Periodontal Disease and Cysts

#### **Chapter 10**

## 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.

#### **Figure 1.**

*Traumatic injuries to the periodontal tissues.*

#### *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 displacement 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.

#### *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 restorations 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].

Gingivitis artefacta are the most frequently described self-inflicted MTI to the gingival 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, complications could develop after surgery [17–20]. In addition to increased plaque and calculus production, gingival inflammation may also be one of the main postoperative 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 identification, 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 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 laboratory 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 multivitamins and topical analgesics such triamcinolone acetate and benzocaine to ease discomfort [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 cementum 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 movement 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. Periodontal 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 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, subluxation 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 ligaments, 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


#### *4.1.1 Alendronate*

It is a constituent of the diphosphonate family and has been used to treat osteoporosis 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


**Table 1.**

*Aetiology for chemical burns of the oral mucosa.*

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 cellmediated 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, aspirin'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) (C17H21NO4)*

It is an alkaloid obtained from *Erythroxylum coca* leaves. Europe has the secondhighest 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, endodontic sealants, impression pastes, and dressings for dry sockets. Unprocessed eugenol is combined with zinc oxide to create zinc oxide-eugenol, which demonstrates a

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 frequently 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 indicated 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 H2O2 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 hypersensitivity 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 softtissue 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

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 contact, depth of tissue penetration, and mechanism of action. Chemical burns on the mucosa manifest as diffuse erosive lesions that can range in severity from conventional desquamation to full mucosal detachment with penetration into the submucosa [50]. Chemical exposure causes changes in the vascularity, colour, texture, and consistency 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 analysis [56]. Salivary gland duct involvement may result in temporary obstructive salivary 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

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 gastrointestinal 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*

H2O2 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, hemorrhagic, 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].

#### **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 permanently. Multiple irrigations with sterile water or betadine. If needed, analgesics, corticosteroids 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 extensively researched. Occlusal trauma, also known as traumatism or trauma from occlusion(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 information from well-controlled prospective trials in people, making it difficult to comprehend this intricate host interaction [75].

#### **5.1 Definitions**


#### **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 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 (horizontal) 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 changing the direction of occlusal pressures. The main fibres are positioned along the long

*Trauma and the Periodontal Tissues: A Narrative Review DOI: http://dx.doi.org/10.5772/intechopen.108202*

#### **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].*

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


*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 disappear 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 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. Insertion 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' adaptive 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 periodontal 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 widening 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 opposition. 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. Following insult to the fibroblasts and other connective tissue cells, portions of the ligament undergo necrosis.

#### *Trauma and the Periodontal Tissues: A Narrative Review DOI: http://dx.doi.org/10.5772/intechopen.108202*

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 created. 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

**Figure 4.** *Physiological response, intra-socket adaptation of the tooth to the normal occlusal forces [28].*

**Figure 5.** *Response to orthodontic forces—results in areas of pressure and tension [28].*

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 material 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.

*Trauma and the Periodontal Tissues: A Narrative Review DOI: http://dx.doi.org/10.5772/intechopen.108202*

**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].*

Accommodation of PDL to force widening of PDL to promote mobility is not pathologic 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.

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.


#### **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:


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

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 mobility 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.


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:


This treatment sequence is altered if the following conditions are met:


### **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 outcomes [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*


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 overhanging 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. Particularly 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 positioned deep inside the sulcus or within the junctional epithelium, restorations may have an impact on the biologic width. With apical migration of the junctional epithelium and re-establishment of the attachment apparatus at a higher apical level, this may encourage inflammation and loss of clinical attachment.

#### **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


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.


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.

#### **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 wellcontoured 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 restoration 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.*

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]. However, 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 developed in this situation. By doing so, additional traumas that might exacerbate the prognosis—which is not always favourable—would be avoided. Because it is impossible 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 attachment 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.

*Trauma and the Periodontal Tissues: A Narrative Review DOI: http://dx.doi.org/10.5772/intechopen.108202*

#### **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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[97] Marcum JS. The effect of crown margin depth upon gingival tissue. The Journal of Prosthetic Dentistry. 1967;**17**: 479

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[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

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[102] Andreasen JO, Andreasen FM. Textbook and Color Atlas of Traumatic Injuries to the Teeth. Copenhagen: Munksgaard; 1994

#### **Chapter 11**

## Perspective Chapter: Antioxidants as an Adjuncts to Periodontal Therapy

*Sura Dakhil Jassim and Ali Abbas Abdulkareem*

*Some dreams cannot be actualized but without a doubt part of them can breathe the wonder of life ultimately*

#### **Abstract**

It has been established that periodontal diseases are related with the hyperactivity of neutrophils. Reactive oxygen species are produced mainly by neutrophils. In order to maintain the balance with reactive oxygen species, the need for antioxidants is increasing. As for supplements to the conventional periodontal therapy, different antioxidants have been applied in an attempt to provide new possibilities in the periodontal treatment. This chapter focused on recent studies that used different antioxidants as adjuncts to conventional periodontal treatments.

**Keywords:** antioxidant, periodontal diseases, periodontal treatments, reactive oxygen species, neutrophils

#### **1. Introduction**

The most important immune response against periodontal pathogens attacks includes an increase in the numbers of neutrophils seen in gingival crevicular fluid (90%), junctional epithelium (50%), and connective tissue.

In order to control bacterial invasion, neutrophils have numerous mechanisms, which include extracellular and intracellular, non-oxidative, and oxidative killing mechanisms [1]. When macrophages and neutrophils are stimulated, they generate a "respiratory burst", which is characterized by a rise in the consumption of oxygen, Hexose-Monophosphate shunt activation, and generation of Reactive Oxygen Species (ROS) and Free Radicals (FR). There is significant overproduction of FR and reactive species at sites of chronic inflammation, including periodontal diseases. **Figure 1** shows the mechanisms of increased ROS production in periodontal disease.

Free radical may be defined as a molecular or atomic group capable of free existence with one or more unpaired electrons in its composition [3]. At low concentrations, these FRs are involved in performing a variety of cell signaling functions but at elevated concentrations, they react with certain cellular components such as proteins, DNA, and lipids, exerting oxidative stress in the periodontal ligament, gingival tissues, and alveolar bone associated with tissue damage.

#### **Figure 1.**

*Reactive oxygen species production in periodontal disease. Nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, hydroxyl radical (•OH), hypochlorous acid (HOCl) and singlet oxygen (1O2) [2].*

Antioxidants define as the agents that scavenge ROS or FR; therefore, they prevent damage associated with them. Based on their mode of function, antioxidants can be categorized into two groups [4]. The first one includes preventive antioxidants which involve enzymatic antioxidants such as catalase (CAT), superoxide dismutase (SOD), DNA repair enzymes, glutathione reductase, and, glutathione peroxidase (GPx) as well as some metal ion sequestrators such as albumin. The second group involves chain-breaking antioxidants or scavenging antioxidants such as carotenoids (including retinol-vitamin A), ascorbic acid (vitamin C), a-tocopherol (vitamin E), polyphenols (flavonoids), reduced glutathione, and uric acid, **Table 1** shows types of antioxidants.

Many studies have tried to detect the uses of antioxidants in the management of periodontitis because antioxidants are associated with a strong defense function against ROS. It has been concluded that enhanced clinical periodontal parameters, lower levels of systemic and local ROS as well as higher activities of systemic and local antioxidants in comparison with usual periodontal treatment resulted from periodontal treatments that are supplemented with antioxidants like lycopene, vitamin C, and vitamin E [5–7].

Muniz et al. performed a review and they examined the effects of the supplemental application of vitamin C, lycopene, vitamin E, capsules with fruits/vegetables/ berry and dietary changes on periodontal treatment [8]. It established that only the


use of vitamin E and lycopene is related with improved clinical periodontal parameters [8]. These results are associated with a beneficial effect not only on periodontal status but also on systemic oxidative status.

#### **2. Methodology**

For the assessment of the association between antioxidant and periodontal diseases all available studies that we could find were included. PubMed, Scopus, and Google Scholar were searched to select appropriate papers. The following combinations of search terms were used: "periodontal disease" OR "periodontitis" OR "periodontal therapies" OR "antioxidants" OR "periodontitis AND antioxidants" OR "periodontal disease AND antioxidants" OR "periodontal therapies AND antioxidant".

Only studies written in the English language were accepted, while pilot studies and case reports were not accepted for this chapter. All reference lists of the selected studies were screened for additional papers.

#### **3. Lycopene**

Lycopene is one of the most efficient antioxidants which provides prevention against various chronic disorders, and it was found in a wide range of foods [9]. It has been classified into the class of components known as carotenoids, which are the red, yellow, and orange pigments produced by plants [10].

Lycopene is considered as the most competent biological antioxidant agent because it has the exceptional characteristic of binding to chemical groups that react with oxygen [11].

Di Mascio et al. showed that lycopene is the most effective biological carotenoid singlet oxygen quencher [12].

It has been concluded by Chandra et al. [13] and Arora et al. [5] that systemic lycopene and oral prophylaxis showed a statistically significant drop in Gingival index, compared to the placebo oral prophylaxis group. Patients were followed up in both studies for 2 weeks in gingivitis patients and 2 months in chronic periodontitis patients respectively.

Kaur et al. evaluated the influences of systemically administered extracts of piperine, curcumin, and lycopene as an adjunct to conventional periodontal treatment in patients with moderate gingivitis. They recognized a reduction in gingival index, plaque index, and bleeding scores with statistically significant differences between the control and the test groups at the 21st day period [14].

#### **4. Vitamin C**

For a long period of time, the importance of ascorbic acid (vitamin C) for periodontal health was known. In the eighteenth century, sailors often suffered from scurvy, the disease of vitamin C deficiency, associated with loosening of the teeth and bleeding of the gums. James Lind in 1747 performed his classic experiments aboard the ship "the Salisbury"; he cured scurvy with lemons and oranges in this experiment [15].

Vitamin C is considered as an important dietary nutrient that is essential as a cofactor needed by numerous enzymes. As well as vitamin C is considered as an electron donor and this characteristic accounts for every identified function of vitamin C. In addition, vitamin C is a strong water-soluble antioxidant in humans by its electron donor property. It has been suggested by many lines of studies that vitamin C is a potent antioxidant in vitro [16]. Although records from clinically controlled trials have not confirmed that elevated consumption of ascorbic acid only will assist in the protection against chronic pathological conditions, however, the verification that vitamin C is considered as an essential antioxidant in several body tissues is persuasive [17].

Even though the precise function of ascorbic acid insufficiency in periodontitis is not well recognized, ascorbic acid is considered as a candidate for handling periodontal diseases for a long period of time [18]. It has been identified that supplemental ascorbic acid is necessary for tissue regeneration and infectious diseases, however, low ascorbic acid intake does not cause periodontitis [19].

Collagen fibers, which are present in different forms of the periodontal ligament, connective tissues, and bone, depending on vitamin C for synthesis as well as other intercellular substances depend on it [20]. In addition, vitamin C has immune-regulatory role in affecting the vulnerability of the body to infectious diseases [21].

Sulaiman and Shehadeh [22], found that the supplemental dose of ascorbic acid did not provide additional improvements in comparison to non-surgical periodontal therapy alone. They attributed their finding to the possibility that vitamin C is considered as a poor antioxidant in vivo and its antioxidant activity could have no physiologic function, or its function could be inconsiderable. As well as they supposed that the antioxidant functions of ascorbic acid occur only at particular locations and may be particular to definite reactions [22].

Shimabukuro et al. [23] used dentifrice containing L ascorbic acid 2-phosphate magnesium salt, they found that gingival redness and gingival index significantly decreased in the test group in comparison with the control group [23].

Rajaram et al. evaluate the effects of a diet rich in antioxidants, vitamin C, and fiber on clinical outcomes in patients with gingival inflammation for 1 month. They concluded that gingival inflammation is significantly reduced with a diet rich in antioxidants, vitamin C, and fibers [24]. However, interventional studies, evaluating vitamin C alone, are necessary for proper evaluation of the nutritional impact on periodontal status.

#### **5. Vitamin E**

Vitamin E is a well-known antioxidant that prevents the production of ROS formed from fat oxidation [25]. Vitamin E gained its antioxidant effects by its incorporation into cellular membranes, where it inhibits the peroxidation of lipids [26, 27].

Rattanasuan et al. [28] studied the adjunctive use of vitamin E supplementation (vitamin E soft gel 200 mg/day) to the conventional periodontal therapy and they found that antioxidant defense, as well as periodontal healing, were improved [28].

#### **6. Melatonin**

It has been reported by several studies that melatonin is considered as an active component with antioxidant properties [29]. It is secreted mainly by Pinealocytes; it is a derivative of tryptophan (indoleamine) [30]. Regulation of the sleep cycle is the main function of melatonin. In addition, studies showed that melatonin is involved in energy metabolism and homeostasis [31].

Melatonin has the ability to activate brown adipose tissue and consequently increase energy expenditure. Furthermore, another research pointed out its immunomodulatory, anti-inflammatory, and antioxidant properties [32]. Melatonin can enhance the expression of antioxidant enzymes (CAT, GPx, and SOD) as well as scavenges free radicals [33].

Javid et al. investigated the anti-inflammatory and antioxidant properties of melatonin in patients with periodontal disease and type 2 diabetes mellitus (T2DM) who experience non-surgical periodontal therapy, they found that the adjunctive effects of melatonin and nonsurgical periodontal therapy may improve antioxidant and inflammatory parameters in T2DM patients with periodontal disease [34].

#### **7. Green tea**

Green tea is associated with active ingredients, which include polyphenols. The majority of them are catechins (flavan-3-ols). Furthermore, entire green tea has other antioxidants in the structure of vitamins, such as tocopherols, ascorbate and carotenoids [35].

The mechanism of action of polyphenols as antioxidants is summarized via the stimulation of antioxidant enzymes for example superoxide dismutase and glutathione S-transferase.

In a study performed by Kushiyama and co-workers, they showed that when green tea is taken regularly, it has a protective outcome. Green tea may even decrease the development of existing periodontitis [36].

Generally, green tea catechins have anti-bacterial properties besides their antioxidant properties by their actions on pathological periodontal bacteria such as *Prevotella intermedia* and *Porphyromonas gingivalis.* Inhibition of cysteine proteases of *P. gingivalis* is considered as the mechanism of action [37, 38].

Kudva et al. [39] and Chava and Vedula [40] used green tea as a supplementary to nonsurgical periodontal therapy and they follow the patients for a period of 21 days and 4 weeks respectively, and they found declines in probing pocket depth parameters in test groups with statistically significant differences in comparison to control groups [39, 40].

#### **8. Discussion**

This chapter evaluated the efficacy of antioxidants as an adjunct to scaling and root planing. It has been concluded that systemic lycopene and oral prophylaxis showed a statistically significant drops in clinical periodontal parameters [5, 13, 14].

Although vitamin C has a strong effect on gingival parameters and gingival health conditions, some studies showed that there is no benefit from using vitamin C as an adjunct to periodontal therapy this maybe due to the weak antioxidant capacity of vitamin C in vivo [22].

Adjunctive use of both vitamin E and melatonin in the conventional periodontal therapy results in an improvement in antioxidant defense and periodontal healing [28, 34].

Green tea not only decreases the development of existing periodontitis but also when used as supplementary to nonsurgical periodontal therapy, it resulted in a drop in periodontal parameters.

Although antioxidants have a wide range of beneficial effects for overall health, numerous studies have raised doubt about possible side effects. It has been shown that antioxidants may have a harmful effect in the development of lung cancer [41]. The antioxidants reduced the expression of p53, a key tumor suppressor protein. However, further studies are required to improve a procarcinogenic role of antioxidants.

#### **9. Conclusion**

Uses of antioxidants as an adjunct to periodontal treatment is not a new concept. Nearly all of the evaluated studies showed that there was an improvement in clinical periodontal parameters when using antioxidants as an adjunct to periodontal treatment.

#### **Author details**

Sura Dakhil Jassim1 \* and Ali Abbas Abdulkareem2

1 Department of Periodontology, College of Dentistry, University of Babylon, Iraq

2 Department of Periodontology, College of Dentistry, University of Baghdad, Iraq

\*Address all correspondence to: suradak85@yahoo.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.

*Perspective Chapter: Antioxidants as an Adjuncts to Periodontal Therapy DOI: http://dx.doi.org/10.5772/intechopen.105016*

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[18] Nishida M, Grossi SG, Dunford RG, Ho AW, Trevisan M, Genco RJ. Dietary vitamin C and the risk for periodontal disease. Journal of Periodontology. 2000;**71**:1215-1223

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[23] Shimabukuro Y, Nakayama Y, Ogata Y, et al. Effects of an ascorbic acid-derivative dentifrice in patients with gingivitis: A double-masked, randomized, controlled clinical trial. Journal of Periodontology. 2015;**86**:27-35

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#### **Chapter 12**

## Management of Periodontal Emergency during COVID-19 Pandemic

*Desy Fidyawati, Adrianus Wicaksono, Veronica Septnina Primasari and Suci Amalia*

#### **Abstract**

The novel coronavirus disease (COVID-19) caused by the SARS-CoV-2 virus presents with nonspecific symptoms such as fever, dry cough, shortness of breath, weakness, headache, and diarrhea. The primary mode of transmission of SARS-CoV-2 is through direct or indirect inoculation of the mucous membranes (eyes, nose, or mouth) with infectious respiratory droplets or fomites. Periodontal tissue can serve as a barrier to the SARS-CoV-2 virus in infected individuals. There are similarities between COVID-19 and periodontal disease, based on pro-inflammatory cytokines released by the body. A periodontal emergency arises when an acute condition involving the periodontium causes pain, forcing the patient to seek urgent care; therefore, most periodontal treatment can be considered as dangerous work compared to other dental procedures regarding the aspect of bioaerosol generation procedure. Transmission can occur through direct doctor-patient contact, as well as contamination from instruments or surfaces in the dentist's practice room, and it is recommended to use PPE, to avoid aerosol splashes that occur during the work procedure, where aerosol granules and droplets can last 30 minutes after the treatment procedure is performed. The use of teledentistry is very important in periodontal care, in communication with patients regarding chief compliant, risk factor control, and oral hygiene instruction.

**Keywords:** COVID-19, periodontal disease, dental management, periodontal emergency, periodontal treatment

#### **1. Introduction**

Coronavirus disease 2019 (COVID-19) was first reported in Hubei Province of China at the end of December 2019. Later, in March 2020, after observing the nature of the virus and its course, the World Health Organization (WHO) announced it as a pandemic [1]. SARS-CoV-2 is mainly transmitted *via* direct contact with respiratory droplets, through cough, sneeze, and droplet inhalation, or *via* indirect contact of oral, nasal, and mucous membranes with contaminated fomites or saliva, which may be of particular interest for dental settings, that invariably carries the risk of

SARS-CoV-2 transmission, especially considering the interpersonal proximity, the exposure to blood and saliva, the handling of sharp instruments, and the variety of aerosol-generating dental procedures [2, 3]. Therefore, dental patients are very vulnerable and at risk of transmission of the SARS-CoV-2 virus infection, where this virus can be transmitted through direct contact through the mouth and nose in the form of droplets and aerosols containing the virus, originating from infected individuals or through indirect contact with contaminated dental instruments or contaminated teeth [4]. Not only patients but also clinicians who treat patients are also at risk of transmission caused by direct contact with patients who are not wearing masks, as well as aerosols and droplets produced from the mouth of the patient [5]. So, caution is needed for clinicians and patients in carrying out dental actions and treatments.

#### **2. COVID-19 and periodontal disease**

*Severe acute respiratory syndrome* coronavirus 2 (SARS-CoV-2) is a new type of novel coronavirus that causes COVID-19 [6]. The target of SARS-CoV-2 infection is cells in the respiratory tract, where Protein S in SARS-CoV-2 will bind to (angiotensin-converting enzyme 2 (ACE2) as the receptor [7]. ACE2 is found in pulmonary epithelial cells, myocardial cells, gastrointestinal system, proximal cells of renal tubules, arterial smooth muscle cells, and oral epithelial cells, where the expression of ACE2 will increase in patients with certain conditions, such as, in elderly individuals, obesity, kidney disease, and lung disease that results in individuals with the condition being more susceptible to the transmission of COVID-19 [8–10]. The SARS-CoV-2 virus will replicate, and the virus that has entered the body will be presented by *antigens-presenting cells* (APCs) and will induce T cells and B cells as humoral and cellular immune responses [11].

Periodontal disease is an inflammatory disease of dental support tissue that is commonly found in individuals over the age of 30 years and is often found in the elderly population. Severe periodontitis, now known as stage III and IV periodontitis, is the 6th rank disease commonly suffered by adults, affecting 11% of the adult population globally Several studies have shown a link between COVID-19 and periodontal disease, and this is due to the similarity of pro-inflammatory cytokines released by the body. Periodontal disease is a multifactorial disease caused by the involvement of microorganisms and a host response characterized by the production of pro-inflammatory cytokines [12, 13]. Pathogenesis of periodontal begins from the expansion of the subgingival plaque into the gingival sulcus, where microorganisms residing in the subgingival plaque can cause changes in the coronal attachment of the epithelium on the surface of the tooth, and this is due to the presence of an immune response to pathogenic bacteria and endotoxins through the activity of neutrophils, macrophages, and lymphocytes. Host factors also influence the development of periodontal disease, where an inadequate host response in destroying bacteria can damage periodontal tissue [14]. Pathophysiology periodontitis stimulates the occurrence of cytokine responses. Research conducted by Wu et al. (2020) on COVID-19 shows that there is an unfavorable relationship that can cause cytokine storms, where certain elements have similarities with cytokine profiles commonly encountered in periodontitis. Individuals infected with the COVID-19 virus that was accompanied by aggravation so that they had to be treated in the ICU showed an increase in IL-2, IL-7, IL-10, macrophage, monocytes, and TNF alpha. Th17 cells were also found in individuals suffering from SARS-Co V and MERS-CoV [15]. Th17 cells are found in

#### *Management of Periodontal Emergency during COVID-19 Pandemic DOI: http://dx.doi.org/10.5772/intechopen.106714*

cytokine storms, {Formatting Citation} pulmonary edema, and damaging tissues that may result in lung infections caused by the SARS-CoV-2 virus [16]. An increase in IL-17 was also found in individuals experiencing inflammatory gingivitis and periodontitis [17]. Gupta et al. (2021) found the accumulation of the corona virus in gingival crevicular fluid (GCF) in asymptomatic or mildly symptomatic COVID-19 patients, where the condition is in line with the hypothesis in a study conducted by Badran et al. (2020) where periodontal can serve as a reservoir for the SAR-CoV-2 virus in infected individuals [18, 19].

#### **3. Dental management during COVID-19**

Dental care during the pandemic should not be delayed, especially in emergency cases, dental care during the pandemic should be linked to patient risk assessment, patient triage, and infection prevention measures for clinicians or health professionals and nosocomial transmission in dental clinics (**Figure 1**) [20].

Treatment in the field of dentistry can generally be categorized as an emergency, urgent, nonurgent, and advise/self-care (**Figure 2**). In principle, emergency care in the field of dentistry is associated with acute pain that is urgent for treatment, as well as life-threatening possibilities, including uncontrolled bleeding, significant infections, bending, and orofacial trauma that has the potential to block the airway. Meanwhile, urgent (essential) treatment is the treatment of severe or uncontrolled symptoms that require patients to see a dentist. Nonurgent care or categorized as daily care is a routine treatment carried out by individuals, while advise/self-care treatment is dental care that can be done through telemedicine, related to it the instruction and prescribing of either analgesic or antimicrobial (**Figure 3**) [21].

**Figure 1.** *Illustration of COVID-19 transmission in dental clinic.*


#### *Management of Periodontal Emergency during COVID-19 Pandemic DOI: http://dx.doi.org/10.5772/intechopen.106714*


#### **Figure 2.**

*Dental care management that occurs during COVID-19.*

#### **Figure 3.** *Medical dosage recommendations.*

Note: Patients with substantial swellings can progress to life-threatening emergencies, which can increase risks in the setting of reduced health care availability. For that patient, extraction of the causative pathogenic teeth should be prioritized over the restorative rescue. Close follow-up by telephone is recommended [21].

#### **3.1 Recommendations for clinicians to reduce airborne viral contamination**

Dental care is usually done in an enclosed space, so the dentist needs to equip himself with some protection, such as masks, gloves, goggles, head coverings, and gowns that reduce saliva splashes that may occur during dental procedures. Aerosol granules or droplets can stay in the air for 30 minutes after the dental treatment procedure is carried out [22]. In addition, the regulation of air circulation in the clinic room is also must be noted, and the common thing to do is to eliminate airborne transmission in the clinic room is to equip the room with the use of a good quality air filter and the presence of an ultraviolet room as part of the air ventilation system [23]. Another tool that should be present to reduce contamination through the air is extraoral suction or known as a high-volume evacuator (HVE), in dental treatment procedures, and a good extra oral suction has a wide opening or mouth and is connected to a drain that reduces the volume of air to 100 cubics of per minute. Several previous studies have suggested that the use of HVE can reduce airborne virus contamination by up to 90%, if the clinic room is not equipped with HVE, and it is recommended to use air vents to facilitate air exchange [24, 25].

#### **3.2 Dental treatment procedures that must be carried out to eliminate viral contamination through the air**

To reduce the risk of transmission, it is necessary to have a good strategy in terms of carrying out dental procedures, including [26].

1.The use of rubber dam

The use of a rubber dam is needed for dental treatment procedures that require isolation of the work area, and if it is not possible to isolate the work area such as curettage or other periodontal measures, it is recommended to use hand instruments instead of ultrasonic tools, to reduce the chances of aerosols being generated.


#### *Management of Periodontal Emergency during COVID-19 Pandemic DOI: http://dx.doi.org/10.5772/intechopen.106714*


#### **Figure 4.**

*Recommended PPE during COVID-19.*

#### **3.3 PPE (personal protective equipment)**

For professional dentists, the risk of transmission can be prevented by the use of PPE. The recommended use of PPE (**Figure 4**) includes head coverings, gowns, gloves, face shields, masks, footwear covers, or other equipment that aims to protect against injury or contamination bacteria derived from aerosols or droplets produced during dental treatment procedures [26]. The recommended use of masks is N95/ PFF2 because it provides good protection and is recommended internationally; in addition, if needed due to inadequate amount of availability, N95/PFF2 masks can be disinfected first before reuse [26, 35, 36].

#### **4. Periodontal management during COVID-19**

#### **4.1 Prevention of droplet transmission before treatment measures**

Dentists who perform periodontal treatment are at risk of being contaminated with the COVID-19 virus through droplets or aerosols generated during the periodontal treatment procedure, through the use of ultrasonic scalers, rotary instruments, and water syringes and air polishers that potentially increase the risk of transmission through cross-transmission between dentists and patients [37–39]. All dental health care facilities are required to implement triage protocols including detailed medical record data, which contains specific questions that can identify individuals suspected of COVID-19. All patients seeking treatment should be considered potentially infectious. All patient screening actions must be carried out in strict health protocols, and operators should be equipped with PPE during the patient screening process [37, 40]. When the screening process is carried out, the dental professional should ask questions related to patient complaints that lead to emergency care and conduct an assessment to determine whether or not emergency care is necessary [39, 41, 42]. To reduce the occurrence of transmission through direct contact, screening can be done via telemedicine or tele-triage, which can be done via the internet or telephone, and if the patient states to have had contact with an infected individual with COVID-19 recently or is known to have the symptoms of COVID-19, the patient can be prescribed if needed [39, 43].

#### **4.2 Prevention of droplet transmission during treatment measures**

Some preventive measures that can be carried out before periodontal treatment include cleaning the surface of the dental unit with material containing 0.5% sodium hypochlorite for 1 minute and sterilizing non-disposable tools [44]. Using an extraoral suction, air purifier and exhaust fan are still being evaluated for effectiveness for dental clinics, if there are patients who are suspected of having COVID-19, and it is recommended that their dental treatment should be carried out in a negative pressure room to reduce the spread of the virus through droplets and aerosols [45]. However, the use of negative pressure rooms has issues because it requires quite expensive costs [38, 45]. After the initial examination, the periodontist is advised to take periodontal treatment measures that are not emergency in nature unless there is pain that is a complaint. The effectiveness of the use of ultrasonic scalers is basically the same as that of manual scalers except that on ultrasonic scalers, and it is more risky in aerosol dispersing, which allows to stick to the corners of the eyes and nose operator [46]. However, if the patient complains of pain leading to emergency measures, it is advisable to perform a scaling procedure manual rather than scaling by using an ultrasonic scaler. The use of mouthwashes containing povidoneiodine 0.2% or 0.5–1% of hydrogen peroxide is recommended before the periodontal treatment procedure to reduce the accumulation of virus in the saliva and also as an infection control for operators [37]. Patients should not do self-medication independently, and if necessary, it is recommended to consult through telemedicine in advance for planning pain-related treatments complained by patients [40]. Dental care and periodontal is a treatment that requires close physical contact, so it would be better if the treatment was made as short as possible, or the treatment procedure was carried out in the area that became complaints only, and the patient's recall time for maintenance is made a bit long, at least 2 weeks to see the possibility of COVID-19 symptoms in patients [5, 47]. Periodontal disease is a disease with biofilm plaque as the primary etiology, so plaque control is very important, and the use of mouthwashes as an ingredient in dentrifices gives good results especially when combined with scaling treatment. The administration of antibiotics in the treatment of periodontitis is not recommended, since it allows the occurrence of resistance, except in certain cases such as aggressive periodontitis and recurrent periodontitis, which requires evaluation of certain specific bacteria [48]. For periodontal surgical therapy, in the current pandemic situation, it is rather difficult to do, given the necessity of a strict control schedule, so for cases of intra bony defects that require regenerative therapy, and it is advisable to do conservative therapy, such as the use of enamel matrix derivative, for control that can be done via telemedicine/teledentistry as already described above to get good results after regenerative or conservative therapy. It is necessary to motivate the maintenance of good oral hygiene so that good results are obtained well. On the contrary, mucogingival surgery is advised not to be performed or done limitedly during the COVID-19 pandemic [5, 48]. Complex periodontal cases that require cooperation between disciplines as one of the ways to control the inflammation of periodontitis and also rehabilitate the mastication function [49] must be carefully analyzed to obtain the right diagnosis and treatment plan which is accurate, avoid excessive maintenance, and minimize surgical procedures [50]. Teledentistry plays a very important role in periodontal care (**Figure 5**) among others to regulate patient schedule based on complaint priority, pre-check triage monitoring, diagnosis determination based on staging, grading, and also communication with patients regarding risk factor control and oral hygiene instruction [5].

*Management of Periodontal Emergency during COVID-19 Pandemic DOI: http://dx.doi.org/10.5772/intechopen.106714*

**Figure 5.**

*Periodontal care flowchart during COVID-19 pandemic.*

#### **5. Periodontal emergency management during COVID-19**

Cases of periodontal emergence arise when an acute condition that causes pain in the periodontal tissue forces the patient to seek treatment on the spot. Time management is key to avoiding more severe periodontal tissue damage as well as its effect psychically and functionally on patients [51]. Cases related to periodontal emergencies are basically limited, including acute abscesses involving periodontal tissue or


#### **Table 1.**

*Periodontal condition based on treatment needs.*

endo-perio lesions, necrotizing ulcerative gingivitis and periodontitis caused by stress during the pandemic, dentin hypersensitivity, and lesions oral effects on the quality of life such as ulcers, viral and fungal infections, and cases requiring biopsy [52]. During the pandemic, pharmacological treatment is the best and safest option [37]. According to group disease conditions through the periodontal disease classification approach and the latest conditions 2017, it is actually very unfortunate that there is no grouping of cases periodontal as an emergency, urgent, or elective (**Table 1**) because the disease can initially be recognized as urgent which can then become an emergence if ignored, which then can trigger irreversible damage, and it should all be done in parallel with the periodontal treatment procedure, minimizing the production of aerosols produced during the treatment periodontal [47, 49].

#### **5.1 Necrotizing periodontitis**

**Clinical and etiology:** Necrotizing periodontitis is also known as an inflammatory disease of severe dental support tissue (**Figure 6**), associated with the presence of biofilm plaques, which are grouped into acute necrotizing ulcerative gingivitis (ANUG) and necrotizing ulcerative periodontitis (NUP) [51]. ANUG, the necrotic

**Figure 6.** *(left) NUG and (right) NUP.*

#### *Management of Periodontal Emergency during COVID-19 Pandemic DOI: http://dx.doi.org/10.5772/intechopen.106714*

state of tissue, only involves the gingival with a clinical picture of the presence of ulcers and necrotic tissue in the attached gingival, while in NUP there has been damage to periodontal tissue and alveolar bone which results in loss of attachment. Periodontal necrotizing is characterized by the presence of pseudo-membranes. The pain felt by the patient is generally based on the expansion and severity of the lesion area, sometimes accompanied by halitosis. In NUP, there is an interdental crater. This inflammation generally hits the anterior region of the lower jaw. ANUG or NUP is often associated with HIV/AIDS disease or immunosuppressant disease. The etiology of the disease is associated with infection of organisms and is often associated with Spirochaeta and fusiform bacteria, with compromised immunology predisposing factors [53].

**Emergency treatment:** For the elimination of plaque deposits and calculus through superficial debridement, it is recommended to use an ultrasonic scaler instead of a hand instrument to minimize pressure on the ulcerated soft rareness, during the pandemic currently, and the use of ultrasonic scalers should be done briefly and quickly, combined with hand instruments. Debridements should be performed daily in the acute phase for 2–4 days. Patients are advised to brush their teeth on a limited basis to avoid pain and disruption of the healing process. Patients are also recommended to rinse their mouth with chlorhexidine 0.2% as much as 2x a day or with 3% hydrogen peroxide diluted with warm water 1: 1 and also with other mouthwashes that function as oxygen-releasing agents, which have an antibacterial effect through the release of oxygen [54]. If it does not also improve, then the patient can be given a systemic antibiotic with metronidazole content (400 mg 3x1 a day) as a drug of choice for cases of periodontitis necrotizing [55].

#### **5.2 Abscesses**

#### *5.2.1 Gingival abscesses*

**Clinically and etiology:** Gingival abscesses are generally purulent and localized on the marginal or interdental gingival. A common cause of a gingival abscess is the "trapping" of a foreign body inside a healthy gingival in the sub-gingival region. Foreign objects include fish bones or nail pieces from individuals with a bad habit of biting nails (**Figure 7**) [51, 56].

**Emergency treatment:** Preparation of incision and irrigation with saline solution to reduce symptoms. Short-term treatment is recommended through the use of chlorhexidine mouthwash (0.2%) or warm saline solution, especially for areas where brushing is not possible [51].


**Figure 7.** *Periodontal abscess features.*

#### *5.2.2 Periodontal abscess*

**Clinically and etiology:** Periodontal abscesses are defined as the accumulation in the periodontal pocket produced by the destruction of collagen fibers accompanied by bone damage [51, 57]. The most prominent clinical sign is the presence of enlargement in the gingival along the length of the lateral root of the tooth, which is characterized by redness, diffuse, and soft consistency. There is a deep periodontal pocket accompanied by bleeding during probing (**Figure 7**) [51]. The presence of suppurations that come out through fistulas or walls of periodontal pockets spontaneously or through suppression is also accompanied by the presence of tooth shakes and pain during percussion. Generally, patients complain that their teeth feel rather high. Periodontal abscesses generally come from further periodontitis, derived from pockets, bifurcation abnormalities, or vertical defects [58].

**Emergency treatment:** Treatment in the case of periodontal abscess is found in the pre-elimination phase, including the management of acute conditions, and drainage, either through a pocket or an external incision. Sometimes, an occlusal adjustment is needed to eliminate the symptom. The administration of antibiotics is necessary if there are indications of infection (fever or lymphadenopathy). If the tooth is no longer maintainable, then the most likely treatment is the removal [51].

#### *5.2.3 Pericoronitis or pericoronal abscess*

**Clinically and etiology:** Pericoronitis is an inflammation of the soft tissue surrounding the crown of a partially erupted tooth. Pericoronal abscesses are generally localized accumulations on the gingival flaps that envelop the crown of a tooth that has not been perfectly erupted [57]. The clinical picture of a periodontal abscess lesion is the gingival redness, softness, suppurative, and pain when touched aching. There is a bending at the angle of the mandible, trismus pain that radiates to the ear area, accompanied by fever and bending lymphadenopathy. The etiology of pericoronitis is the accumulation of plaque on the operculum that covers part of the molar 3 mandibles that are partial eruption and can also be caused by trauma from the opponent's teeth (**Figure 7**) [51].

**Emergency treatment:** The operculum area should be cleaned with an irrigation solution slowly, to remove debris, if needed, that can be done under anesthesia. The operculum removal and occlusal adjustment should be performed to eliminate trauma to the 3-mandibular molar tooth. Antibiotic administration is carried out if there is an indication of infection [51].

#### *5.2.4 Peri-endo abscess*

**Clinically and etiology:** It is a combination of periodontal/endodontic lesions, localized, covering areas that have infection originating from periodontal/pulp tissue. It is the result of "communication" between the periodontal tissue and the pulp. The clinical picture is characterized by the presence of periodontal pockets surrounding non-vital teeth, and soft lesions of the gingival, accompanied by the formation of exudate and fistulas. Teeth that have a peri-endo abscess will hurt when there is percussion and shake, and sometimes there is a vertical fracture of the root (crack). The etiology of this lesion is the presence of an infection that begins with inflammation of the pulp which then extends to the periodontal ligament, or it can also be preceded by inflammation of the periodontal tissue through the formation of a pocket that extends to the musty from the tooth and then radiates to the pulp through the accessory canal (**Figure 7**) [51, 55].

**Emergency treatment:** For the drainage through periodontal canal debridement or root canal treatment, incision can be done if the abscess appears to be fluctuating. If necessary, occlusal adjustments should be done. The administration of antibiotics is recommended for the comfort of the patient and if there is an indication of the expansion of infection [51].

#### **6. Discussion**

Several studies have shown a link between COVID-19 and periodontal disease, and this is due to the similarity of pro-inflammatory cytokines released by the body [13]. The pathogenesis of periodontal disease begins with the expansion of the subgingival plaque into the gingival sulcus, where microorganisms in the subgingival plaque can cause changes in the coronal attachment of the epithelium on the tooth surface, and this is due to the immune response to pathogenic bacteria and endotoxins through the activity of neutrophils, macrophages, and lymphocytes [14]. Research conducted by Wu et al. (2020) on COVID-19 shows that there is an unfavorable relationship that can lead to cytokine storms, where certain elements have similarities with cytokine profiles commonly encountered in periodontitis [15]. Treatment in dentistry can generally be categorized as an emergency, urgent, nonurgent, and advise/self-care [21]. Dental and periodontal care are treatments that require close physical contact, so it would be better if the treatment was made as short as possible or done as a complaint only, and the patient's recall time for maintenance was made rather long, at least 2 weeks to see the possible symptoms of COVID-19 in the patient [5, 47]. Cases of periodontal emergence arise when an acute condition that causes pain in the periodontal tissue forces the patient to seek treatment on the spot. Time management is the key to avoiding more severe periodontal tissue damage and its effect psychically and functionally on patients [51]. Cases related to periodontal emergencies are essentially limited, including acute abscesses involving periodontal tissue or endo-perio lesions, necrotizing ulcerative gingivitis and periodontitis resulting from stress during the pandemic, hypersensitivity to dentin, and oral lesions that affect the quality of life such as ulcers, viral and fungal infections, and also cases requiring biopsy. During the pandemic, pharmacological treatment is the best and safest option [37, 52]. During the treatment, if direct contact is required, dentists recommended to use PPE to avoid aerosol splashes that occur during the work procedure, where aerosol granules and droplets can last 30 minutes after the treatment procedure is performed [21, 26]. The use of teledentistry is very important in periodontal care, including organizing patient schedules based on complaint priority, pre-checking triage monitoring, diagnosing determination based on staging, grading, and also communicating with patients regarding risk factor control and oral hygiene instruction [5].

#### **7. Conclusion**

Periodontitis is an inflammatory disease of periodontal tissue that is multifactorial; in some cases, it can be aggravated by the presence of systemic abnormalities so that individuals with certain systemic disorders become more at risk, which allows the use of telehealth to be one of the ways of communicating between patients and professionals of various disciplines. Control of routine maintenance of periodontal

tissue, monitoring of periodontal tissue health, and control of risk factors aim to reduce the progression of periodontal disease and reduce the risk of tooth loss, which during this pandemic is difficult to do, so far teledentistry is quite reliable for monitoring the health of periodontal tissue, motivating, and provision of periodontal health maintenance instructions. Increased motivation related to the prevention of periodontal tissue abnormalities can be done through teledentistry and other applications by increasing individual motivation and awareness related to periodontal tissue maintenance, especially for individuals with risk factors for systemic disorders who have a more severe risk of transmission of COVID-19.

#### **Acknowledgements**

The authors would like to express their gratitude to everyone who facilitated and enabled us to carry out this successfully.

#### **Conflict of interest**

There were no conflicts of interest as declared by the authors.

### **Author details**

Desy Fidyawati1,2\*, Adrianus Wicaksono1 , Veronica Septnina Primasari1 and Suci Amalia1

1 Department of Periodontology, University of Prof. Dr. Moestopo (B), Jakarta, Indonesia

2 Faculty of Dentistry, Doctoral's Candidate, University of Indonesia, Jakarta, Indonesia

\*Address all correspondence to: desyfidyawati@dsn.moestopo.ac.id

© 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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#### **Chapter 13**

## Perspective Chapter: Salivary Duct Cyst

*Saurabh R. Nagar, Gabriela Fernandes, Shivani Bansal, Rajiv S. Desai and Diya Jayanth Kamdar*

#### **Abstract**

Salivary duct cysts (SDCs) are true cysts caused by obstruction of salivary ducts and are rare in minor salivary glands. Intraoral SDCs and mucoceles represent clinically salivary gland neoplasms, making diagnosis difficult and subject to errors in treatment. It is important for Oral and Maxillofacial Surgeons to include SDC in the differential diagnosis of swelling affecting buccal mucosa.

**Keywords:** salivary duct cyst, minor salivary glands, oral pathology, oral surgery, maxillofacial surgery

#### **1. Introduction**

The two major groups of oral cysts are divided based on odontogenesis: odontogenic cysts (OCs) and non-odontogenic cysts (non-OCs). The odontogenic cysts are distinguished by specific odontogenic markers. They have histological similarities with odontogenic structures and anatomical considerations, whereas the non-odontogenic group includes cysts that originate from specific areas or organs of the oral cavity such as naso-palatine duct/mid-palatine cysts, nasolabial cysts, and salivary cysts. There are some cysts that are included in this group, that are ubiquitous in the body such as aneurysmal bone cysts, lympho-epithelial cysts, and dermoid cysts [1].

Odontogenic cysts develop from the tooth-producing tissues and on the other hand, they originate from the remnants of dental lamina epithelium entrapped within the gingival named epithelial rests of "Serres," or the epithelial remains of the "Malassez." These cellular remnants have limited growth potential and they fall within the concept of the post-functional state of the dental lamina. The two types of dental cysts are generated by the two types of embryological residues. Periodontal cysts originate from the remnants of Serres and the orthokeratocysts, which are a more aggressive type of cyst with a neoplastic variant. The inflammatory radicular cyst originates from the residues of the Malassez. For this particular type of cyst, an infectious and/or inflammatory stimulus acting on a genetic predisposition has been proposed as the first pathogenic event causing the proliferation of cellular odontogenic remnants.

Cytokeratins are ideal markers for differential diagnosis of these cysts, being involved in physiological odontogenesis epithelium-specific markers of differentiation and have been proposed as ideal markers for differential diagnosis of these cysts, being involved in physiological odontogenesis, thoroughly cytokeratins 5 and 14 are present in the basal cell layer of keratinized and non-keratinized epithelia along with a depletion in the layers above. Cytokeratins 1 and 10 are particular with respect to the spinous layer; cytokeratin 19 is specific with regard to the basal stratum layer of the non-kertinized epithelia; cytokeratins 13 as well as 4 are particular to the supra-basal cells of the tongue epithelium; there is the presence of K2p in the supra-basal epithelial cells of the hard palate and gingiva. In the course of odontogenesis, the cytokeratins form a unique expression; in the early bell stage, cytokeratin 14 is present in the "stellatum reticulum"


• Aneurysmal bone cyst

#### **Table 1.** *Cysts of the oral cavity.*

*Perspective Chapter: Salivary Duct Cyst DOI: http://dx.doi.org/10.5772/intechopen.105494*

along with cytokeratin 7; CK19 is expressed along with these cytokeratins in the cells of the enamel epithelium; although cytokeratin 14 is present during the early bell stages which are ultimately substituted by cytokeratin 19 in differential ameloblasts; cytokeratins 7 and 13 are present in the "rests of Serres." The structure of cytokeratins and their expression within the cells are based on the conditions of the environment and changes that occur in the functioning of the cell. Hence, an altered expression when detected becomes extremely helpful for the differential diagnosis of multiple diseases like cysts and tumors. Therefore, cytokeratins 5 and 6 are found in every single layer of the odontogenic cysts, cytokeratin 13 is present among the supra-basal cell layer of odontogenic cysts, while cytokeratin 20 is not present in any of the odontogenic cysts.

In this chapter, we suggest a simplified classification with regard to the cysts of the oral cavity. We plan to divide the various types of cysts into two main groups: (1) cyst of the osseous and periodontal tissue and (2) soft tissue origin non-odontogenic cyst. After which, these groups are further divided into subgroups depending on their relationship with the anatomical area, histological origin as well as clinical behavior (rate of recurrence, frequency, and malignant potential; **Table 1**). **Table 1** depicts the classification of the cysts of the oral cavity.

#### **2. Cysts of the oral bone and periodontal tissue**

#### **2.1 Odontogenic cysts of inflammatory origin**

Radicular necrotic cyst (RC) is the most common cyst of the oral cavity which is caused by the loss of pulp of the tooth (biological barrier) due to carious lesions or dental trauma. There is the presence of pulp necrosis and the cyst is derived from the cellular remnants of the "Malassez." This can preside to form inflammatory radicular necrotic cyst which can either be periradicular or periapical. Initially, the granuloma forms, and after which it gives rise to a cyst whose epithelium demonstrates odontogenic CK19 in the superficial cell layers and co-expresses CK5 in the cyst lining. Residual radicular cysts are a unique variant of the radicular cyst which develops from apical granulomas or residual fragments of RC.

Collateral inflammatory cysts (Juvenile paradental cyst and Paradental cyst) have overlapping histological features with radicular cysts. Their etiology is also considered inflammatory or meta-traumatic. It is present on the lateral surface of a tooth which is vital. It occurs as a result of a chronic inflammatory process in the periodontal pocket. In a young patient, the juvenile paradental cyst is seen in the root area of the mandibular molars whereas it is present distally to a lower wisdom tooth in adults. These lesions are considered the same unit, regardless of the localization. The histological features of these cysts cannot be distinguished from those of the inflammatory radicular cysts but this appearance emphasizes the origin from the remains of the Mallasez.

It becomes important to differentiate these cysts from the other radiolucent jaw lesions, such as unicystic ameloblastoma, keratocystic odontogenic tumor, dentigerous cysts, and LPC. A combination of immunohistochemical markers such as CK10, CK13, CK17, PCNA, UEA, and perlecan can help in the differential diagnosis.

#### **2.2 Odontogenic cysts of developmental origin**

Dentigerous cysts surround the crown of a tooth that has not migrated into the oral cavity. They are named follicular, germinal, and eruptive cysts. There is an

accumulation of pathological fluid in the layers of the reduced enamel epithelium or between it and the crown of an unerupted tooth. CK5, CK6, and CK19 are present while CK7 is absent in this type of cyst.

Periodontal tissues (parodontal cysts and Botryoid cysts) form a single nosological group named "cyst of the periodontal tissue" because they are of dental origin and the periodontal tissue is contiguous to the teeth and bone. The cysts which affect the periodontal tissue are gingival cysts which are frequently present in adults and periodontal cysts (lateral parodontal cyst and its variant; botryoid cyst). The periodontal cysts are unicystic with a differential diagnosis of ameloblastoma. Two or three layers of flattened cells mimicking a squamous epithelium are present along with areas of nodular type thickening and clear cells rich in glycogen. The lateral parodontal cysts (LPC) have a multilocular variant defined as "Botryoid cyst." They arise from the remnants of Serres incorporated into the periodontal tissue or from the reduced enamel epithelium of the follicle which expands to occupy a space in the periodontal ligament during the eruptive phase producing a paradontal cyst, while a gingival cyst may form due to a portion remaining in the gum after the eruption. CK13 and CK17 are expressed in the surface layers of the lateral parodontal cyst, whereas perlecan and UEA are present on the cell border of the whole layer. LPC is negative for CK10.

Botryoid odontogenic cyst is a rare pathological multilocular cyst that may or may not have close proximity to a root of a tooth. This is considered a variant of lateral parodontal cyst and it is derived from more groups of converging cellular debris of Serres. It has also been considered to represent a variant of glandular odontogenic cyst due to the presence of mucous cells and the columnar cells. Presence of CK18 and CK13 which is specific for rests of Serres, show the origin from the odontogenic tissues. CD56 and calreatin help in differentiating ameloblastoma from BOC as these markers are absent in the latter.

Gingival cysts of infants are also known as Newborn gingival cysts, Dental lamina cysts, or Bohn's nodules. They are present in newborns and develop from the remains of the dental lamina. Presence of squamous epithelium lining with areas of parakeratosis and keratin-filled cavities.

#### **2.3 Non odontogenic cysts**

Epstein's Pearl are also known as Mid palatal raphe non-odontogenic cysts of infants. They have similar histological and clinical features to gingival cysts. They arise from non-odontogenic epithelial remnants after medican palatal fusion.

Nasopalatine duct cysts are formed by the proliferation of epithelial remnants that are organized in clusters or cords and are present in the incisive canal of the maxilla. These remnants cause the formation of the cyst with the presence of a squamous ciliated epithelium layer.

#### **2.4 Cysts of the globulomaxillary area**

These cysts display constant clinical and radiological features, however, they do not present the same histological features always. Various histological features such as stratified squamous (odontogenic), parakeratinic (orthokeratocystic), or cylindrical respiratory (non-odontogenic) epithelium have been described in these cysts. In this group of cysts, we can always include intraosseous cysts that develop between the roots of the lateral incisior and the canine teeth which causes divergence. Moreover, cysts originating from the respiratory epithelium remained trapped in the globule maxillary site and parodontal cyst. It is possible to find neoplastic cysts in this site.

#### **2.5 Cysts with malignant variants with neoplastic characteristics**

Orthokeratinized odontogenic cysts are characterized by a keratinized lining epithelium. The term keratocystic odontogenic tumor (KCOT) is preferred when the epithelium displays significant parakeratosis or orthokeratosis and presents more aggressively with a tendency to recur. Whereas, these two cysts show a different pattern of expression of CKs: OOC expresses CK1, CK2, CK10, and loricrin, while KCOT expresses CK4, CK10, CK13, CK16, CK17, and CK19, similar to the dental lamina. The differential immunohistochemical expression of CD-56, CD-105, and calreatin help in distinguishing these cysts from ameloblastoma from a clinical view point.

Calcifying odontogenic cyst (COC) have three entities, simple intraosseous COC, extra osseous peripheral COC, and the malignant form calcifying cystic odontogenic tumor. Radiologically, they show cystic imaging with small scattered areas of calcification which often resembles an odontoma. They have a peculiar histological pattern with their epithelial lining consisting of a basal layer of columnar cells and an overlying epithelium, which is thick and vacuolated. Furthermore, groups of eosinophilic cells with non-stainable cellular structures are visible in the epithelial lining, connective tissue capsule, or both. These cells are referred to as "ghost cells" and are considered dystrophic cells with aberrant keratinization or apoptotic cells with intracellular calcification. These particular cells are present in different pathological entities such a craniopharyngioma, odontoma, pilomatrixoma, ameloblastic fibroma, and some visceral tumors. They lose the cytoskeletal components and become CK1013 negative as they accumulate some substances during the differentiation process. While, CK14 is expressed in the basal layer, CK10/13 are present in the upper layer of the cyst. P63 expression is present in all layers of COC examined.

Glandular odontogenic cyst (GOC) contain acidophilic cuboidal or columnar cells arranged in glandular structures with papillary growth and projections into cyst-like spaces. This cyst can be differentiated by mucoepidermoid carcinoma based on the diverse immunohistochemical expression of mammary serine protease inhibitor (MASPIN) as well as Ki67 and P63 tumor markers.

Cysts of the maxillary sinus have three types of primary cysts, the first type is the true cysts which are due to an occlusion of the excretory ducts of the sinus mucous glands. The second type is mucoceles which are formed from the non-external drainage of normal mucous and the third type is secondary mucoceles. They are formed as a result of post-radical sinus surgery and probably due to residues of sinus mucosa forming a new mucocele in a closed compartment. Pseudocysts are also present, they are formed between the inner surface of the bone wall and the connective tissue layer while the sinus mucosa remains on the outside. These cysts may be formed due to allergies, inflammation of the maxillary sinus and mucosal odontogenic inflammation. Sometimes, the secondary odontogenic cysts develop in the bone base of maxilla and invade the maxillary sinus. These cysts are particularly "intrusive sinus oral cysts."

#### **3. Pseudocysts present in the oral cavity**

Solitary bone pseudocysts (SBP) are devoid of any epithelium lining. They have a traumatic origin hence they are also known as bone pseudocysts or bone traumatic pseudocysts, whereas aneurysmal bone cysts (ABP) are blood-filled sinusoidal or cavernous spaces without cystic epithelium. The pathology of this cyst is similar to ABP. A trauma could lead to a bone hemorrhage and the clot may not be re-canalized which eventually leaves the cavity devoid of content and may present as continuous micro-hemorrhages. This causes a local reaction of macrophages or vascular dilation. The ubiquitous protease USP-6 which is mapped on chromosoma 16q22 are used as a diagnostic tool for ABPs.

#### **3.1 Soft tissue non-odontogenic cysts**

Nasolabial cysts are considered as one of the soft tissue non-odontogenic cysts. The concept that it is considered a fissural cyst is because it is related to the globulemaxillary cyst and its peripheral form is no longer valid. Histologically, it consists of a cyst that is lined by a bi-layered epithelium with a cuboidal basal layer and sometimes pseudo-stratified with goblet cells along with areas of squamous metaplasia. CK7 and CK19 are present in all layers whereas CK5 and CK6 are expressed only in the basal layer. The mucin in the goblet cells is positive for MUC-2 and MUC-5 AC. It is a developmental non-odontogenic cyst that originates from the lower portion of the naso-lacrimal duct.

Dermoid and epidermoid congenital cysts are positive for CK10. They are derived from embryonic pluripotential cells trapped which was trapped during the early weeks of intrauterine life and subsequently develop into one or into all three layers ectoderm, mesoderm, and endoderm. They are present in the floor of the mouth, tongue, parotid gland, and mandible.

Salivary cysts and pseudocysts are soft tissue cysts. While salivary retention cysts are considered as a pseudo-cyst. Histologically, oncocyte-like cells and pseudostratified columnar epithelium are present. The Ranula represents a mucocele on the floor of the mouth. It is formed due to salivary accumulation in the sublingual or the submaxillary gland which is followed by a rupture and extravasation of saliva in the surrounding connective. The presence of an epithelial coating is not there. Ranulas are located above the mylohyoid muscle which is known as the simple type or can grow downwards forming an hourglass shape which is known as the complex type.

Salivary duct cysts represent less than 10% of all salivary gland disorders, especially in the major salivary glands. Sialocyst is another name given to the salivary duct cyst (SDC). Salivary gland cysts can be either ephemeral or persistent. It is caused due to ductal obstruction that leads to cystic dilation of salivary ducts. Different terminologies have been given to these lesions; although, "salivary duct cyst (SDC)" is the most adequate by virtue of its origin being related to the epithelial lining of salivary gland ducts. SDCs typically occur in the major salivary glands with 80% occurring in the parotid and minimal cases are reported in the submandibular and sublingual glands. They present as dome-shaped, sessile, slow-growing, unilateral, asymptomatic, and compressible nodules in adult patients [2]. They are fluctuant to palpation but usually painless and if a sialolith is present then it may feel firmer. Secondary infection may present as mucus or pus from dilated ductal orifices when palpated. Blue tinge due to the Tyndall effect is present. They do not typically wax or wane over time, whereas its occurrence in minor salivary glands is rare and occurs more commonly in the sixth decade of life. Symptoms generally involve eating there was no pain or increase in the size of swelling. Intra-oral examination depicts a painless, mobile, non-compressible, soft, nodular, solitary swelling along with a soft brownish cystic sac filled with slimy gel-like material (**Figure 1**). Majority of the swellings range from 1 to 3 cm. Hematoxylin & Eosin (H&E) stained sections demonstrate a dilated salivary gland duct with intraluminal mucous plug (**Figures 2** and **3**) with dense chronic inflammatory infiltrate composed chiefly of lymphocytes around the dilated duct [3, 4]. Salivary

#### **Figure 1.**

*Clinical image shows surgical exposure of salivary duct cyst in the left buccal mucosa and gross specimen showing cystic sac filled with slimy gel-like material (inset).*

#### **Figure 2.**

*Histopathological image showing cystically dilated salivary gland duct with intraluminal mucous plug and squamous metaplasia of the lining epithelium (H&E stain; ×100 magnification).*

duct cysts may be congenital or acquired in origin. However, studies show that the vast majority of the cases are acquired and occur following obstruction in the duct. The exact factors that cause the obstruction are usually unknown, some suggestions include the involvement of mucus plugs, calculi, or postoperative or postinflammatory structures. Salivary secretion reduces with an increase in the age which may lead to

#### **Figure 3.**

*Histopathological image revealed cystic lining exhibiting ciliated, mucous, and oncocytoid metaplasia (H&E stain; ×400 magnification).*

the formation of a mucous plug. This has detrimental effects as it blocks the salivary gland ducts that eventually result in dilation of the duct and the intraluminal pressure increases. Another study suggests that restriction of the duct is frequently reported to be associated with mouth wash which includes hydrogen peroxide, fragrant mouth washes, and toothpaste that control tartar accumulation. Luminal pressure marginally increases due to a continuous flow of saliva as a result of recreation. This invariably leads to ductal dilation.

Cysts in the salivary ducts often present themselves as an asymptomatic, unilateral swelling that usually occurs in sites that are less prone to trauma. They are evenly distributed between the contiguous area of the buccal mucosa, lower lip mucosa, mandibular vestibule, the floor of the mouth, hard and soft palate, as well as minor salivary glands with a size range of 0.8–10 cm in size [5]. They are rarely present in the major salivary glands and if involved, are usually found in the superficial lobe of the parotid with no involvement of the facial nerve. Salivary duct cysts may affect children to older adults, mostly those over 30–40 years of age. SDCs affect the male and female population equally.

Salivary gland cysts can often be an early manifestation of a salivary gland tumor, therefore diagnosis and early treatment interventions play an important role in the prognosis of this lesion. Presence of epithelial alterations, such as metaplasias and focal papillary proliferations observed, are comparable to similar changes seen in odontogenic cysts and maybe an early markers of tumor manifestation [6]. On rare occasions, these cysts can progress and develop into benign and malignant neoplasms such as adenocarcinoma and mucoepidermoid carcinoma from the lining of a salivary duct cyst.

Primary diagnostic interventions involve imaging and histopathology. Imaging helps with determining the extent of the involvement, the borders, and the core content. Internal blood flow is absent in color Doppler while CT reports the cyst as a well-circumscribed lesion with low-density areas. On MRI, these lesions appear as

#### *Perspective Chapter: Salivary Duct Cyst DOI: http://dx.doi.org/10.5772/intechopen.105494*

high signal areas and no enhancement is observed upon administration of gadolinium while ultrasonography demonstrates a posterior acoustic enhancement lesion with imperceptible walls. Finally, sialography permits only indirect visualization of the cyst, evaluated by the displacement of the ducts around them [7].

Histologically, these lesions appear unilocular along with a ductal epithelium that may be cuboidal or columnar in conjunction with a completely, or partially lined squamous epithelium. Occasionally, oncocytic metaplasia is present. The lesions composed of oncocytic cells range from oncocytic metaplasia, and hyperplasia to benign and malignant neoplasms, including oncocytomas and oncocytic carcinomas [8].

SDCs may present clinical-pathological characteristics similar to those of salivary gland neoplasms, making diagnosis difficult and subject to errors in treatment. Pleomorphic adenoma, cystoadenoma, and low-grade mucoepidermoid carcinoma may present in a similar manner to that of SDCs. Salivary duct cysts comprise 0.5–10% of all salivary gland cysts and ideally arise from the salivary duct as nonneoplastic lesions and a majority of these lesions are between 1 and 3 cm in dimension. Since these cysts demonstrate an epithelial cystic lining histopathologically, they are considered to be a "true cyst." These cysts tend to develop post-obstruction because of the calculi, mucus plugs, trauma, or post-inflammatory scarring. In pediatric patients, the most common pathology lesions involving the parotid gland are benign neoplasms that are not limited to sialocele, lymphoepithelial cyst, first branchial cleft cyst (BCC), and a vascular or lymphatic malformation. Salivary duct cysts can be easily histopathologically differentiated from branchial cleft cysts by the presence of their epithelial lining since the former have epithelium lining of duct cells similar to intercalated, striated, or excretory duct cells whereas the latter is lined with squamous or respiratory epithelium. SDCs are extremely rare and should not be overlooked as part of the differential for any cystic salivary gland lesion since they easily and very quickly progress into a larger lesion in a few months. Sometimes, there might resemble a lymphatic malformation such as chyle-filled cysts lined with endothelium that can be macrocystic or microcystic. And these lesions can appear identical on radiographs and both display high signal intensity on T2-weighted MRI. However, these can be distinguished via MRI and STIR images since SDCs tend to be well-circumscribed masses while lymphatic malformations can be infiltrative and permeate across fat planes [9].

One of the differential diagnoses for SDCs is papillary cystadenoma lymphomatosum (Warthin Tumor). In this, there is the presence of lymphoid stroma in the cyst wall and multiple papillary infoldings with a bilayer of columnar and oncocytic epithelial lining. The second differential diagnosis is gingival cyst of the adult. These transpire only on the gingiva which has no minor salivary glands. The third differential diagnosis is cystadenoma, low-grade mucoepidermoid carcinoma (LG-MEC). Cystadenoma presents often as a well-circumscribed or encapsulated neoplasm together with a collection of the proliferation of ducts. These cysts often occur in the parotid gland and their histological variants include papillary cystadenoma, papillary oncocytic cystadenoma, and papillary mucinous cystadenoma. SDCs may present clinical-pathological characteristics similar to those of mucocele. Clinically, both represents an asymptomatic nodule, but salivary duct cysts are rare in appearance comparing mucocele. In the latter, the presence of true salivary gland duct epithelial lining is absent and instead, this is mimicked by epithelioid macrophages at the periphery of the extravasated mucin. Mucocele is present in the lower lip mucosa and a younger age group contrary to SDCs.

The treatment option for salivary duct cysts includes cryosurgery, carbon dioxide laser surgery, and conservative surgical excision. Because of the fact that benign

tumors of the salivary glands are able to clinically mimic salivary duct cysts, excision is extremely necessary. Complete surgical excision along with the feeding minor salivary gland is curative. In this method, iatrogenic intraoperative damage may occur to the neighboring salivary gland parenchyma which would contribute to the development of postoperative mucocele. Then partial or total removal of the feeding major salivary glands may be needed. Chlorhexidine mouthwash and oral antibiotics are provided for secondarily infected SDCs. Sialagogues are also provided which may help in decreasing the risk of salivary stasis within dilated ducts by stimulating salivary flow.

In conclusion, intraoral salivary duct cysts are reactive ductal ectasia that develops secondary to intraluminal obstruction that may require clinical attention when it reaches a particular size. Although the SDCs is considered a rare condition in the oral cavity, it is important to include this lesion in the differential diagnosis of lesions that affect the buccal mucosa and may sometimes transform into a malignant lesion such as adenocarcinoma and mucoepidermoid carcinoma from the lining of a salivary duct cyst along with an association of a latent Epstein–Barr virus infection. With an increase in the aging population, SDC should be considered as one of the differential diagnoses in geriatric patients.

### **Conflict of interest**

The authors declare no conflict of interest.

### **Author details**

Saurabh R. Nagar1,2,3\*, Gabriela Fernandes4,5, Shivani Bansal6 , Rajiv S. Desai6 and Diya Jayanth Kamdar7

1 Department of Pathology, Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Mumbai, India

2 Homi Bhabha National Institute, Mumbai, India

3 Department of Oral Pathology and Microbiology, Government Dental College and Hospital, Mumbai, Maharashtra, India

4 Department of Periodontics and Endodontics, SUNY Buffalo, Buffalo, New York, USA

5 Department of Oral Biology, SUNY Buffalo, Buffalo, New York, USA

6 Department of Oral Pathology and Microbiology, Nair Hospital Dental College, Mumbai, India

7 Faculty of Dental Sciences, Bangalore, Karnataka, India

\*Address all correspondence to: saurabh.nagar90@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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