Dental biofilm is a polymicrobial entity that resides on biotic and abiotic surfaces of the oral cavity ^[1]. These surfaces can range from hard or soft tissues of the oral cavity as well as the inanimate surfaces such as orthodontic bands, clear aligners, or prosthesis ^[2][3]. The supra and subgingival dental plaque biofilm can form on the tooth or implant surface. Being close to the gingival epithelium can deteriorate the periodontal and peri-implant health ^[3]. Dental plaque biofilms are also formed in some inaccessible regions of the oral cavity from where it is difficult to remove, thus compromising the home-care oral hygiene management. Although scaling and root planing (SRP) is considered the gold standard for mechanical plaque debridement ^[4], it also has its own disadvantages ^[5][6][7]. Nowadays, an alternative novel approach is being practiced for removing the biofilm by visualizing it with a disclosing agent and subsequently removing it with specialized air abrasive powder. Lastly, it is followed by the removal of supra and subgingival calculus using specialized instruments. This concept has been named guided biofilm therapy (GBT) ^[8].

2. Dental Biofilm and Its Relation to Periodontal and Peri-Implant Diseases
The oral cavity is an inhabitant of many microbial species, ranging from healthy microorganisms to those with pathogenic potential. The association between dental plaque and periodontal diseases is a well-established fact. However, until 1980, it was believed that the microorganism present in dental plaque remains in suspended or planktonic states [9]. Accordingly, the majority of the treatment was directed towards the removal of the dental plaque. Later, Casterton and colleagues have shown in their research that the microorganisms are not free-floating entities; rather, they are attached to the tooth surfaces [9]. Currently, it is well accepted that the microorganism lives in a complex environment known as biofilm [9,10]. It is known to contribute as the etiological agent for dental caries and periodontal disease [10,11]. A mature biofilm is a polymicrobial entity that primarily consists of bacteria, but it can also harbor protozoa, viruses, and fungi [12]. In 2002, Donlan and Casterton defined biofilm as a sessile microbiological community characterized by cells adhered to a substrate, to an interface, or each other, embedded in an extracellular polymeric substance matrix that produces and presents an altered phenotype, in terms of growth rate and gene transcription [13]. The biofilm has been considered as a single unit consisting of spatial arrangement of microorganism wherein the microorganisms display characteristics as a whole unit rather than a single entity [14]. Usually, the bacteria residing in the biofilm are considered beneficial bacteria and are known as commensal. However, during diminished host response predisposed by certain clinical situations, there is a shift in the composition of microbial flora where pathogenic bacterial species dominate over the healthy microbial flora. This phenomenon is known as “dysbiosis” [3].
The bacteria residing in the biofilm are responsible for the inflammatory cascade and, subsequently, the destruction of the supporting tissues [15,16]. Presently, periodontal and peri-implant disease are based on “polymicrobial synergy and dysbiosis” [17]. This is based on the hypothesis that the keystone pathogens such as P. gingivalis are initially introduced into the biofilm. Later, by undermining the host’s immunity, they succeed in modifying the composition of the microbial community, thus making it more pathogenic and competent to instigate disease [18]. These microbial alterations are accentuated by local environmental changes, thus establishing a microbiota capable of sustaining the dysbiosis and progressing the disease. It is also suggested that instead of directly causing the disease, the keystone pathogens bring about change in the metabolic activity of commensal which in turn increases the pathogenicity of the bacteria and thus manifests the disease [19]. The dysbiosis leads to an upsurge in the generation of inflammatory mediators, which triggers the host cell to produce toxic products. When these toxic products are produced, more than the threshold level leads to destruction of the tissues around the tooth and implant [3]. Additionally, the pathogenic bacteria trigger the innate immune response, which tries to cleanse the invading microorganism [20]. In the innate immune system, the pathogens trigger the Pattern Recognition Receptors (PRRs) that attach to the pathogen associated Molecular Patterns (PAMPs). These receptor types include toll-like receptors, nucleotide-binding oligomerization domain (NOD) proteins, cluster of differentiation 14 (CD14), complement receptor-3, lectins, and scavenger receptors [20,21]. The toll like receptors plays a crucial role in the progression of periodontal/peri-implant inflammation and bone resorption [22]. It has been reported that PAMPs activates T and B cells’ immune response leading to activation of cytokines and osteolytic pathway [22]. In conjunction with innate immunity, periodontal and peri-implant tissue produces various cytokines and chemokines which maintain the equilibrium. However, in the presence of dysbiosis, there are certain cytokines such as IL-1β, tumor necrosis factor (TNF)-α and IL-6 which lead to destruction of the tissues [3]. Apart from these mechanisms, there are three protein pathways, namely nuclear factor kappa B (NFκB), cyclo-oxygenase (COX) and lipo-oxygenase (LOX), which has an established role in the progression of periodontal/peri-implant diseases [3]. Hence, understanding its structure and biology is fundamental to unfold the etiopathogenesis behind the periodontal disease and peri-implant disease. Furthermore, researchers have found that 65% of infectious diseases are linked with the biofilm mode of growth of the microorganism [23].
The biofilm formed on the natural tooth or dental implant shares the common pattern of microbial colonization [24]. Within 30 min of implant insertion in the oral cavity, it is coated with a salivary pellicle and later becomes colonized with primary colonizers and subsequently with the late colonizers. Among the late colonizers, Porphyromonas gingivalis (P. gingivalis) and Porphyromonas intermedia (P. intermedia) are primarily responsible for peri-implantitis [25]. Surface roughness is a common feature incorporated in the implant to achieve osseointegration, but it also invites more biofilm microbial entities for colonization [24]. Biofilm formation is an inevitable phenomenon, but at the same time, its control and elimination cannot be overlooked, as it is the main culprit in the etiopathogenesis ofperiodontal or peri-implant diseases.
3. Rationale and Approaches for Non-Surgical Management of Dental Biofilm
The dental biofilm resides in the close vicinity of the gingiva epithelium. If proper oral hygiene measures are not taken care of, this supragingival biofilm will accumulate along the gingival epithelium and become a potential source of gingival inflammation [3,15]. It is generally considered that the dental biofilm is noxious in nature, and if not disrupted it can progress to periodontitis, provided there is a simultaneous diminished host response [26,27]. In order to maintain periodontal stability after non-surgical periodontal therapy (NSPT) or surgical periodontal therapy, supportive periodontal therapy (SPT) plays an important role [28]. It is commonly observed that periodontal pockets can be easily recolonized with bacteria. Hence, regular recall visits in the form of periodontal maintenance therapy are of utmost importance [29]. Similarly, the biofilm formed on the dental implants has a similar microbiota as the neighboring tooth [30]. It is observed that the subgingival microbiota shares common periodontal pathogens as in periodontal disease. Hence, maintenance of the implant by removing the biofilm should be the principal management to combat the development of peri-mucositis or peri-implantitis. Initially, based on the non-specific plaque hypothesis, the removal of the dental plaque was aimed at removing the bulk of the bacteria [31]. Later, the focus was shifted to specific bacterial removal based on specific plaque hypotheses [32]. Nevertheless, many hypotheses have been presented, but dental plaque remains a common etiological factor. Thus, a dental plaque was taken into consideration for the prevention of periodontal or peri-implant disease. Oral hygiene is maintained at home by personal care, which includes the usage of the toothbrush with dentifrices [26,33]. Despite meticulous cleaning, some amount of dental biofilm is left behind in undetected areas. Dental anatomical structures such as furcation,cervical enamel projection, deep groves, and concavities can be a potential ecological niche for bacteria [34]. Professional management of dental biofilm will enable professionals to reach inaccessible areas where dental plaque remains hidden. SRP is a gold standard in non-surgical mechanical debridement, based on the biofilm’s mechanical disruption [3].Although it is a conventional treatment option, it has its own disadvantages such as being a time-consuming procedure, technically demanding, and occasionally uncomfortable to the patients [35]. After SRP, it has been reported that the lingual tooth surface and furcation areas are prone to residual calculus [6,7].
Moreover, furcation areas are seen to have incomplete root planing [7,36]. Additionally, gingival recession, and irreversible root damage has been reported if SRP is performed repeatedly as a protocol for supportive periodontal therapy(SPT) [5]. These untoward events will lead to dentinal hypersensitivity [37]. Furthermore, it has been observed that the outcome of SRP also depend on the skills of the operator [38]. Considering these drawbacks, various technologies and machines have been introduced to remove the dental biofilm, such as vector scaling systems, lasers, and an air polishing agent.

Figure 1. Steps in guided biofilm therapy (GBT).

Figure 2. (A–F): Guided biofilm treatment (GBT) procedure in a patient with generalized bleeding on probing with plaque accumulation and localized calculus. (A) Pre-operative view; (B) application of disclosing agent on left half of the patient’s mouth; (C) application of disclosing agent over the patient’s entire mouth; (D) removal of supragingival biofilm and stains with air-polishing device (AIRFLOW^® Handy); (E) removal of the calculus removal from natural teeth with PIEZON^® PS allows thorough cleaning; (F) immediate post-operative view of the patient’s mouth after implementing the GBT protocol.

 4. Role of Disclosing Agent
The plaque detector or disclosing agent is a non-toxic substance that binds and colors bacterial plaque deposits to be visible and can be removed accurately. According to Wilkins (1959), a disclosing agent is a selective dye in solution and/or tablets used to visualize and identify dental biofilm on tooth surfaces [39]. The plaque detector helps the patient understand the state of dental hygiene at home and helps the clinician. It can be used during the active phase as well as in the professional hygiene maintenance phase. It will enable the clinician to follow the progress over time as well as provide an absolute certainty that all plaque deposits have been completely removed after periodontal therapy [40]. By applying the disclosing agents immediately before tooth brushing, SRP, or periodontal surgery, it is possible to precisely identify plaque and achieve a better degree of biofilm removal in terms of professional oral hygiene, thereby improving clinical results [40,41].
Many clinicians adopt disclosing agents to motivate and make patients’ oral hygiene home care performance measurable. This method has been given the name “colorimetric technique” [42]. The disclosing agent in the correct form and technique helps the patient perform better oral hygiene [43]. With the use of disclosing agents, the patients can clearly visualize the areas around the teeth, including the bacterial biofilm, thus facilitating the clinician to motivate patients to prevent periodontal disease.In 1914, Skinner introduced the first disclosing agent (Skinner’s iodine solution) with the aim of teaching a home method of plaque identification [44]. At that time, it was not an established fact that the biofilm is the etiological agent for periodontal diseases and dental caries. Later, many monotonic dyes were introduced in the market, such as mercurochrome, Bismark brown, Genetian violet, and erythrosine [44]. Currently, various monotonic, bitonic and tritonic disclosing agents are available in the market. As the name suggests, the monotonic dyes highlight all deposits on dental surfaces with a single shade, whereas the bitonic compounds are able to differentiate between young and mature plaque. Recently, a new generation tritonal plaque detector gel has been introduced in the market. It is capable of identifying not only “young” and “mature” plaque, but also being the most acidic, it is capable of demineralizing the hard tissues of the tooth [45]. These are dispensed in various forms, including soluble tablets (mainly for home use) gel, solution, wafer, lozenges, mouth rinses, or pre-loaded pallets. On administration, these agents color
the areas of the oral cavity where the biofilm is present, whereas the intensity of the color depends on the thickness of the plaque [46]. Ideally, a disclosing agent should be stable, odorless, tasteless, non-allergic, diffusible, and should adequately stain the tissue [47]. Likewise, in GBT the basic principle is to visualize the dental biofilm—the main etiologic agent for periodontal disease and peri-implant disease—and subsequently its removal with specialized instruments and equipment. These disclosing agents act as a professional guide to visualize the most inaccessible area of biofilm and thereby achieve mechanical plaque control by a minimally invasive procedure concept [8]. Many patients are visual learners and are impressed to view the plaque disclosed areas with the help of
intraoral camera images on the computer monitor. This helps to motivate patients about the treatment and oral hygiene. The Electromedical system (EMS) provides the disclosing solution in pre-loaded pellets, in which the sponge is pre-soaked with disclosing agent. Hence, it can be easily applied on tooth surfaces with less effort and cleanliness. There are some technical considerations to be kept in mind before applying the disclosing agents.
(a) It should be used with caution on the restorative material as it can cause staining;
(b) It should not be applied before the application of a sealant;
(c) Solutions containing alcohol should not be stored for more than 2 to 3 months as the alcohol will evaporate, making the solution too concentrated;
(d) Clinical assessments of soft tissue color, such as gingival status and gingival bleeding index, should be performed prior to the use of the plaque detector as dyeing the solution may mask the clinical status of the tissues;
(e) Always assess for any kind of allergies of patients before using the detectors in any form [44].
6. Air Polishing Devices
The usage of air polishing devices was introduced in 1945, wherein aluminum hydroxide [Al(OH)3] powder was used for cavity preparation [48]. Various technical advances have improvised the devices, and currently, these air polishing devices are used for biofilm removal. The principle of air-polishing device was to deliver the slurry consisting of abrasive air particles (powder) mixed with water under pressure through a specialized nozzle [48].

The air-polishing device is based on two principles. First, the “venturi” powder chamber principle [49], where the powder mainly exits from the bottom of the chamber. In this technique the mixture of air and powder is created by the combination of carburetor technique and swirling [49]. In this technique, the amount of air powder discharged through the tube is dependent on the positioning of a sloping deflector at the filler cap [48]. As per the second principle, the air-powder slurry is formed by forcing the pressurized air into the powder chamber and reaching the outlet by swirling action [50]. The amount of powder emission is dependent on the screw setting. It has been observed that the amount of powder emission can be regulated by the first principle, whereas according to the second principle, the setting powder emission is inconsistent. In the second type, a decrease in the
powder mass can decrease the powder output [48]. Currently, two systems(devices) are available for an air-polishing device: a hand-held device and a standalone device. These units are connected with the air turbine coupling of the dental unit. In the hand-held device, the powder chamber is smaller, thus requiring frequent refilling. Furthermore, the coupling unit of the hand-held device is bulkier. Hence,it is not ergonomic to use in inaccessible areas [48]. Essentially there are two types of nozzles used for air polishing, namely the supragingival and subgingival nozzle (Table 1). The supragingival nozzle, otherwise known as the standard nozzle, is basically used to remove the supragingival plaque and stains. On the other hand, subgingival nozzles can be used for treatment of periodontal pockets as well as in peri-implantitis. The supragingival nozzle is available at a 120 or 90◦ angle for posterior and anterior teeth, respectively [51]. Conversely, the subgingival nozzle is designed to have markings with either two outlets (Acteon) or three outlets (EMS). In the EMS system (PERIOFLOW®), the two outlets are located approximately 2 mm above the third nozzle
which is situated at the tip. The outlets on the sides allow the exit of the air and powder mixture whereas the third outlet at the tip helps in the emergence of water [28]. It has been reported that a minute change in the size, diameter, length of the tube, and curvature can significantly affect the efficacy of the equipment [52]. It is also of prime importance to keep the nozzle at thecorrect distance from the tooth structure and the angulation of the slurry with the tooth surface. The incorrect angulation of the handpiece and distance from the tooth structure can have an adverse effect on soft tissues [53].

7. Air Abrasive Powders
The mechanism by which the air abrasive removes the biofilm, calculus, or tooth substance depends largely upon the particle size, mass hardness, and angularity of the abrasive delivered through the pressurized jet of water [48]. However, the increased pressure and water setting increase the efficacy of the instrument. Furthermore, it is also believed that water enhances the activity of air abrasive powder by removing the embedded particles on the surface. On the contrary, it is also believed that water film on the object will decrease the effect of air abrasives. Additionally, water’s kinetic energy will help break the particle and reduce its size, hence adversely affecting its efficiency [48]. Since the 1970s, various air abrasives have been used in clinical practice. Currently,
sodium bicarbonate (NaHCO3), glycine powder, erythritol powder, and bioactive glasses are some of the commercially available air abrasive powders [5]. These air abrasive powders mainly differ in particle size, shape, and consequently in their outcome. The particle size ranges from 1–250 µm with the glycine powder having a particle size of 45–60 µm and erythritol powder with a particle size of about 14–31 µm. The smallest particle size is found to be of bioactive glass (1–10 µm). Comparing the particle shape of air abrasives, NaHCO3 has chiseled and sharp edges. The particle shape of glycine is similar to NaHCO3, but it is less chiseled. Erythritol has extra fine grains whereas bioactive glass have has regular shape [5].
Another factor that can influence the treatment outcome is time duration. Instrumentation time is basically userdependent, and it may adversely affect the hard tissue or soft tissue if proper technique is not followed [48]. Additionally, the effectiveness of the technique is also modulated by the amount of powder present in the pressurized chamber. It has been reported that the usage of the slurry in the pressurized chamber decreases the efficacy and efficiency of the device [48].
7.1. Sodium Bicarbonate (NaHCO3)
It is a non-toxic, water-soluble powder used mainly for supragingival biofilm removal [5]. It has been reported that NaHCO3 can alter the outer enamel layer, root cementum, and dentine [5,35] even if used for a shorter span of time. Furthermore, it is corrosive to certain restorative materials such as gold, amalgam, and composites [35]. Considering its abrasive nature, nowadays, low abrasive agents such as glycine and erythritols are commonly used [5]. However, in vitro studies pertaining to usage of NaHCO3 on Titanium disc has shown promising results as an air abrasive [55,56].
7.2. Glycine Powder
Glycine is an amino acid, consisting of non-toxic, biocompatible organic salt crystals which have slow solubility in water. It is approximately 80% less abrasive than NaHCO3, and accordingly, studies have reported less soft tissue damage using glycine powder. Rarely, air emphysemas have been reported as an adverse reaction which wasresolved within four days [57].
7.3. Erythitol Powder
It is an artificial sweetener and a food additive. It is chemically neutral, non-toxic, water-soluble polyol. Compared to glycine, it has a smaller particle size and is more stable [58]. Its usage in periodontitis patients has been reported to lower the counts of P. gingivalis [58] and is more acceptable and tolerant to the patients [59,60]. Some authors have reported that erythritol powder causedno significant damage to soft or hard tissue after using erythritol powder. Furthermore, erythritol powder showed a smooth surface on dentin compared with NaHCO3 and glycine powder. It was also found in a 12 month follow-up period that erythritol powder resulted in significant reduction in probing pocket depth (PPD) and bleeding on probing (BOP) [61].

This entry is adapted from the peer-reviewed paper 10.3390/microorganisms9091966