Based on the 2018 classification of periodontal disease, a series of articles have been published describing the decision points of periodontal therapy and how the findings collected at those decision points can be used as guidelines for periodontal therapy.
While the new classification gives definitive parameters for the stage and grade of periodontal disease, it does not give treatment recommendations for the different stages. Treatment was addressed by the EFP in 2020 
. While multiple treatment possibilities were outlined by the EFP, specific decision points to guide clinical treatment were difficult to ascertain. Due to the need for clinical guidance, specific decision points for treatment were developed by a group of academic and clinical periodontists with many years of experience in the private practice of periodontics, teaching of periodontics within an academic institution, and clinical periodontal research. These decision points were outlined by Harrel et al. in 2022 
. The decision points were based on the 2018 classification system, and they defined points during the clinical treatment of a patient with periodontal disease where reassessment of the patient’s periodontal condition was required. The purpose of the decision points was to define where reevaluation of the response to the treatment performed up to that point should be assessed so a determination could be made as to whether treatment had been successful. Based on the finding of the reevaluation, a decision could then be made regarding whether the patient could be placed in a periodontal maintenance program or if more advanced periodontal therapy was indicated. The decision points aided in defining critical phases where further evaluation was necessary but did not define what further treatment may be indicated. Later in 2022, the same group who had developed the decision points published clinical guidelines for periodontal therapy 
. These guidelines for periodontal treatment combined the 2018 classification of periodontal disease with the previously defined decision points in therapy.
All clinical treatment of periodontal disease is based on the basic tenet of eliminating inflammation and then maintaining an inflammation free state 
. At a purely scientific level this requires the removal of any contaminated material from the periodontal sulcus and the establishment of a stable microbiota of non-harmful organisms. The clinical application of this goal is stated simply as the removal of plaque and calculus from the tooth and establishing acceptable conditions for the patient to perform adequate oral hygiene. All clinicians who treat periodontitis know that accomplishing these goals can be very difficult. If these goals are not achieved, there will always be a continuation of periodontal inflammation and an ongoing risk for progression of periodontitis. The determination of whether these goals have been accomplished and maintained can only be achieved by routine and rigorous reevaluations of the patient’s periodontal condition.
If signs of inflammation are present at the reevaluation following initial periodontal treatment or at any periodontal maintenance appointment, further periodontal treatment is indicated. This may be a repetition of the treatment performed during initial therapy, but in most instances advanced periodontal therapy is required. Advanced periodontal therapy may take the form of non-surgical debridement with advanced visualization, localized minimally invasive surgery, or generalized surgical access. In all instances, whether non-surgical or surgical, advanced therapy starts with gaining visual access to accomplish instrumentation for the removal of calculus that was not removed during initial therapy. After calculus removal, advanced therapy may also include surgical treatment to allow for improved oral hygiene (osseous surgery) or regeneration of the damaged periodontal supporting structure. However, the common denominator needed for the success of advanced therapy is the removal of calculus that remains after initial therapy. Thus, the need for advanced therapy is based on a therapist’s inability to remove calculus during initial therapy. The retention of calculus is central to the instances where there is a failure of debridement procedures and the progression of periodontal disease following treatment 
Researchers will look at the following clinically relevant issues: (1) The previously published decision points and guidelines as they apply to clinical decisions for further periodontal treatment; (2) The role of calculus and the incomplete removal of calculus during initial therapy on the need for advanced periodontal treatment; (3) The pathologic risk factors for periodontal disease that can be addressed by the practitioner performing active therapy; and (4) The ethical considerations of periodontal reevaluations and the recommendation for further therapy.
2. Initial Therapy
In all cases, no matter what stage of the disease, the initial treatment of periodontitis will consist of debridement of the teeth and the periodontal sulcus in conjunction with oral hygiene instructions (OHI). This debridement generally takes the form of scaling and root planing (SRP) 
. In most instances, SRP is performed simultaneously with OHI aimed at teaching the patient how to remove the constantly renewed plaque and biofilm on their teeth. While it is well recognized that OHI is an integral part of maintaining periodontal health, the actual application of the OHI and the daily maintenance of oral hygiene is in the hands of the patient 
. Because this is a patient dependent activity, this portion of periodontal therapy will not be addressed other than to state that oral hygiene is mandatory for clinical success and should be evaluated, reviewed, and reinforced at every appointment.
3. Debridement and the Removal of Calculus
SRP is the most frequently performed periodontal treatment procedure 
. Part of the definition of SRP is the complete removal of all soft and hard deposits on the tooth and root 
. The required complete removal of hard material (calculus) from the root surface is technically and physically very demanding and becomes more difficult as the periodontal sulcus becomes deeper with periodontal disease progression 
. Several studies have looked at the efficacy of performing SRP without enhanced (endoscope or videoscope) visualization 
. SRP without enhanced visualization is often referred to as “blind SRP”. These studies found that when an expert clinician with adequate instrumentation and time performed blind SRP, between 27 to 73% of the planed root surface still had detectable calculus following subsequent surgical exposure of the root surface 
. Studies have also shown that when extracted teeth that had SRP performed using direct visualization under 3.5× loupe magnification with unfettered access for instrumentation, 20% of the root surface continued to have what were termed microislands of calculus remaining 
. Figure 1
shows microislands of calculus remaining after SRP using loupes for magnification. A recent scanning electron microscope (SEM) study has shown that residual calculus fragments, referred to as fractured calculus, are present on root surfaces that have undergone SRP 
. It is likely that the fractured calculus seen with SEM may represent the microislands of calculus detected in other studies. These studies collectively reveal that a residuum of subgingival calculus remains in most instances where SRP has been performed in a routine “blind” manner. This routine retention of calculus is a major factor in disease recurrence and represents incomplete and inadequate treatment for the control of periodontal disease 
Figure 1. Microislands of calculus remaining on a root surface after ultrasonic and hand scaling until the root of the extracted tooth was deemed calculus free when visualized with 3.5× magnification loupes. The root surface is illuminated with a 655 nm laser to aid visualization of calculus. (Videoscope photo 40× magnification).
4. Calculus as a Risk Factor for Periodontal Degeneration
There is general agreement that plaque/biofilm consisting of a community of bacteria and other microbiota, e.g., viruses and protozoa, is the initial cause of periodontal disease 
. Because of the extensive literature supporting plaque as the “cause” of periodontal disease, there has been a relative deemphasis on the role of calculus in the persistence and progression of periodontal disease. Most have indicated that calculus plays a secondary role acting mainly in the retention of plaque and that the removal of calculus is solely to allow for improved oral hygiene 
However, there is both classic and recent literature indicating that calculus plays a more direct role in periodontal inflammation and destruction. For example, an in vivo animal study showed that sterile calculus when placed in Guinea pigs resulted in generalized inflammation and granulation tissue production 
. In addition, a study using non-surgical endoscopic visualization in humans revealed that nearly 70% of inflammation (assessed via tissue coloration) of the soft tissue wall in deep periodontal pockets was associated with calculus covered by biofilm and less than 20% of the inflammation was associated with biofilm alone 
Recently a potential alternate pathway for cell death in periodontal tissues has been reported. Ziauddin et al. 
. demonstrated that sterile calculus, when phagocytized by connective tissue cells in cell culture, induced cell death 
. In a later study, Ziauddin et al. 
. confirmed the cytotoxic effects of sterile calculus using an in vitro model consisting of HSC-2 oral epithelial cells and THP-1 macrophages. This pathway of cell death was described as pyroptosis, i.e., an inflammatory form of lytic programmed cell death. The authors postulated that the calculus crystals are phagocytized by the epithelial cells utilizing a defense mechanism designed to bring bacterial products into the cell where they are neutralized. However, when the phagocytized agent is the crystallin structure of calculus, the cells die. While this pathway of induced cell death has yet to be demonstrated in humans, it is logical to presume that such a pathway will act in humans in a similar fashion as seen in the cell culture studies 
. If this presumption were to prove true, then it explains the clinical observations that most inflammation in the gingival sulcus soft tissue is associated with calculus and that residual calculus is found at sites of inflammation following SRP.
The complete removal of calculus is imperative for the adequate treatment of periodontal disease but frequently it is not completely removed with standard nonsurgical treatment. It is clinically and ethically unacceptable to place patients in a periodontal maintenance program when calculus and associated inflammation remain.