Trauma and the Periodontal Tissues: A Narrative Review

Abstract

The health of the periodontium including the soft tissues – gingiva and periodontal ligament; and the hard tissues – cementum and alveolar bone is of key importance in the overall homeostasis of the dentition. Injury to the periodontal tissues in any form such as microbial, physical, thermal, chemical, mechanical, occlusal and habitual injury affects the harmony of the periodontal attachment apparatus thereby altering the entire functioning of the dentition. The type of tissue damage when trauma is unintentional and iatrogenic tends to be acute and self-limiting. On the other hand, mechanical and occlusal forces could result in chronic damage. This book chapter provides a review on the various forms of non-microbial trauma to the periodontal tissues, their clinical manifestations and its management.

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Chapter
Trauma and the Periodontal
Tissues: A Narrative Review
Santo Grace Umesh, Lakshmi Ramachandran,
Janani Karthikeyan and Sindhuja M. Shankar
Abstract
The health of the periodontium including the soft tissues –gingiva and periodontal
ligament; and the hard tissues –cementum and alveolar bone is of key importance in
the overall homeostasis of the dentition. Injury to the periodontal tissues in any form
such as microbial, physical, thermal, chemical, mechanical, occlusal and habitual
injury affects the harmony of the periodontal attachment apparatus thereby altering
the entire functioning of the dentition. The type of tissue damage when trauma is
unintentional and iatrogenic tends to be acute and self-limiting. On the other hand,
mechanical and occlusal forces could result in chronic damage. This book chapter
provides a review on the various forms of non-microbial trauma to the periodontal
tissues, their clinical manifestations and its management.
Keywords: periodontal trauma, gingival trauma, chemical injury, trauma from
occlusion, iatrogenic trauma
1. Introduction
A traumatic dental injury represents acute transmission of energy to a tooth and its
supporting structures, which results in fracture and/or displacement of the tooth and/
or separation or crushing of the supporting tissues (gingival, periodontal ligament,
PDL and bone) [1, 2]. Dental injuries can be divided into different categories based on
their genesis, anatomy, pathology, or treatment implications (Figure 1) [3, 4].
1.1 Injuries to the hard dental tissues: pulp, periodontal ligament, alveolar
process and supporting tissues
1.1.1 Crown-root fracture
A fracture involving enamel, dentin and cementum. It may or may not expose the pulp.
1.1.2 Root fracture
A fracture involving dentin, cementum and the pulp. Root fractures can be further
classified according to displacement of the coronal fragment.
1

1.1.3 Fracture of the alveolar socket wall
A fracture of the alveolar process which involves the alveolar socket.
1.1.4 Fracture of the alveolar process
Fracture of the alveolar process that may or may not involve the alveolar socket.
1.1.5 Concussion
An injury to the tooth- supporting structures without abnormal loosening or dis-
placement of the tooth, but with marked pain to percussion.
1.1.6 Subluxation (loosening)
An injury to the tooth-supporting structures resulting in increased mobility, but
without displacement of the tooth.
1.1.7 Extrusive luxation (peripheral dislocation, partial avulsion)
Partial displacement of the tooth out of its socket.
1.1.8 Lateral luxation
Displacement of the tooth in a direction other than axially. Displacement is
accompanied by comminution or fracture of either the labial or the palatal/lingual
alveolar bone.
1.1.9 Intrusive luxation (central dislocation)
Displacement of the tooth into the alveolar bone. This injury is accompanied by
comminution or fracture of the alveolar socket.
Figure 1.
Traumatic injuries to the periodontal tissues.
2
Dental Trauma

1.1.10 Avulsion (exarticulation)
The tooth is completely displaced out of its socket.
1.1.11 Abrasion
A superficial wound produced by rubbing or scraping of the skin or mucosa
leaving a raw, bleeding surface.
1.1.12 Contusion
A bruise without a break in the skin or mucosa. Subcutaneous or submucosal
haemorrhage in the tissue. A contusion may be isolated to the soft tissue but may also
indicate an underlying bone fracture.
1.1.13 Laceration
A shallow or deep wound penetrating into the soft tissue, usually produced by a
sharp object. May disrupt blood vessels, nerves, muscles and involve salivary glands.
Most frequently seen in lips, oral mucosa and gingiva. More seldom the tongue is
involved.
1.1.14 Soft tissue avulsion
Avulsion (loss of tissue) injuries are rare but seen with bite injuries or as a result of
a very deep and extended abrasion.
2. Thermal traumatic injuries (TTI)
The use of overheated handpieces and ultrasonic scalers can iatrogenically result in
thermal traumatic injuries to the gingiva. Thermal burns, however, have been listed as
one of the potential side effects that could be brought on by using ultrasonic scalers
[5]. TTI can also be brought on by consuming unusually hot/cold meals or drinks.
However, persons with psychiatric illnesses have been documented to experience
severe cases of intraoral and laryngopharyngeal burn brought on by hot foods or
beverages [6]. Because the supporting periodontal tissue is unconstrained by space
and has a larger blood supply than the pulp, heat-generating devices are more likely to
cause a temperature increase in the periodontal ligament than the pulp [7].
3. Mechanical traumatic injuries (MTI)
Accidents, assaults, falls during play or sports, and convulsions can all lead to
mechanical traumatic injuries (MTI) to the gingival tissue. It has also been noted that
malocclusions such a deep bite or an enhanced overbite can harm the gingiva [8, 9].
Dental appliances that were manufactured incorrectly and defective dental restora-
tions might cause iatrogenic mechanical stress [10, 11]. MTI can also occur when one
bites or sucks on a fingernail or other hard, sharp object, improper flossing [12].
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Gingivitis artefacta are the most frequently described self-inflicted MTI to the gin-
gival tissue [13]. According to reports, gingivitis artefacta minor is more prevalent,
whereas gingivitis artefacta major is more severe and spreads to the periodontium’s
deeper tissues. In gingivitis artefacta minor, there is typically a previous source of
irritation, such as a habit of biting one’s fingers or eating foods that are abrasive. As a
result, the condition can be treated effectively by removing the irritant from its source.
On the other hand, gingivitis artefacta major requires specialised treatment approaches
because the condition may have an emotional and extraoral component [14].
Stewart and Kernohan [15] grouped gingival injuries resulting from self-inflicted
physical trauma into three categories: Type A injuries are those that are added on top
of pre-existing lesions (or irritations) where the patient continues to cause harm to the
area, Type B injuries are those that are caused by habits like fingernail biting or finger
sucking, and Type C injuries are those with unknown and/or complex etiologies that
are typically brought on by emotional disturbances [15]. Oral piercing is another MTI
to the oral soft tissues that is self-inflicted [16]. The prevalence of oral and peri-oral
piercings among young adults ranged from 0.8 percent to 12 percent, according to a
comprehensive review [17].
Oral and peri-oral tissues are perforated in order to place jewellery on various
facial features, including the tongue, lips, cheek, and labial frenum. However, com-
plications could develop after surgery [17–20]. In addition to increased plaque and
calculus production, gingival inflammation may also be one of the main post-
operative periodontal problems [17, 20]. Chronic bad oral hygiene, particularly in
people who smoke a lot, can lead to secondary post-operative periodontal problems.
Additionally, when the jewellery material is porous, there may be a change in the
bacterial population and a rise in the pathogenic potential of the periodontopathogens
bacteria leading to mucogingival defects and abscesses of the supporting tissues
[17, 20].
While the only reasons for getting an oral piercing may be a trend, group identifi-
cation, attractiveness, other types of self-inflicted MTI to the gingival tissue may be
caused by potentially dangerous oral behaviour [16, 21]. Neuroses, occupational
habits, and other habits were used to categorise these oral behaviour [22]. Neuroses
include biting the lips, cheeks, pencils, pens, and fingernails. Occupational habits
include holding nails in the mouth by upholsterers, carpenters and biting thread by
tailors. Miscellaneous habits include smoking pipes or cigarettes, thumb sucking,
mouth breathing, and using the wrong toothbrushing technique [22].
3.1 Clinical presentations and management of trauma to the gingiva
The numerous factors already mentioned lead to a wide range of potential clinical
manifestations. Depending on the unique characteristics of each instance, the history
elicited will vary from case to case. Patients who engage in self-harming behaviour
may have a history of continuous gingival irritation, which leads to picking or
scratching of the gingiva, as well as a history that may point to an emotional disorder
or psychological imbalance [13, 14, 23]. A history may also indicate long-standing
behaviour like compulsive toothbrushing, digit sucking, or biting on potentially
harmful things, as well as interaction with other potentially harmful mechanical,
chemical, or thermal objects.
When examined, there may be significant ulcerative lesions affecting the lips,
tongue, and gingival oral mucosa in addition to intense burns, scorching, and bleeding
[13]. The ulcer may occasionally appear as coagulative necrosis coated in slough. In
4
Dental Trauma

factitious injuries, bite marks on the lips and nail marks on the gingiva can both be
seen [14]. Usually, there is gingival recession, which can be severe and widespread,
affecting numerous teeth. Depending on the affected location, mouth opening may be
restricted and chewing may be challenging. It’s possible that there is not any labora-
tory or radiologic proof of an underlying systemic illness.
Complete re-epithelialization of the gingival tissue, complete or considerable root
covering, and an expansion of the zone of keratinized gingiva are the treatment’s
primary objectives [24]. Additionally, it’s crucial to stop a recurrence by getting rid of
any identified causal factors. Therefore, the first step in treatment is to cure any
improper oral hygiene habits and get rid of any dangerous substances. To eliminate
the accumulated plaque, gentle mechanical oral hygiene techniques are implemented;
if necessary, this may be done with topical or local anaesthetic medications. In the
beginning, regular brushing in the other areas may be continued while chemical
plaque management is advised as the only oral hygiene measure in the affected area.
Two times a day, chlorhexidine mouthwash may be recommended. Warm saline
mouth wash and Betadine has also been found helpful [25, 26].
Supportive symptomatic care is provided to preserve the patient’s overall health,
and this includes the recommendation of a non-spicy, soft food, as well as multivita-
mins and topical analgesics such triamcinolone acetate and benzocaine to ease dis-
comfort [26]. Topical steroid triamcinolone should be administered in conjunction
with carboxymethyl cellulose in cases of significant tissue injury [25]. To eliminate the
infection, antibiotic treatment could be required. Factitious situations may necessitate
professional psychiatric care, which may involve the use of antidepressants and/or
antianxiety medications [14]. A significant loss of gingival tissue may need the use of a
free gingival graft to repair the damage [12].
3.2 Trauma to periodontal ligaments
The soft complex connective tissue that serves as an interface between the cemen-
tum covering the roots and the inner wall of the alveolar bone is vascular, highly
cellular, and specialised [27, 28]. The periodontal ligaments may become
overextended and inflamed in circumstances where there are too many bilateral
opposing vector stresses. The term “sprained tooth syndrome”is sometimes used to
describe this (STS.). This can happen when someone unintentionally bites down on a
hard object, when a tooth is improperly or excessively filled, when teeth are drifting,
or in cases of sinusitis or allergies. The aberrant outward lateral pressure from the
tongue to the teeth that results in temporary orthodontic pressure and outer move-
ment outward and abnormal tooth mobility has been linked to STS in cases of upper
respiratory tract infection.
Every effort must be made to avoid iatrogenic forms of trauma to the periodontal
ligament because its attempts at healing may have unpredictable outcomes. Periodon-
tal ligament may heal favourably without resorption or with repair related surface
resorption and it can also heal unfavourably with osseous replacement resorption
(ankylosis) or with inflammatory resorption [29].
Treatment for sprained teeth focuses mostly on reversing the opposing vector forces
that caused the strain. A broken tooth, on the other hand, can wait a few days to see
whether it heals by itself. Rest is necessary for the treatment of a sprained tooth because
using the injured teeth for chewing and speaking causes further discomfort [23].
Radiographic evaluation, tooth realignment, surgical or orthodontic extrusion of
the afflicted tooth, splinting, occlusal correction, antimicrobial therapy, endodontic
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treatment, and follow-up are all necessary for the management of invasive luxation
[30]. All of the aforementioned procedures are likewise necessary for lateral and
extrusive luxation, with the exception of tooth extrusion. While concussion simply
needs a radiographic evaluation and follow-up to monitor the tooth over time, sub-
luxation only needs a radiographic evaluation, splinting, and follow-up [30]. Only if
there is no contamination and the tooth was transported and stored in a manner that
ensured the health of the periodontal ligaments could an avulsed tooth be successfully
reimplanted. After reimplantation, the tooth will be immobilised, and endodontic
procedure may be initiated later [31].
It has been established that higher temperatures have detrimental effects on the
periodontal ligament [32]. Clinical signs of protein denaturation in periodontal liga-
ments, disruption of the blood supply to the periodontal ligament, and tooth ankylosis
may result from thermal injury to periodontal disorders [32, 33]. Thermal injuries are
mostly managed by prevention. Using enough cooling water for tooth preparation or
when dry cutting is required, applying gentle pressure, and limiting the bur-contact
duration to less than 20 seconds at a time are just a few of the clinical recommendations
that have been made to help prevent thermal injuries during dental treatment [17].
4. Chemical burns
4.1 Classification
Chemical burns majorly occur by the action of irritants on the mucosal tissues
(Table 1). Mucosal damage caused by chemical burns could be
1.Iatrogenic as in irrigation performing endodontic procedures
2.Inappropriate application of chemicals and non-therapeutic agents by the
patients.
4.1.1 Alendronate
It is a constituent of the diphosphonate family and has been used to treat osteopo-
rosis caused on by glucocorticoids as well as a number of other bone disorders.
Alendronate may have side effects, such as esophagitis on the mucosa of the upper
Dental materials Medications Nontherapeutic agents Drugs
•Arsenic [34]
•Calcium hydroxide [35, 36]
•Cavity varnish [37]
•Chromic acid [38]
•Dentine-bonding agent [39]
•Ferric sulfate [40]
•Formocresol [41]
•Iodine [42]
•Paraformaldehyde [42]
•Eugenol [43, 44]
Alendronate [45, 46]
Aspirin [47, 48]
Chlorpromazine [49]
Promazine [49]
Tetracycline
hydrochloride [50–52]
•Arrack [53]
•Battery acid [49]
•Denture cleansers
[54, 55]
•Garlic [56]
•Gasoline [57]
•H
2
O
2
[58, 59]
•Minard’s Liniment [60]
•Mouthwashes [61–64]
•NaOCl [65, 66]
Amphetamine
[67] Cocaine
[68–72]
MDMA [72]
Table 1.
Aetiology for chemical burns of the oral mucosa.
6
Dental Trauma

aerodigestive tract is the most typical one. Patients must be instructed to take the drug
with a glass of water, not to chew or suck the tablet, and to stand up straight for
around 30 minutes in order to avoid this side effect [45].
4.1.2 Aspirin
Acetylsalicylic acid, popularly known as aspirin, is a frequently prescribed drug for
the treatment of pain, fever, and inflammation. Aspirin and its derivatives, commonly
prescribed for alleviating oral and tooth pain, are responsible for the majority of
chemical burn incidences when they are sucked, administered as a gel, mouthwash,
powder, or as a tablet near to a sore tooth in an effort to relieve pain [73]. When
aspirin is applied to the mucosa for a long time, it exerts a caustic impact. A cell-
mediated response might result in an aphthous-like ulceration of the oral mucosal
layer due to the acidic nature of acetylsalicylic acid (pH 3.5–5.0) [47]. Further, aspi-
rin’s organic and inorganic components adhere to the oral cavity epithelium, causing
denaturation and coagulative necrosis [48].
4.1.3 Calcium hydroxide
Calcium hydroxide (Ca(OH)
2
) is frequently used in the field of endodontics due to
its notable characteristics of mineralisation induction and promotion, antimicrobial
capabilities, and necrotic material disintegration. Its adverse effects include cellular
damage, epithelial damage, necrosis of bone, and cytotoxicity.
4.1.4 Cocaine (benzoylmethylecgonine) (C
17
H
21
NO
4
)
It is an alkaloid obtained from Erythroxylum coca leaves. Europe has the second-
highest prevalence of cocaine use, with about 910,000 persons taking it. Cocaine’s
nonionized form diffuses across the lipid membranes of neurons. It transforms back
into the active cationic form in the axoplasm, binds to the sodium channels, and stops
the action potential from forming, producing a reversible anaesthetic effect [72].
4.1.5 Denture cleansers
Patients clean their dentures with a variety of homemade and store-bought
cleaners. Potassium monopersulfate, sodium perborate, sodium carbonate, surfactant,
sodium bicarbonate, citric acid, and an additive are ingredients in immersion-type
denture cleaners sold as tablets or powders. The perborate breaks down into an
alkaline peroxide solution when the tablet or powder is dissolved in water, and it
continues to break down to release oxygen. Debris is mechanically loosened by this
process. The newly formed oxygen may interact with substances required for cell
metabolism, interact with cell structures, or accelerate metabolism at the expense of
cell growth [54].
4.1.6 Eugenol
Eugenol has a scorching flavour, a strong carnation aroma and is a pale yellow
liquid. It has been included in a number of products, including dental cement, end-
odontic sealants, impression pastes, and dressings for dry sockets. Unprocessed euge-
nol is combined with zinc oxide to create zinc oxide-eugenol, which demonstrates a
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combination of physical and therapeutic qualities and can be used as a foundation
material, root canal filler, and temporary restorative material. The tissue reaction
caused by eugenol’s byproducts might range from mild local allergic reactions to the
uncommon catastrophic anaphylactic reactions [43, 44].
4.1.7 Formocresol
Ever since Buckley introduced formocresol to dentistry in 1904, it has been fre-
quently utilised in paediatric dentistry. In pulpotomy, formocresol is employed as a
medication because of its ability to repair tissue when exposed to pulp. In the field,
there has been a lot of concern stated and debated regarding the safety of using
formocresol. There have been reports of widespread necrosis of soft tissues in the oral
cavity due to improper formocresol use.
4.1.8 Garlic burn
Allium sativum, also known as garlic, is regarded as a valuable herbal remedy and
has been used for ages to treat a variety of illnesses. Additionally, studies have indi-
cated that garlic has fibrinolytic, antihypertensive, and lipid-lowering properties. It
has antiviral, antifungal, and antibacterial effects. Garlic’s most frequent adverse
reactions are nausea, diarrhoea, heartburn, and digestive distress. Rhinitis, asthma,
anaphylaxis, contact dermatitis, and pemphigus are manifestations of garlic allergy. In
1987, Parish et al. reported the first instance of garlic burn. Garlic’s precise ingredients
that cause skin lesions are still a mystery. Allicin, diallyl disulfide, and allyl propyl
disulfide are presumed to be the causes of chemical burn [56].
4.1.9 Hydrogen peroxide
The method by which H
2
O
2
exerts its antimicrobial effects is owing to the release
of nascent oxygen, which is harmful to anaerobes. The action of H O on bacterial cell
wall debridement is the other antibacterial property mechanism [58]. H2O2 is used in
mouthrinses (1–3%) and as a bleaching agent (3–5%) among other applications. Oral
use of solutions containing 3 percent H2O2 may result in nausea, minor mucosal
irritability, and burns to the mouth, throat, oesophagus, and stomach. Ingestion of
greater concentrations (>10 percent) can have more hazardous side effects, like burns
to the gut mucosa and mucous membranes [59]. It is because it can directly react with
proteins to create conjugates and reactive haptens that it triggers localised hypersen-
sitivity reactions to oral mucosa, known as “contact stomatitis,”and to the dermis,
known as “contact dermatitis,”in lower doses [43, 44].
4.1.10 Sodium hypochlorite
NaOCl is a transparent, straw-coloured solution with 5% accessible chlorine in it. It
creates chloramines upon ionisation, those are providing the antibacterial properties.
The drawback of NaOCl is that if it is used outside of a root canal, it can lead to soft-
tissue irritation and necrosis [40]. It reacts with the oral mucosa’s proteins and lipids,
which could cause subsequent infections [42]. NaOCl should be used as an irrigant in
the root canal at a concentration of between 0.5 percent and 5.2 percent. Localised or
widespread tissue necrosis has resulted from NaOCl’s extension into the periradicular
tissue. In the epidermis and subcutaneous tissues, a significant acute inflammatory
8
Dental Trauma

response causes rapid intraoral and extraoral tissue swelling. It causes acute sinusitis if
it spreads into the maxillary sinus [65].
4.2 Clinical features
The degree of tissue damage, the causative agent’s destructive qualities, and the
method of application all affect how chemical burns look clinically [56]. Clinical
lesions can range in severity from mild to severe depending on the substance used, pH
level, chemical agent concentration, quantity used, method and length of tissue con-
tact, depth of tissue penetration, and mechanism of action. Chemical burns on the
mucosa manifest as diffuse erosive lesions that can range in severity from conven-
tional desquamation to full mucosal detachment with penetration into the submucosa
[50]. Chemical exposure causes changes in the vascularity, colour, texture, and con-
sistency of the tissues. The general chemical burn appears as a shallow, wrinkled
lesion that ranges in colour from white to yellow.
The characteristics of coagulative necrosis are seen through histopathological anal-
ysis [56]. Salivary gland duct involvement may result in temporary obstructive sali-
vary glanditis, but subsequent ductal opening scarring may result in chronic
obstruction. Excision of the duct or gland may be necessary in cases of chronic
sialadenitis [41]. Chemical burns frequently have a localised distribution and are not
always restricted to the anatomic distribution of the masticatory mucosa [74].
4.2.1 Alendronate
Clinically, it may present as ulcers located on the palate, tongue, and lower lip. The
ulcers cause intense pain [45].
4.2.2 Aspirin
It causes a localised white scurf with a reddened and thickened border [47, 73],
while chromic acid produces a characteristic yellow lesion with a flat border [74].
4.2.3 Calcium hydroxide
Patients present with a swollen lip and mucosa, no history of pain and an extensive
necrotic zone on gingiva with perforation [37].
4.2.4 Cocaine
Lesions develop at the site of application. A white slough, which could easily be
removed, showing underlying ulceration and erythema seen on the gingiva. Patients
may report painful, retracted gingiva [72].
4.2.5 Denture cleansers
Denture cleansers on chewing and swishing it around the mouth show burning
sensation, swelling of the floor of the mouth and the salivary glands, inflammation of
the soft palate and tongue. The orifices of the submandibular glands can also present
with red and ulcerated with sloughing of the mucosa. There have been several reports
of upper digestive tract injury associated with the accidental ingestion of denture
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cleansers. Furthermore, it can depict as diffuse erosive lesions ranging from simple
desquamation to complete obliteration of the oral mucosa with extension past the
basement membrane into the submucosa. On ingestion, it also presented with
perioral, glossal, and laryngeal edema and respiratory stridor leading to death. On
autopsy, it showed extensive hemorrhagic bronchopneumonia and widespread gas-
trointestinal ulceration [54].
4.2.6 Eugenol
Eugenol burns usually presents with burning sensation and pain over the exposed
area. Patient also complains of itching sensation. Intraoral examination may reveal
allergic reaction “contact stomatitis”over the gingiva and adjacent mucosa [43].
4.2.7 Formocresol
Formocresol burns usually presents with pain and swelling on the exposed area.
Extensive ulcerative lesion extending along exposed surface will appear like
coagulative necrosis covered by slough. Patient also presents with symptoms of
restricted mouth opening and reduced food intake [41].
4.2.8 Garlic
Garlic burns are clinically manifested as an area of slough and mucosal ulceration
extending along the area of placement. The lesion may be painful on palpation [56].
4.2.9 Hydrogen peroxide
H
2
O
2
burns present as extensive areas of ulceration and erythema involving the
alveolar mucosa and the marginal and attached gingival regions. Focal areas of
ulceration and sloughing with necrosis of the surface layers of the epithelium may be
seen [59].
4.2.10 Sodium hypochlorite
NaOCl burns manifest clinically as soft-tissue inflammation and necrosis if it is
expressed outside the confines of root canal. The swelling may be edematous, hemor-
rhagic, or both and may extend beyond the region that might be expected with an
acute infection of the affected tooth. The sudden onset of pain is a hallmark of tissue
damage and may occur immediately or be delayed for several minutes or hours.
Associated bruising and ecchymosis of adjacent tissues may occur due to bleeding into
interstitial spaces [65].
4.2.11 Tetracycline hydrochloride
Tetracycline hydrochloride burns are manifested as loosely adherent yellowish
white slough on gingiva. It may show erythematous margins, and patients complain of
severe pain [38].
10
Dental Trauma

4.3 Treatment
A correct clinical history must be obtained in order to diagnose a chemical burn
because the patient may not be aware of the relevance of these potentially harmful
chemicals [41]. Early patient screening and prompt implementation of therapeutic
measures will guarantee a speedy recovery and potentially stop additional mucosal
damage [74].
The reason might be entirely eliminated by just getting rid of the agent perma-
nently. Multiple irrigations with sterile water or betadine. If needed, analgesics, corti-
costeroids and benzocaine applied topically. Dietary supplements in the form of
multivitamins would accelerate the recovery. When necessary, medications to stop
secondary infections. Encourage the patient to follow a soft, chilled diet devoid of
spices for a week. After a week, recall.
5. Occlusal trauma
The role of occlusion and how it interacts with the periodontium has been exten-
sively researched. Occlusal trauma, also known as traumatism or trauma from occlu-
sion(TFO), is an injury that causes tissue alterations inside the attachment apparatus
as a result of occlusal force. Clinicians’knowledge of the impacts of damaging occlusal
forces and the periodontium’s adaptive, reparative, and destructive responses is
mostly based on retrospective observations of human postmortem specimens and
laboratory animal investigations. Unfortunately, there is a scarcity of scientific infor-
mation from well-controlled prospective trials in people, making it difficult to com-
prehend this intricate host interaction [75].
5.1 Definitions
•Trauma from occlusion was defined by Stillman [76] as “a condition where injury
results to the supporting structures of the teeth by the act of bringing the jaws
into a closed position.”
•According to Carranza (AAP, 1986) [77], when occlusal forces exceed the
adaptive capacity of the tissues, tissue injury results, the resultant injury is
termed trauma from occlusion.
•WHO in 1978 defined trauma from occlusion as “damage in the periodontium
caused by stress on the teeth produced directly or indirectly by teeth of the
opposing jaw.”
•In the “Glossary of Periodontic Terms”(AAP 1986); occlusal trauma was defined
as “An injury to the attachment apparatus as a result of excessive occlusal force”.
5.2 Glickman’s concept
Glickman asserted that a plaque-associated gingivitis can be altered by abnormal
occlusal forces [28]. That suggests that the Periodontal apparatus is gradually being
affected by these forces. The response of a traumatised tooth with subgingival plaque
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is different when compared to tissues around a tooth without deliterious forces. He
suggested that there exists two distinct zones (Figure 2).
Zone of irritation: The interdental gingival papillae and marginal gingiva make up
the zone of irritation, which is restricted by the gingival fibres. In this area, local
irritations cause inflammation. The most harmful effects are epithelium ulceration,
suppuration, and gingival connective tissue degeneration and necrosis. Even (hori-
zontal) bone loss is could occur [78].
Zone of co-destruction: This contains the alveolar bone, the root cementum, and the
periodontal ligament. Transseptal collagen fibre bundles (interdental and
dentoalveolar) demarcate it coronally. The formation of an angular bony defect may
result from the progression of inflammation from the zone of irritation directly into
the periodontal ligament [79].
5.3 Adaptive capacity of the periodontium to occlusal forces
Adaptive capacity varies from person to person and from time to time within the
same person. The size, direction, duration, and frequency of occlusal forces on the
periodontium all determine their effect (Figure 3).
When occlusal stresses are raised in amplitude, the periodontium responds with
1.The periodontal ligament space is being widened.
2.The quantity and width of PDL fibres significantly increased.
3.An increase in the alveolar bone density [76].
The reorientation of stress and strains inside the periodontium is caused by chang-
ing the direction of occlusal pressures. The main fibres are positioned along the long
Figure 2.
Spread of inflammation in TFO-Glickman Concept-zone of irritation, zone of co-destruction [28].
12
Dental Trauma

axis of the tooth to best tolerate occlusal stresses. The periodontium is more prone to
be injured by lateral (horizontal) and torque (rotational) forces.
5.4 Trauma caused by occlusion
5.4.1 Acute vs chronic TFO
5.4.1.1 Acute TFO
Acute TFO is a type of TFO that occurs suddenly. It is usually caused by
1.Biting down on a hard object causes an abrupt occlusal impact.
2.Prosthetic appliances that interfere with or change the direction of occlusal force
are known as restorations [80].
Characteristics: Tooth pain, percussion sensitivity, and increased tooth movement.
Consequence: If the force is removed by a shift in the position of the tooth or by
wearing away or correcting the restoration, the injury heals and the symptoms disap-
pear if not, injury may worsen, leading to necrosis and the creation of a periodontal
abscess.In some instances, it may persist as a symptomless chronic illness or end up in
formation of cemental tears.
5.4.1.2 Chronic
It’s more common and has a higher clinical impact. Rather than developing as a
result of acute TFO, it develops as a result of gradual alterations in occlusion caused by
Figure 3.
Response to occlusal forces (a) normal periodontium can withstand normal occlusal forces, and (b) excessive
occlusal forces causes damage to the periodontium [28].
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tooth attrition combined with parafunctional habits like as bruxism and
clenching [81].
Characteristics: Increasing mobility is one of the clinical characteristics.
5.4.2 Primary vs secondary TFO
5.4.2.1 Primary TFO
Occlusion trauma is the key etiologic cause in periodontal deterioration, and
occlusion trauma is the only local modification to which a tooth is susceptible. Inser-
tion of a “high filling”insertion of a prosthetic replacement that places excessive
forces on the abutment and antagonist teeth drifting movement or extension of teeth
into spaces created by unreplaced missing teeth drifting movement or extension of
teeth into functionally unacceptable positions drifting movement or extension of teeth
into spaces created by unreplaced missing teeth.
The amount of connective tissue attachment is not altered by original trauma, and
pocket development is not initiated. This is likely because the supracrestal gingival fibres
are unaffected, preventing the junctional epithelium from migrating apically [81].
5.4.2.2 Secondary TFO
Occurs when bone loss caused by marginal inflammation impairs the tissues’adap-
tive capacity to bear occlusal stresses. This changes the leverage on the remaining tissues
by reducing the periodontal attachment area. The periodontium becomes more prone to
injury, and occlusal forces that were previously tolerated become traumatic [82].
5.5 Tissue response to increased occlusal forces
5.5.1 Effect on periodontal ligament
5.5.1.1 Stage I: injury
Excessive occlusal forces result in tissue destruction. The periodontium is modified
to buffer the impact of the offending force if it is chronic. The ligament widens at the
expense of the bone, resulting in angular bone defects and loose teeth without peri-
odontal pockets. The fulcrum or axis of rotation, which in single-rooted teeth is
located in the junction of the middle third and the apical third of the clinical root,
rotates under the stresses of occlusion. On opposite sides of the fulcrum, pressure and
tension are created. These various lesions may coexist in the same region if jiggling
pressures are applied.
Slightly too much pressure induces alveolar bone resorption, resulting in a widen-
ing of the periodontal ligament space. Blood vessels become more numerous and
smaller in places with increased pressure.
Excessive tension promotes elongation of the PDL fibres and alveolar bone oppo-
sition. The size of blood vessels expands in locations of high strain.
Greater pressure caused a gradation of alterations in the periodontal ligament,
beginning with the compression of the fibres, resulting in areas of hyalization. Fol-
lowing insult to the fibroblasts and other connective tissue cells, portions of the
ligament undergo necrosis.
14
Dental Trauma

Within 30 minutes, blood vessels appear to be constricted and stagnant with
erythrocytes, which begin to fragment at the end of 3 hours.
Disintegration of the blood vessel walls and discharge of the contents into the
surrounding tissue occurs between 1 and 7 days.
Resorption of alveolar bone and root surface also occurs.
Severe strain causes periodontal ligament expansion, thrombosis, bleeding, ripping
of the periodontal ligament, and alveolar bone resorption.
Necrosis of the periodontal ligament and bone occurs when there is enough pressure
to drive the tooth against the bone. Undermining resorption occurs when bone is
resorbed from viable periodontal ligament close to necrotic areas and from marrow gaps.
The furcations are the parts of the periodontium that are most vulnerable to harm
from high occlusal stresses. When the periodontium is injured, there is a temporary
decrease in mitotic activity and fibroblast proliferation, as well as in the creation of
collages and bone. After the forces have dissipated, these restore to normal levels.(6).
5.5.1.2 Stage 2
Repair TFO induces greater reparative activity in the typical periodontium, which
is always occurring. In order to heal the injured periodontium, the damaged tissues are
eliminated and new connective tissue cells and fibres, bone, and cementum are cre-
ated. The body seeks to reinforce the thinned bony trabeculae with new bone when
bone is damaged by high occlusal forces. This attempt to compensate for missing bone
is known as buttressing bone growth, and it is a key part of the TFO recovery process.
Within the jaw, buttressing bone production occurs when endosteal cells deposit new
bone, which repairs the bony trabeculae and minimises the size of the marrow gaps.
On the bone, buttressing bone development can also occur [77].
5.5.1.3 Stage3: periodontal adaptive remodelling
If the repair process is unable to keep up with the occlusion’s damage, the
periodontium is reformed in an attempt to establish a structured relationship in which
forces are no longer harmful to the tissues. This causes a thicker periodontal ligament
with a funnel-shaped crest, as well as angular flaws in the bone and no pocket
formation. The teeth that are implicated grow loose. There has also been evidence of
increased vascularization [83].
Apart from occlusal forces, the forces such as orthodontic forces, jiggling forces
etc. also play a role in remodelling (Figures 4–7).
5.5.2 Pathologic tooth destruction
Each tooth is expected to have a force threshold at which an occlusal traumatic lesion
in the attachment apparatus occurs. This threshold force may be extremely strong, but it
may be greater than a tooth’s resistance to wear. Wear on the occlusal and incisal
surfaces. As a result of the trauma, cartilage-like material might form in the periodontal
ligament spare. It has also been demonstrated that erythrocytes can form crystals [84].
5.5.3 Soft-tissue effects
Because occlusal forces only affect the attachment apparatus of the periodontium,
they have no effect on the supracrestal soft tissues of the periodontium. Excessive
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force on a tooth does not harm the attachment of gingival soft tissues coronal to the
bone (the C.T. attachment and JE). Pocketing and recession are marginal disease
entities (occlusal trauma is not a marginal illness) that are initiated at the gingival
margin by plaque-related pathosis [84]. As a result of the trauma, cartilage-like mate-
rial might form in the periodontal ligament spare. It has also been demonstrated that
erythrocytes can form crystals.
5.6 Clinical and radiographic
5.6.1 Signs
Increased tooth mobility is the most prevalent clinical symptom of periodontal
damage. Destruction of PDL fibres increases mobility in the early stages.
Figure 5.
Response to orthodontic forces—results in areas of pressure and tension [28].
Figure 4.
Physiological response, intra-socket adaptation of the tooth to the normal occlusal forces [28].
16
Dental Trauma

Accommodation of PDL to force widening of PDL to promote mobility is not patho-
logic in the ultimate stage. It becomes pathogenic when it gets worse over time [85].
5.6.2 Radiographic features
The following radiographic features of TFO may be seen:
1.Wider periodontal space, often accompanied with thickening of the lamina dura
along the lateral face of the root, in the apical region, and at bifurcation points.
Figure 6.
Response to excessive occlusal forces by a compromised periodontium results in tooth mobility [28].
Figure 7.
Periodontal response to jiggling forces results in multiple areas of pressure and tension causing extensive tissue
damage [28].
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These changes may be due to thickening and strengthening of the periodontal
ligament and alveolar bone as a positive reaction to increasing occlusal stresses,
and so are not necessarily detrimental.
2.Interdental septum damage that is “vertical”rather than “horizontal.”
3.Alveolar bone radiolucence and condensation.
4.Resorption of the roots.
5.7 Traumatic lesions can be reversed
Occlusion-related trauma is reversible. When the artificially induced force is
removed from experimental animals, the tissues begin to heal. TFO, on the other
hand, does not always fix itself (by going away or intruding), hence it is not always
transitory or of minor clinical relevance. For repair to take place, the injurious force
must be alleviated. Periodontal injury persists or worsens in people if the teeth are
unable to escape or adapt to severe occlusal force. Inflammation may make this
reversibility more difficult [86].
Occlusal trauma cannot be identified without a block section biopsy since TFO is
characterised and diagnosed based on histologic abnormalities in the periodontal
supporting system. Because this is manifestly unfeasible in periodontics therapy, the
doctor must rely on clinical symptoms of possible occlusal trauma. These are some of
the indicators:
1.Fremitus
2.Flexibility (progressive)
3.Occlusal inconsistencies
4.Additional signs such as wear facets.
5.Migration of teeth
6.Broken tooth/teeth
7.Sensitivity to heat
The method in which the teeth make contact can also be used to assess the
occlusal relationship of the teeth. This is accomplished by gradually retruding the
patient’s jaw (retruded occlusion/centric relation) and softly closing the patient’s
mouth, until the first tooth-to-tooth contact is made After that, the patient is asked to
close their mouth to a comfortable intercuspated position (central occlusion/habitual
occlusion). The centric relation to centric occlusion slide (or CR/CO shift) is the
distance the patient moves from the retruded position to the greatest intercuspation. It
is possible to capture both the initial contact point and the approximate amount of
slide. Tooth interactions are also documented in eccentric jaw positions (i.e. lateral
and protrusive jaw positions). Contacts are frequently noticed and may also be
18
Dental Trauma

documented with a thin inked silk ribbon or Mylar film to record tooth contact during
an examination.
5.8 Occlusal therapy
After nonsurgical treatment is completed, occlusal treatment is frequently carried
out. When the periodontal supporting structures become inflamed, the teeth’s mobil-
ity often increases. The periodontal ligament may be inflamed, resulting in more
movement. When inflammation is under control, teeth are less dynamic, resulting in a
more stable occlusal association after occlusal therapy. To make the patient more
comfortable, occlusal treatment may be recommended as the first stage of periodontal
therapy in these circumstances [87]. If occlusal therapy is started before inflammation
is controlled, it will almost certainly be essential to do additional occlusal treatment
once the inflammation has been controlled. Prior to starting treatment, the patient
should be advised about this.
There are two primary techniques to occlusal therapy.
(1) Using a bite device (bite guard) and/or (2) Altering the occlusal connections
between the teeth to adjust the occlusion.
Orthodontic therapy or selective occlusal surface grinding can permanently alter
the relationship between teeth.
Coronoplasty/Selective grinding- Selective grinding is a process that involves
modifying the occlusal surfaces of teeth to improve the overall contact pattern. Tooth
structure is eliminated selectively until the reshaped teeth make contact in a way that
achieves the treatment goals [88].
The following are some of the goals of coronoplasty that have been met as a
consequence of occlusal adjustment:
1.Afferent impulse pattern and intensity change.
2.Excessive tooth movement is reduced.
3.To provide occlusal stabilisation, multiple simultaneous contacts are dispersed
across the occlusal scheme.
4.A beneficial adjustment in chewing or swallowing habits.
5.Mandibular movement patterns in multiple directions.
6.Occlusal stresses on implants are verticalized.
The occlusion is generally modified once gingival inflammation and periodontal
pockets have been removed in treatment planning for the following reasons:
1.Evidence of aetiology and healing features suggests that coronoplasty effects are
incomplete unless inflammation is addressed initially.
2.When the inflammation is gone, the teeth frequently shift back to their original
place. As a result, if the occlusion is modified before the inflammation has
subsided, it may need to be corrected again once gingival health has been restored.
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This treatment sequence is altered if the following conditions are met:
a. In infrabony pockets, where excessive occlusal stresses are vital in deciding the
pattern of osseous defects, the occlusion is altered to give best conditions for
development of bony flaws.
b. Bacterial plaque is often thought to be the cause of periodontal disease. It’s
possible that a localised mechanism interacts with bacterial plaque when high
occlusal stresses are applied. It’s also possible that high occlusal forces produce
an environment in which bacterial plaque’s harmful effects are amplified, or
that there’s a whole new process at work that has not been discovered yet.
Treatment of the occlusion to reduce occlusal interferences, in combination
with other modalities of periodontal treatment, may, however, have a positive
impact on the progression and treatment of periodontal deterioration. Excessive
occlusal forces is a risk factor that can be reduced using current clinical tools, as
can any risk factors that can be reduced using current clinical tools.
6. Food impaction
Food impaction is the forceful wedging of food into the tooth supporting tissues by
occlusal force. It may occur interdentally or in the buccal and palatal surfaces. It is
perceived to be the most common cause of gingival and periodontal inflammation. If
left unidentified it could alter the pathogenesis and leads to adverse therapeutic out-
comes [89]. Food is typically prevented from being forced into the mouth by the
integrity and placement of the proximal contact, the contour of the marginal ridge and
developing grooves, and the contour of the lingual and facial surfaces (Figure 8).
6.1 Types of food impaction
6.1.1 Vertical impaction
A. Open contacts
B. Irregular marginal ridge
Figure 8.
Food impaction—wedging of food into the deeper tissues by plunger cusp [89].
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Dental Trauma

C. Plunger cusp: Cusp that tend to forcibly wedge food interproximal region of
opposing teeth.
6.1.2 Horizontal/lateral food impaction
Periodontal disease/gingival recession results frequently in enlargement of gingival
tissues in the interdental embrasure area which is subjected to forces from the lips,
cheek and tongue resulting in food lodgment in the proximal areas.
6.2 Management
6.2.1 Periodontal treatment
Curettage, interproximal brushing, flossing, and scaling.
6.2.2 Occlusal adjustment
Plunger cusp—Go around these angular plunger cusp peaks. The palatal cusp of
maxillary teeth, the buccal cusp of mandibular teeth, and occasionally the palatal
incline of the maxillary buccal cusp and the buccal incline of the lingual cusp are the
functional cusps that make up these plunger teeth. Additional advantages could result
from reviewing the study cast to assess the relationship between the lingual cusps.
Equalise the marginal ridges’occlusal heights.
7. Iatrogenic injury
In 1912, Black recognised the strong connection between iatrogenic causes and
periodontal degeneration [90]. It has been well established for many years that dental
restorations and periodontal health are related. The position of the restoration in
relation to the gingival margin, the presence of overhangs, the presence of marginal
leakage, the roughness of the surfaces, and the type of restorative material are a few
examples of the various aspects of the periodontal-restorative interaction that have
received attention in numerous studies [91]. The most consistent way that dental
restorations can harm marginal health is by increasing plaque formation, but over-
hanging metal restorations have also been linked to changes in the subgingival
microbiota, including an increase in potential periodontal pathogenic microflora [92].
The areas of restorative dentistry and periodontics that overlap are the marginal
periodontium. In contrast, special attention should be paid to how the periodontium
reacts to the irritants caused by negligent procedures, which might start or exacerbate
gingival inflammation already present. If the illness is not identified and treated in its
early stages, loss of periodontal support and subsequent tooth loss may follow. Partic-
ularly when they are subgingivally positioned, dental restorations or appliances are
usually linked to the development of gingival inflammation. This may be true for
orthodontic bands, crowns placed onlays, fillings, and subgingivally. By being posi-
tioned deep inside the sulcus or within the junctional epithelium, restorations may
have an impact on the biologic width. With apical migration of the junctional epithe-
lium and re-establishment of the attachment apparatus at a higher apical level, this
may encourage inflammation and loss of clinical attachment.
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7.1 Margins of restorations
The following characteristics of dental restorations and detachable partial dentures
are important for maintaining periodontal health:
1.Where the gingival margin should be placed for the restoration
2.The distance between the restoration’s edge and the unprepared tooth
3.The design of restorations
4.The occlusion
5.The restoration’s components
6.The practical restoration process
7.The removable partial denture’s design
When positioning the restorative margins, especially in the aesthetic zone where
the major treatment objective is to cover the junction of the margin with the tooth, the
biologic width information should be used. The placement of the restoration margin
depends greatly on:
1.Aesthetics.
2.The need for extra restorative retention.
3.The level of oral hygiene.
4.The person’s vulnerability to root caries.
5.The marginal gingiva’s susceptibility to irritants.
6.The marginal gingival’s morphological features.
7.The severity of gingival recession.
8.Significant cervical abrasion.
9.Dental restorations with overhanging margins.
Overhanging dental restoration margins increase the severity of periodontal
disease by changing the gingival sulcus’ecological balance to one that favours
the growth of disease-associated organisms (mostly gram-negative anaerobic
species) at the expense of healthy organisms (primarily gram-positive
facultative species) [93] and by preventing the patient’s access to remove
accumulated plaque.
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Dental Trauma

7.2 Placing the matrix/rubber dam
After cavity preparation, a correctly planned and contoured matrix needs to be
implanted so that it may be accurately adjusted to the margins without harming the biologic
width. For class II restorations, extra interdental wedge placements are necessary for a well-
contoured restoration, but they must be done carefully. To repeat proper form and avoid
intracrevicular overhangs, the matrix should be stiff and well-contoured (Figure 9).
7.3 Hypersensitivity to dental materials
Nonprecious alloys used in dental restorations have been linked to inflammatory
gingival reactions, according to reports [94]. Although the frequency of these events is
debatable [95], the reactions have typically been to alloys containing nickel. Rarely do
precious alloys cause hypersensitivity reactions, and these alloys offer a simple fix for
the issues with nonprecious alloys.
7.4 Marginal fit
Marginal fit has unmistakably been linked to the periodontium’s inflammatory
response. According to research, the degree of gingival inflammation might rise in
direct proportion to the degree of marginal opening [96]. Significantly open marins
(more than a few tenths of a millimetre) are capable of hosting huge numbers of
bacteria and may be the cause of the observed inflammatory response. However, the
periodontium is significantly more affected by the quality of the marginal finish and
the location of the margin in relation to the attachment than by the distinction
between a 20-m fit and a 100-m fit [97].
7.5 Crown contour
The preservation of periodontal health has been said to depend heavily on restora-
tion contours [98]. Access for hygiene is made possible by proper contour, which also
Figure 9.
Improper rubber dam placement can cause injury to the periodontal tissues.
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has the capabilities to create the ideal gingival form and has a pleasant visible tooth
contour in places that matter aesthetically.
Studies on both humans and animals conclusively show a link between gingival
inflammation and over-contouring, whereas under-contouring has no negative effects
on periodontal health [99]. Inadequate tooth preparation by the dentist is the most
frequent cause of over-contoured restorations, which compels the technician to create
a bulky restoration to make place for the restorative material. A flatter contour is
always acceptable in parts of the mouth where aesthetic concerns are not important.
8. Discussion
There is a potential risk that the periodontium’s soft tissues will sustain accidental,
intentional, or fictitious trauma, which can have a negative impact on periodontal
health. Also, studies on animals and humans have suggested a connection between
periodontal disease progression and occlusal trauma/occlusal differences [100]. How-
ever, all researchers came to the consensus that high occlusal forces do not cause
plaque-induced periodontal disease or loss of periodontal attachment, and more
recent research confirms this [101]. The treatment strategy for traumatic dental
injuries differs depending on the amount of damage to the teeth and supporting
tissues. It should be remembered that the treatment strategy must be properly devel-
oped in this situation. By doing so, additional traumas that might exacerbate the
prognosis—which is not always favourable—would be avoided. Because it is impossi-
ble to determine the exact extent of damage to the tooth and supporting structures,
follow-up after any form of trauma is crucial [102].
9. Conclusion
In order to maintain the general homeostasis of the dentition, the periodontium,
which includes the cementum and alveolar bone as well as the soft tissues gingiva and
periodontal ligament, must be in good health. The harmony of the periodontal attach-
ment system is affected by injury to the periodontal tissues in any form, including
microbiological, physical, thermal, chemical, mechanical, occlusal, and habitual
injury, which changes how the dentition functions as a whole. Prior to receiving any
other dental treatment, the periodontium must first be restored which comprehends
that gingival irritants are eliminated, functional and occlusal interferences are fixed,
morphologic and pathologic gingival problems are treated, and bone abnormalities of
the supporting periodontium are corrected.
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Author details
Santo Grace Umesh*, Lakshmi Ramachandran, Janani Karthikeyan
and Sindhuja M. Shankar
SRM Dental College, Ramapuram, Chennai, Tamil Nadu, India
*Address all correspondence to: grace.santo@gmail.com
© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of
the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0),
which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.
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DOI: http://dx.doi.org/10.5772/intechopen.108202

References
[1] Gottrup F, Andreasen JO. Wound
Healing Subsequent to Injury. Textbook
and Color Atlas of Traumatic Injuries to
the Teeth. 4th ed. Oxford: Blackwell;
2007. pp. 1-61
[2] Andreasen JO, Andreasen FM,
Andersson L, editors. Textbook and
Color Atlas of Traumatic Injuries to the
Teeth. John Wiley & Sons; 2018
[3] Andreasen JO, Andreasen FM.
Classification, etiology and
epidemiology. Textbook and Color Atlas
of Traumatic Injuries to the Teeth. 1994;
3:151-179
[4] Glendor U, Marcenes W, Andreasen
JO. Classification, epidemiology and
etiology. Textbook and Color Atlas of
Traumatic Injuries to the Teeth. 2007;4:
217-254
[5] Thennukonda RA, Natarajan BR.
Adverse events associated with
ultrasonic scalers: A manufacturer and
user facility device experience database
analysis. Indian Journal of Dental
Research. 2015;26(6):598
[6] Iyama K, Ueki T, Yamano S, Tajima
G, Inokuma T, Hirao T, et al. An adult
case of laryngopharyngeal burn by
drinking hot water. Acute Medicine &
Surgery. 2017;4(2):198-201
[7] Kwon SJ, Park YJ, Jun SH, Ahn JS, Lee
IB, Cho BH, et al. Thermal irritation of
teeth during dental treatment
procedures. Restorative Dentistry &
Endodontics. 2013;38(3):105-112
[8] Ustun K, Sari Z, Orucoglu H, Duran I,
Hakki SS. Severe gingival recession
caused by traumatic occlusion and
mucogingival stress: A case report.
European Journal of Dentistry. 2008;2
(02):127-133
[9] Gupta ND, Maheshwari S, Prabhat
KC, Goyal L. A critical review of the
management of deep overbite
complicated by periodontal diseases.
European Journal of General Dentistry.
2012;1(01):2-5
[10] Meeran NA. Iatrogenic possibilities
of orthodontic treatment and modalities
of prevention. Journal of Orthodontic
Science. 2013;2(3):73
[11] Safa’a AA, Fadel EI. Hazards of
prosthodontic devices and materials.
Tanta Dental Journal. 2017;14(1):7
[12] Dilsiz A, Aydin T. Self-inflicted
gingival injury due to habitual fingernail
scratching: A case report with a 1-year
follow up. European Journal of
Dentistry. 2009;3(02):150-154
[13] Chalkoo AH, Peerzada GY, Makroo
NN. Case report of gingivitis artefacta
(self-injurious behavior). Journal of
Indian Academy of Oral Medicine and
Radiology. 2016;28(3):317
[14] Mazumdar U, Mazumdar B,
Rajkumar IR. Gingivitis artefacta–self
injurious behaviour in adult patients of
depression report of 2 cases. Journal of
Orofacial Research. 2011;1(1):45-48
[15] Stewart DJ, Kernohan DC. Self-
inflicted gingival injuries. Gingivitis
artefacta, factitial gingivitis. The Dental
Practitioner and Dental Record. 1972;22
(11):418-426
[16] Khalia N, Vemanaradhya GG, Mehta
DS. Oral piercing: Style statement or a
state of disharmony? International Journal
of Oral Health Sciences. 2013;3(2):84
[17] Hennequin-Hoenderdos NL, Slot
DE, Van der Weijden GA. The
26
Dental Trauma

prevalence of oral and peri-oral piercings
in young adults: A systematic review.
International Journal of Dental Hygiene.
2012;10(3):223-228
[18] Bone A, Ncube F, Nichols T, Noah
ND. Body piercing in England: A survey
of piercing at sites other than earlobe.
BMJ. 2008;336(7658):1426-1428
[19] Hickey BM, Schoch EA, Bigeard L,
Musset AM. Complications following
oral piercing. A study among 201 young
adults in Strasbourg, France.
Community Dental Health. 2010;27(1):
35-40
[20] Gill JB, Karp JM, Kopycka-
Kedzierawski DT. Oral piercing injuries
treated in United States emergency
departments, 2002–2008. Pediatric
Dentistry. 2012;34(1):56-60
[21] Mishra P, Gupta M, Shrivastava K,
Singh N, Singh P. Oral tattoos:“beauty
lies in the eyes of the beholder”.
Advances in Human Biology. 2015;5(2):
17-21
[22] Bathla S. Periodontics Revisited.
India: JP Medical Ltd; 2011
[23] Odai ED, Ehizele AO. Trauma to the
soft tissues of the periodontium: A
review. Nigerian Journal of Dental and
Maxillofacial Traumatology. 2019;2(1&
2):7-14
[24] Griffin TJ, Cheung WS, Zavras AI,
Damoulis PD. Postoperative
complications following gingival
augmentation procedures. Journal of
Periodontology. 2006;77(12):2070-2079
[25] Girish MS, Anandakrishna L,
Chandra P, Nandlal B, Srilatha KT.
Iatrogenic injury of oral mucosa due to
chemicals: A case report of formocresol
injury and review. IOSR Journal of
Dental and Medical Sciences. 2015;14:1-5
[26] Gonçalves PS, Mendez DA, Santos
PS, Damante JH, Rios D, Cruvinel T. The
diagnosis and treatment of multiple
factitious oral ulcers in a 6-year-old boy.
Case Reports in Dentistry. 2017;2017
[27] Mcculloch CA, Lekic P, Mckee MD.
Role of physical forces in regulating the
form and function of the periodontal
ligament. Periodontology 2000. 2000;24
(1):56-72
[28] Lindhe J, Lang NP, Karring T.
Clinical Periodontology and Implant
Dentistry. 5th ed. Pan America, Mexico:
Wiley-Blackwell; 2012. pp. 3-49
[29] Goswami M, Chaitra TR, Chaudhary
S, Manuja N, Sinha A. Strategies for
periodontal ligament cell viability: An
overview. Journal of Conservative
Dentistry: JCD. 2011;14(3):215
[30] Pedrini D, Panzarini SR, Poi WR,
Sundefeld ML, Tiveron AR. Dentists’
level of knowledge of the treatment
plans for periodontal ligament injuries
after dentoalveolar trauma. Brazilian
Oral Research. 2011;25:307-313
[31] Trope M. Clinical management of
the avulsed tooth. Dental Clinics of
North America. 1995;39(1):93-112
[32] Kocak FZ, Talari AC, Yar M,
Rehman IU. In-situ forming pH and
thermosensitive injectable hydrogels to
stimulate angiogenesis: Potential
candidates for fast bone regeneration
applications. International Journal of
Molecular Sciences. 2020;21(5):1633
[33] Gluskin AH, Ruddle CJ, Zinman EJ.
Thermal injury through intraradicular
heat transfer using ultrasonic devices:
Precautions and practical preventive
strategies. The Journal of the American
Dental Association. 2005;136(9):1286-
1293
27
Trauma and the Periodontal Tissues: A Narrative Review
DOI: http://dx.doi.org/10.5772/intechopen.108202

[34] Maron FS. Mucosal burn resulting
from chewable aspirin: Report of case.
Journal of the American Dental
Association (1939). 1989;119(2):279-280
[35] Santos-Pinto L, Campos JA, Giro
EM, Cordeiro R. Iatrogenic chemical
burns caused by chemical agents used in
dental pulp therapy. Burns: Journal of
the International Society for Burn
Injuries. 2004;30(6):614-615
[36] De Bruyne MA, De Moor RJ, Raes
FM. Necrosis of the gingiva caused by
calcium hydroxide: A case report.
International Endodontic Journal. 2000;
33(1):67-71
[37] Murrin JR, Abrams H, Barkmeier
WW. Chemical burn of oral tissue
caused by dental cavity varnish. Report
of a case. Illinois Dental Journal. 1978;47
(10):580-581
[38] Dayakar MM, Pai PG, Sooranagi RP,
Vijayan V, Waheed A. Chemical burns of
gingiva and its management. SRM
Journal of Research in Dental Sciences.
2018;9(4):174
[39] Harris JH. Soft-tissue burns from a
dentin bonding agent. General Dentistry.
1991;39(5):350-351
[40] Loe H. Reaction of marginal
periodontal tissues to restorativie
procedures. International Dental Journal.
1968;18:759-778
[41] Ozcelik O, Haytac MC, Akkaya M.
Iatrogenic trauma to oral tissues. Journal
of Periodontology. Oct 2005;76(10):
1793-1797
[42] Pindborg JJ. Atlas of Diseases of the
Oral Mucosa. Copenhegan: Munksgaard;
1980
[43] Deshpande A, Verma S, Macwan C.
Allergic reaction associated with the use
of eugenol containing dental cement in a
young child. Austin Journal of Dental.
2014;1(2):1-3
[44] Sarrami N, Pemberton MN,
Thornhill MH, Theaker ED. Adverse
reactions associated with the use of
eugenol in dentistry. British Dental
Journal. 2002;193(5):257-259
[45] Gonzalez-Moles MA, Bagan-
Sebastian JV. Alendronate-related oral
mucosa ulcerations. Journal of Oral
Pathology & Medicine. 2000;29(10):
514-518
[46] Krasagakis K, Krüger-Krasagakis S,
Ioannidou D, Tosca A. Chronic erosive
and ulcerative oral lesions caused by
incorrect administration of
alendronate. Journal of the American
Academy of Dermatology. 2004;50(4):
651-652
[47] Dellinger TM, Livingston HM.
Aspirin burn of the oral cavity. Annals of
Pharmacotherapy. 1998;32(10):1107
[48] Ramalingam K, Abdalla KA.
Traumatic chemical oral ulceration—
Aspirin burn—A case report from Libya.
CIBTech Journal of Surgery. 2016;5(2):
2319-3875
[49] Neville BW, Damm DD, Allen CM,
Bouquot JE. Oral and Maxillofacial
Pathology. 2nd ed. Philadelphia, PA:
Saunders; 2002. pp. 337-369
[50] Dayakar MM, Pai PG, Madhavan SS.
“Tetracycline hydrochloride chemical
burn”as self-inflicted mucogingival
injury: A rare case report. Journal of
Indian Society of Periodontology. 2012;
16(2):282
[51] Sánchez AR, Rogers RS III, Sheridan
PJ. Tetracycline and other tetracycline-
derivative staining of the teeth and oral
28
Dental Trauma

cavity. International Journal of
Dermatology. 2004;43(10):709-715
[52] Kapoor A, Malhotra R, Grover V,
Grover D. Systemic antibiotic therapy in
periodontics. Dental Research Journal.
2012;9(5):505
[53] Baruchin AM, Lustig JP, Nahlieli O,
Neder A. Burns of the oral mucosa:
Report of 6 cases. Journal of Cranio-
Maxillofacial Surgery. 1991;19(2):94-96
[54] Murdoch-Kinch CA, Mallatt ME,
Miles DA. Oral mucosal injury caused by
denture cleanser tablets: A case report.
Oral Surgery, Oral Medicine, Oral
Pathology, Oral Radiology, and
Endodontics. 1995;80(6):756-758
[55] Bundgaard T. Chemical burns in the
oral cavity and esophagus after
accidental intake of a Steradent denture-
cleansing tablet. Tandlaegebladet. 1985;
89(19):711-713
[56] Bagga S, Thomas BS, Bhat KM.
Garlic burn as self-inflicted mucosal
injury—A case report and review of the
literature. Quintessence International.
2008;39(6)
[57] Isenberg SR, Hier LA, Chauvin PJ.
Chemical burns of the oral mucosa:
Report of a case. Journal (Canadian
Dental Association). 1996;62(3):262-264
[58] Putt MS, Proskin HM. Custom tray
application of peroxide gel as an adjunct
to scaling and root planing in the
treatment of periodontitis: Results of a
randomized controlled trial after six
months. The Journal of Clinical
Dentistry. 2013;24(3):100-107
[59] Shetty K. Hydrogen peroxide burn of
the oral mucosa. The Annals of
Pharmacotherapy. 2006;40(2)
[60] Moghadam BK, Gier R, Thurlow T.
Extensive oral mucosal ulcerations
caused by misuse of a commercial
mouthwash. Cutis. 1999;64(2):131-134
[61] Bernstein ML. Oral mucosal white
lesions associated with excessive use of
Listerine mouthwash: Report of two
cases. Oral Surgery, Oral Medicine, Oral
Pathology. 1978;46(6):781-785
[62] Flötra L, Gjermo PE, Rölla G,
Waerhaug J. Side effects of chlorhexidine
mouth washes. European Journal of Oral
Sciences. 1971;79(2):119-125
[63] Gagari E, Kabani S. Adverse effects
of mouthwash use. A review. Oral
Surgery, Oral Medicine, Oral Pathology,
Oral Radiology, and Endodontics. 1995;
80(4):432-439
[64] Kowitz GM, Lucatorto FM, Cherrick
HM. Effects of mouthwashes on the oral
soft tissues. Journal of Oral Medicine.
1976;31(2):47-50
[65] Singhal A, Vinaya V, Ahuja T,
Longani P. Sodium hypochlorite:
Complications and management. Journal
of Dental Sciences and Oral
Rehabiltation. 2013;4(1):7-10
[66] Mathew ST. Risks and management
of sodium hypochlorite in endodontics.
Journal of Oral Hygiene & Health. 2015;3
(3):1-5
[67] Parry J, Porter S, Scully C, Flint S,
Parry MG. Mucosal lesions due to oral
cocaine use. British Dental Journal. 1996;
180(12):462-464
[68] Gandara-Rey JM, Diniz-Freitas M,
Gandara-Vila P, Blanco-Carrion A,
Garcia-Garcia A. Lesions of the oral
mucosa in cocaine users who apply the
drug topically. Medicina Oral: Organo
Oficial de la Sociedad Espanola de
Medicina Oral y de la Academia
Iberoamericana de Patologia y Medicina
Bucal. 2002;7(2):103-107
29
Trauma and the Periodontal Tissues: A Narrative Review
DOI: http://dx.doi.org/10.5772/intechopen.108202

[69] Blanksma CJ, Brand HS. Cocaine
abuse: Orofacial manifestations and
implications for dental treatment.
International Dental Journal. 2005;55(6):
365-369
[70] Kapila YL, Kashani H. Cocaine-
associated rapid gingival recession and
dental erosion. A case report. Journal of
Periodontology. 1997;68(5):485-488
[71] Brazier WJ, Dhariwal DK, Patton
DW, Bishop K. Ecstasy related
periodontitis and mucosal ulceration–a
case report. British Dental Journal. 2003;
194(4):197-199
[72] Brand HS, Gonggrijp S, Blanksma CJ.
Cocaine and oral health. British Dental
Journal. 2008;204(7):365-369
[73] Gilvetti C, Porter SR, Fedele S.
Traumatic chemical oral ulceration: A
case report and review of the literature.
British Dental Journal. 2010;208(7):
297-300
[74] Touyz LZ, Hille JJ. A fruit—
Mouthwash chemical burn: Report of a
case. Oral Surgery, Oral Medicine, Oral
Pathology. 1984;58(3):290-292
[75] Kar KM. Beobachtungen uber
Pyorrhea alveolaris. Osterreichisch-
Ungarische Vierteljahresschrift fur
Zahnhelkunde. 1901;17:279
[76] Stillman PR. Early clinical evidence
of disease in the gingiva and
pericementum. Journal of Dental
Research. Dec 1921;3(3):25-31
[77] Pihlstrom BL, Anderson KA, Aeppli
D, Schaffer EM. Association between
signs of trauma from occlusion and
periodontitis. Journal of Peridontology.
1986;57:1-6
[78] Glickman I, Smulow J. The
combined effects of inflammation and
trauma from occlusion in periodontics.
International Dental Journal. 1969;19:
393
[79] Glickman I, Sumlow JB. Effect of
excessive occlusal forces upon the
pathway of gingival inflammation in
human. Journal of Periodontology. 1965;
36:141-147
[80] Stillman PR. What is traumatic
occlusion and how can it be diagnosed
and corrected. Journal of the American
Dental Association (1939). 1925;12:1330-
1338
[81] American Academy of
Periodontology. Glossary of Periodontal
Terms. 2001. Available from: https://
www.perio.org
[82] Reinhardt RA, Pao YC, Krejci RF.
Periodontal ligament stressesin the
initiation of occlusal traumatism. Journal
of Periodontal Research. 1984;19:238-
246
[83] Jin LJ, Cao CF. Clinical diagnosis of
trauma from occlusion and its relation
with severity of periodontitis. Journal of
Clinical Periodontology. 1992;19:92-97
[84] Piotrowski BT, Gillette WB,
Hancock EB. Examining the prevalence
and characteristics of abfraction-like
cervical lesions in a population of U.S.
veterans. Journal of the American Dental
Association (1939). 2001;132:1694-1701
[85] Lee WC, Eakle WS. Possible role of
tensile stress in the etiology of cervical
erosive lesions of teeth. Journal of
Prosthetic Dentistry. 1984;52:374-380
[86] Nakatsu S, Yoshinaga Y, Kuramoto
A, et al. Occlusal trauma accelerates
attachment loss at the onset of
experimental periodontitis in rats.
Journal of Periodontal Research. 2014;
49:314-322
30
Dental Trauma

[87] McCauley LK, Nohutcu RM.
Mediators of periodontal osseous
destruction and remodeling: Principles
and implications for diagnosis and
therapy. Journal of Periodontology.
2002;73:1377-1391
[88] Fleszar TJ, Knowles JW, Morrison
EC, Burgett FG, Nissle RR, Ramfjord SP.
Tooth mobility and periodontal therapy.
Journal of Clinical Periodontology. 1980;
7:495-505
[89] Khairnar M. Classification of food
impaction-revisited and its management.
Indian Journal of Dental Advancements.
2013;5(1):1113-1119
[90] Black A. Preventive treatment of
periodontal diseases. NW Dental Journal.
1912;10:60-73
[91] Waerhaug J. Effect of rough surfaces
upon gingival tissue. Journal of Dental
Research. 1956;35:323-325
[92] Lang NP, Kiel RA, Anderhalden K.
Clinical and microbiological effects of
subgingival restorations with
overhanging or clinically perfect
margins. Journal of Clinical
Periodontology. 1983;10:563-578
[93] Icon A. Amalgam restorations and
periodontal disease. British Dental
Journal. 1976;140:377
[94] Pierce LH, Goodkind RJ. A status
report of possible risks in base metal
alloys and their components. The Journal
of Prosthetic Dentistry. 1989;62:234
[95] Pelton L. Nickel sensibility in the
general population. Contact Dermatitis.
1979;5:2-7
[96] Felton DA, Be K, Bayne SC, et al.
Effect of in vivo crown margin
discrepancies on periodontal health. The
Journal of Prosthetic Dentistry. 1991;65:
357
[97] Marcum JS. The effect of crown
margin depth upon gingival tissue. The
Journal of Prosthetic Dentistry. 1967;17:
479
[98] Hochman N, Yaffe A, Ehrlich J.
Crown contour variation in gingival
health. The Compendium of Continuing
Education in Dentistry. 1983;4:360
[99] Parkinson CF. Excessive crown
contours facilitate endemic plaque
niches. The Journal of Prosthetic
Dentistry. 1976;35:424
[100] Reinhardt RA, Pao YC, Krejci RF.
Periodontal ligament stresses in the
initiation of occlusal traumatism. Journal
of Periodontal Research. 1984;19:
238-246
[101] Flores MT, Andersson L, Andreasen
JO, Bakland LK, Malmgren B, Barnett F,
et al. Guideline for the management of
traumatic dental injuries. I. Fractures
and luxations of permanent teeth. Dental
Traumatology. 2007;23(2):66-71
[102] Andreasen JO, Andreasen FM.
Textbook and Color Atlas of Traumatic
Injuries to the Teeth. Copenhagen:
Munksgaard; 1994
31
Trauma and the Periodontal Tissues: A Narrative Review
DOI: http://dx.doi.org/10.5772/intechopen.108202