1. Introduction
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]. Thisis 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 (NF-κB), 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 becomescolonized with primary colonizers and subsequently with the late colonizers. Among the late colonizers,
Porphyromonasgingivalis (P. gingivalis) and
Porphyromonasintermedia (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 of periodontal or peri-implant diseases.
3. Rationale and Approaches for Non-Surgical Management of Dental Biofilm
The dental biofilm resides in the close vicinity ofthe 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 ofgingival 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.
The sequential steps of GBT are described in Figure 1. Similarly, the procedure performed on the patient has been elaborated in Figure 2.
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 NaHCO
3 on Titanium disc has shown promising results as an air abrasive
[54][55].
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
[56].
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
[57]. Its usage in periodontitis patients has been reported to lower the counts of
P. gingivalis [57] and is more acceptable and tolerant to the patients
[58][59]. 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)
[60].
8. Guided Biofilm Therapy in Periodontal Disease and Peri-Implant Disease
The literature search shows many studies have been performed to assess the outcome of GBT on periodontal or peri-implant disease. Few studies have reported reduction in the red-complex bacteria when periodontally healthy individuals underwent GBT treatment
[9]. In addition, studies with periodontitis patients have also found significant reduction in the pocket depth of more than 5 mm along with the reduction in
Tannerella forsythia (
T. forsythia) and
Treponemadenticola (
T. denticola) with subgingival usage of erythritol as air polishing powder along with reduction in Matrix metalloproteinases (MMP-8)
[10]. Furthermore, in another study a significant decrease in the levels of
P. gingivalis was reported after one month in the group treated with erythritol air-polishing compared to SRP
[11]. Contrary to this, there are studies which have observed the same or lesser clinical outcomes of glycine/erythritol air-polishing compared to SRP
[12][13][14][15].
Home care oral hygiene alone does nothave the ability to completely remove the newly formed bacterial deposits from the residual pockets, which is a well-established fact. Hence, patients are supposed to be put on SPT that needs professional dental biofilm management
[16][17]. GBT has been proven to be as effective as conventional SRP treatment in clinical outcomes
[16][13][14]. However, GBT was reported to be more comfortable to patients with less pain perception
[16][18]. In another study, the 12 month post-operative count of
Aggregatibacter actinomycetemcomitas (
A. actinomycetemcomitans) was less at the test site treated with erythritol with 3% chlorhexidine than the control site receiving SRP. However, the role of adding chlorhexidine to erythritol cannot be substantiated with the reduction of bacteria.
Additionally, it has not caused any harm to the soft tissues
[16]. A systematic review and meta-analysis found that air polishing devices are safe and effective in carrying out biofilm removal similar to conventional therapy when used in SPT
[19]. It was concluded that the main advantage of air polishing in supportive periodontal therapy is that it does notcause harm to soft tissue, tooth structure, or root structure. Moreover, it has better compliance among patients and consumes less time. In a recently conducted retrospective study, the clinical outcomes with low abrasive air powder glycine were equally effective as conventional mechanical debridement during SPT. It was also suggested that it should be restricted in the area of furcation where SRP is advisable
[18].
Dental implants have emerged as effective rehabilitation management for a non-restorable tooth or replacement of tooth in a missing area with a reported success rate of 97% in a follow-up period of 10 years
[20]. However, biological complications such as peri-implant disease are reported with a prevalence of 46.83 and 19.83% for peri-implant mucositis and peri-implantitis, respectively
[20]. A plaque score of ≥30% is a risk indicator for peri-implant mucositis, and similarly, a plaque score of ≥25% is associated with peri-implantitis
[21][22].
As per the consensus report, conventional non-surgical mechanical therapy and oral hygiene reinforcement are the standard treatment for peri-implant mucositis. This treatment will help in the reduction of PPD of approximately 0.5–1.0 mm and 15–40% reduction in BOP. On the other hand, NSPT of peri-implantitis usually helps reduce BOP by 20–50% and, in some cases pocket reduction of ≤1 mm. However, in advanced cases complete resolution of disease is unlikely with mechanical plaque control
[23]. Nonetheless, mechanical plaque control remains a mainstay in the treatment of peri-implant disease or during supportive therapy following implant insertion
[24]. As per the consensus statement 2016, the air-polishing device has shown positive clinical outcome for peri-implant mucositis or peri-implantitis
[25]. Following a non-surgical management of peri-implant mucositis or peri-implantitis, a significant reduction in BOP and bleeding index was found when glycine powder was used as monotherapy or adjunctive measure
[25]. In an animal model study, partial regeneration and less inflammation were reported
[26]. Additionally, studies have reported a statistically significant result with an air-polishing device either with glycine or erythritol in the treatment of peri-implant diseases
[27][28][29][30]. Contrary to this, studies have reported either similar or no additional benefit over SRP
[31][32][33][34][35]. Few fundamental studies related to usage of air polishing powder in periodontal and peri-implant disease have been summarized in
Table 2.
Table 2. Studies with glycine/erythritol as an air-polishing agent in the treatment of periodontal diseases/peri-implant diseases.
The GBT concept may have the following advantages over the conventional methods of prophylaxis:
-
The use of a plaque disclosing agent allows the operator to determine the patient compliance in executing proper oral hygiene practices. It also allows the patient to visualize areas that were neglected;
-
The use of an air-polishing device can remove the disclosed plaque effectively and safely without causing soft tissue damage compared to conventional rubber cups, especially during subgingival plaque removal;
-
The removal of plaque using air polishing prior to ultrasonic scaling provides better visible access to calculus deposits. Instead of the indiscriminate use of ultrasonic scalers for the entire dentition, the operator can now target the use of ultrasonic scalers on sites with mineralized deposits. This minimizes soft tissue damage and CAL caused by ultrasonic scaling at sites with shallow pocket depths. From the patient’s perspective, this translates to lesser discomfort and sensitivity experienced during ultrasonic scaling. Overall, treatment time is also reduced;
-
A second plaque disclosure provides quality control and assurance to the patient as well as the operator.
9. Conclusions
With the current evidence, it can be concluded that GBT is an effective means of removing biofilm from the tooth or implant vicinity. Compared to SRP, GBT was reported with better patient compliance and less pain perception in non-surgical periodontal therapy or supportive periodontal therapy. Although, in peri-implant diseases, it does help in the reduction of plaque, its usage as monotherapy needs further investigation with long term studies as the clinical outcome is short-lasting.