fourth day of healing, vasodilation and
vascularity start to decline, and by the 16th day, they nearly cease to exist. Complete restitution of
the connective tissue requires seven weeks(60).
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14.3.6.4 Flap Surgeries
A mucosa segment that is surgically detached to cover the bone and root surface is known as a
GiAperiodontal flap.
0– 24 Hours: The clot, which is made up of erythrocytes, damaged cell debris, capillaries at the
wound’s edge, and a fibrin reticulum containing numerous PMN leukocytes, establishes a
connection between the flap and the tooth/bone surface.
Three to Five days: The connection gap gets smaller and epithelial cells migrate over the flap’s border.
After One Week: Hemidesmosomes and a basal lamina help to establish an epithelial connection to
the root. Granulation tissue replaces the blood clot.
After Two Weeks: Collagen fibres start to show up parallel to the tooth surface.
After a Month: The gingival crevice has completely epithelised and has a distinct epithelial bond.
The supracrestal fibres are arranged in their initial functional configuration(61).
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14.3.6.5 Wound Healing After Regenerative Therapy
Guided bone regeneration
Guided bone regeneration encourages the production of new bone by prevention of non- osteogenic
tissue infiltration. In order to do this, bone defects are essentially well- tightened membranes with
great tissue compatibility and defined permeability(62).
Guided tissue regeneration
Guided tissue regeneration (GTR) is predicated on the idea of controlling the different components
of periodontal tissue’s proliferation as it heals after periodontal surgery. After a week, the membrane’s coronal edge is partially exposed. Granulation tissue with inflammatory cells and blood
vessels is the most apical component of the abnormalities. In interproximal defects, the average
coronal regrowth of granulation is 1.5 mm, or 30% of the height of the maximal defect, compared
to 0.9 mm, or 20%, in maximal defects. After four weeks, inflammatory cells and new connective
tissue are seen. Nine weeks later, the consistency and colour of gingiva becomes normal(62).
Wound healing post- mucogingival surgery
In periodontal therapy, connective tissue grafts are an efficient way to cover the roots. The benefits
of connective tissue grafts are as follows. Improved healing decreased risk of keloid formation,
accelerated wound healing, etc.(63).
Healing around dental implant
Following implant placement, bone healing is similar to processes involved in bone formation.
Early in the healing process, osteoblasts on the surfaces of bone produce woven bone. There is
bone condensation towards the implant surface as well as into the implant threads. Finally, woven
bone is replaced by lamellar bone. The remodelling process takes 4– 12months and longer than
3– 6months for full healing(64– 68).
Healing after electrosurgery
After electrosurgical incisions in human gingiva, the epithelium and connective tissue healed as
follows: On around third day, the epithelium has closed completely. On the sixteenth day, there
isno discernible zone of granulation tissue. Between the 16th and 21st day, connective tissue is
healed and organised(69).
Healing after laser
After seven days, an extensive area covered in a serofibrin membrane reveals an ulcerated area
with deep penetrations of polymorphonuclear and mononuclear inflammatory cells within the
deep region of the fragment and on its surface, respectively. Presence of giant cells is also seen.
Studies show reepithelialisation within an intensely ulcerated region after the 14th day. After
21days, a large number of skeletal muscle fibres are seen. The atrophic, uniformly shaped fibres
replenish the connective tissue. After 28days, the majority of the tissue is acellular connective
tissue, with a few bundles and isolated skeletal muscle fibres scattered throughout(69).
14.4 Healing ofExtraction Socket
Tooth extraction is a frequently performed procedure in the dental offices. Socket healing is the
term used to describe the entire process that follows extraction and leads to the full healing and
repair of the socket(70).
The process of healing happens gradually and starts right after tooth extraction and lasts for
around six months(71).
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14.4.1 Stages ofSocket Healing
There are four distinct stages of socket healing, which can be distinguished as haemostasis and
coagulation, inflammatory, proliferative, and remodelling (Figure14.5)(72, 73).
14.4.1.1 Haemostasis andCoagulation
After a tooth is extracted, the socket fills with blood right away, causing a blood clot to form. The
blood clot is made up of platelets and red and white blood cells entangled in a fibrin network(74).
This blood clot is replaced in the first seven days by granulation tissue(74, 75).
After a tooth is extracted, bleeding causes platelets to engage with ECM and exposed endothelial
cells, which in turn causes platelet aggregation and the creation of a fibrin clot(72). This first
bloodclot serves as a scaffold for cellular attachment. Numerous CKs and GFs are released by
theblood clot(72, 76).
14.4.1.2 Inflammatory Stage
In response to the released CKs and GFs, inflammatory cells are recruited, migrate, differentiate
and proliferate, which starts 48– 72 hours after extraction(70). The cells aid in clearing away debris,
to make room for new tissue(70, 71). TGF- ß assists convertion of circulating monocytes to macrophages. Platelet- released vascular endothelial growth factors (VEGF) and macrophage- released
FGF support ECM formation and angiogenesis(77, 78). Neutrophils are drawn to wound sites by
PDGF and IL- 1.
Neutrophils, then macrophages and finally lymphocytes enter at the site(72, 76– 78). The blood
clot and necrotic tissues are phagocytosed(76). Additionally, as the socket heals, the macrophages
release GFs that activate osteoblasts and fibroblasts, such as FGF, TGF- α, TGF- ß and EGF(78).
Additionally, during the first four weeks following tooth extraction, the fibrin clot organises and
is replaced with granulation tissue (70, 74). Angiogenesis, inflammatory cells and immature
fibroblasts form the granulation tissue(70, 71, 74).
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Inflammatory stage
Hemostasis and coagulation
Stages of
extraction socket
healing
Figure14.5 Stages of extraction socket healing.
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Proliferative stage
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14.4.1.3 Proliferative Stage
This proliferative stage is characterised by fibroplasia, which is the fast deposition of the
provisional matrix and is thought to be triggered by TGF- ß1 and FGF- 2(72). The aforementioned
fibroplasia and woven bone development, where newly generated blood vessels, bone- forming
cells, and a laying down of woven bone around the blood vessels invade the provisional matrix, are
frequently described as the two phases of this stage of socket repair(70, 72). As this stage advances,
the granulation tissue and any remaining periodontal ligaments will gradually be replaced by the
temporary matrix(72). It has been demonstrated that the primary components of this provisional
matrix are closely spaced mesenchymal cells inside a collagen- rich connective tissue matrix,
together with a small number of mononuclear leukocytes and several blood vessels(74).
Woven bone is laid around the vascular structures(70, 72). Haversian system eventually develops
from finger- like extensions of woven bone surrounding the arteries(79, 80). The woven bone is
then mineralised and lined by osteoblasts with high osteocyte content(74). The granulation tissue
is replaced by woven bone by 6– 8weeks of socket healing(71, 74). In 27 human post- extraction
socket biopsies, Trombelli etal. (2008)(74) demonstrated that woven bone occupied a mean value
of 34.0 ± 24.6% of the entire specimen analysed. BMP, together with TGF- ß, have been shown to
play major roles in bone morphogenesis and osteoblastic differentiation(74, 80).
14.4.2 Factors That Affect Socket Healing
There is significant inter- individual heterogeneity in terms of tissue creation and maturation(74).
There are various factors responsible as follows:
Smoking(81)
Flapless tooth extraction(82– 85)
Location(86– 88)
Single versus multiple extractions(89, 90)
Use of chlorhexidine mouth rinse post- extraction(91)
14.4.3 Use ofReconstructive Technologies inExtraction Socket Healing
In order to optimise bone quality and quantity for dental implant placement and osseointegration,
as well as to prevent post- extraction ridge profile changes that could compromise the aesthetics
of a prosthetic rehabilitation, reconstructive technologies are applied at the sites of fresh
extractions(71).
● Graft materials
● Barrier membranes
● Bioactive agents
14.4.4 Complications inHealing ofExtraction Wounds
14.4.4.1 Haemorrhage
The most frequent postoperative haemorrhage a dental surgeon sees is bleeding from an extraction
socket(92). There are three types of bleeding: primary, reactionary (which happens 48 hours after
the procedure when the vasoconstrictor’s effects wear off and reactive hyperaemia develops) and
secondary (a rare aftereffect of tooth extraction that may be caused by an infection that breaks up
the blood clot). It begins roughly seven days following surgery(92, 93).
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Bleeding can result from a variety of local causes, including violent exercise, applying heat,
laceration, trauma, friable granulation tissue, clot dislodgement, infection, haemorrhagic lesions
and prolonged steroid therapy. It can also result from systemic causes, such as coagulopathies,
anticoagulant therapy, anti- platelet drugs, liver dysfunction, chronic liver failure, uraemia, lupus
erythematosus and prolonged steroid therapy(94, 95).
14.4.4.2 Hematoma andEcchymosis
Insufficient postoperative haemostasis or insufficient drainage are the causes of postoperative
hematoma development (92). It might be the result of excessively tight suturing the incision,
which could cause a significant swelling of the face that feels sensitive to the touch(92).
Most surgical extractions will result in mild ecchymosis, particularly in older patients with
compromised tissue elasticity and increased capillary fragility(96).
14.4.4.3 Postoperative Pain
Incomplete tooth extraction, laceration of the soft tissues, exposed bone, infected sockets or injury
to nearby nerves can all cause post- extraction discomfort(93).
14.4.4.4 Dry Socket (Alveolar Osteitis)
It is characterised by postoperative pain at the extraction site that worsens at any point during the
first three days following the procedure, along with a completely or partially disintegrating blood
clot in the alveolar socket, either with or without halitosis. Dry socket occurs in 1– 4% of tooth
extractions overall, and in third molar procedures, it can occur in 20– 30% of cases(97). Clinically,
the initial blood clot has necrosis and disintegrated, leaving an empty alveolus that is covered in a
layer of debris and necrotic tissues that is greyish yellow in colour and has extremely sensitive
bone surfaces. There is excruciating, ongoing throbbing pain in and around the extraction socket
that radiates to other nearby tissues and organs. This pain can endure for many days or weeks and
is difficult to manage with analgesics(97, 98).
Advanced age, female gender, use of oral contraceptives, longer recovery times after surgery,
smoking, traumatised tooth extraction, higher anaesthetic dosage, medical history (e.g. diabetes
mellitus), operator experience, challenging and drawn- out extractions, prior surgical site infection,
inadequate oral hygiene, excessive irrigation of the alveolus repeatedly, noncompliance with postextraction instructions, gingivitis, periodontitis, number and location of extractions, leftover bone
or root fragments, debris remnants, vasoconstrictors in local anaesthetic solutions, medications
such as antipsychotic and antidepressants, flap design, food particles, and bacterial biofilm can all
be risk factors for dry socket(95, 99).
Other complications are:
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1) Swelling
2) Trismus
3) Trauma
4) Delayed healing of wound
5) Sharp bony irregularities
6) Acute osteomyelitis of mandible
7) Dislocation of temporomandibular joint
8) Paraesthesia
9) Oro- antral fistula
10) Aphthous ulcer
11) Surgical emphysema
12) Osteoradionecrosis
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14.5 Healing ofBone Fractures
Jaw fractures are frequent injuries that can range in severity from simple fractures of the alveolar
process to severe damage to the maxillofacial region. Despite the sequence of events appearing to
be a well- understood and extensively described phenomenon, there are surprisingly many issues
regarding the overall characteristics of bone repair that are debatable.
14.5.1 Immediate Impact ofFracture
The Haversian vessels of the bone, as well as the vessels of the periosteum and the marrow cavity
that happen to cross the fracture line, are ruptured at the site of a bone fracture. Acute inflammation is triggered in the soft tissue at the fracture line because of the resultant tissue injury, particularly in the Haversian canals, marrow spaces and periosteal region. Vascular disruption has
resulted in significant blood extravasation in this approximate area, but there is also a lack of local
blood supply and circulation. The anastomosis of uninjured vessels occurs as close to the fracture
site as the actual stopping of circulation.
There is only one vessel in the bone’s Haversian canals. The bone cells, or osteocytes, of the
Haversian system supplied by this channel perish when the blood supply is disrupted by ripping at
the fracture site. The dead bone may be several millimetres or longer in length as it stretches from
the fracture site to the anastomosing circulation point. Rarely is there a clear distinction between
living and dead bone due to the overlapping structure of the blood supply to bone. Alongside the
loss of the blood supply, the bone marrow next to the fracture line also dies. Because the Haversian
vessels are supplied by branches of the periosteal vessels, the periosteal blood vessel tearing also
plays a role in the local death of bone.
It was formerly believed that the blood clot that forms is crucial to the healing of the fracture
because it causes granulation tissue to renew itself, and bone then replaces it. Most authorities
today believe that the blood clot plays only a passive part in the healing process and that the callus,
which is freshly formed bone, forms outside of the replacement of granulation tissue. Although
severe clot necrosis may somewhat impede the healing process, the clot itself is not actually
required for osteogenic cell invasion.
14.5.2 Callus Formation
The Latin term for callus implies ‘overgrowth of hard skin’. Callus, which is made up of different
proportions of fibrous tissue, cartilage and bone, joins the broken ends of bones. The new tissue
that surrounds the exterior of the two bone fragments creates the external callus. The new tissuecoming out of the marrow cavity is called the internal callus.
The periosteum plays a crucial role in the development of calluses and the final healing of
fractures, so maintaining it is crucial. Usually, the periosteum cells that are next to the periosteum
that is torn at the fracture line perish. However, a flurry of cellular activity may be observed in the
vicinity of this location within a few hours following the injury. The proliferation of cells in the
osteogenic, or inner, layer of the periosteum actually lifts the outer, or fibrous, layer of the periosteum away from the surface of the bone, making it relatively inert. A few days following the
fracture, these cells start to create a small quantity of new bone at a distance from the fracture.
These cells resemble osteoblasts.
When new bone starts to grow in the external callus, it typically takes the appearance of irregular
trabeculae that are frequently arranged at an angle to the surface. The deepest region of the callus
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collar is where these cells differentiate into osteoblasts, which then go on to build bone. In the
quickly expanding collar region away from the fracture line, differing numbers of osteogenic layer
cells develop into chondroblasts instead of osteoblasts and actually produce cartilage. There is not
a clear separation between this cartilage and the bone; instead, they blend together.
The pluripotency of the osteogenic layer cells is demonstrated by their ability to differentiate into
chondroblasts instead of osteoblasts, underscoring the fact that the periosteum was originally a
perichondrium in cartilage- formed bones. Numerous factors influence the amount of cartilage
that forms in a callus, which can vary significantly depending on the situation. The local environment’s vascularity is one important aspect. Where there is adequate blood flow, bone tends to form;
where there is insufficient blood flow, cartilage forms. It should be observed that in the callus, bone
grows next to blood arteries, but the cartilage is formed from cells that have multiplied so quickly
that the blood vessels cannot keep up and are now out of reach. Thus, another factor influencing
the amount of cartilage formation is the rate of healing. There is little cartilage production during
sluggish healing. Lastly, significant cartilage development is frequently linked to the fragments’
mobility.
The cartilage cells mature and start to calcify in a manner akin to typical endochondral bone
formation as callus formation advances. This calcification is noticeably close to blood arteries that
are growing nearby. The calcified cartilage is gradually resorbed and replaced by bone.
The bone marrow’s undifferentiated cells and the endosteum of the Haversian canals combine
to generate the internal callus. The endosteum starts to multiply soon after the fracture, and new
bone and cartilage start to grow in a week or two. The new bone that grows at the end of each
fragment gradually joins the others to form a continuous bone.
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14.5.3 Remodelling ofthe Callus
There is always an abundance of new bone created to support the healing site, necessitating remodelling of the exterior and internal calluses that link the two fragments of bone. Furthermore, pieces
of the old dead bone are often used to fuse the newly formed bone. These pieces gradually reabsorb,
to be replaced by a mature bone type that responds to typical stress patterns. It is also important to
rebuild the exterior callus so that the extra bone can eventually be removed. In the end, the bone
at a fracture site is almost identical to the bone that was there prior to the fracture.
Mandibular fractures are common among facial fractures.
14.5.4 Classification ofMandibular Fractures
There are many classifications concerning mandibular fractures such as Dingman and Natvig
(1969)(100), Kelly and Harrigan(101), Sinn etal.(102), WHO, etc.
14.5.4.1 LeFort Classification
Le Fort fractures(103) are complex facial fractures with varying degrees of craniofacial dissociation
affecting various facial buttresses and are as follows:
I Anterolateral margin of the nasal fossa
II Inferior orbital rim
III Zygomatic arch
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