Reconnecting Practicing Hygienists with the Nation's Leading Educators and Researchers.

Guest Editorial: Dental Hygienists Play a Critical Role

The skills and knowledge of this key dental team member are needed today more than ever before.

 The prevalence of periodontal diseases increases with age. According to the United States Centers for Disease Control and Prevention, 47.2% of adults age 30 and older have some form of periodontal disease; this figure increases to more than 70% among adults age 65 or older. Due to educational efforts by the American Academy of Periodontology, the American public is aware of the relationship between periodontal diseases and diabetes, heart disease, stroke, and even some cancers. If one were to ask the average person “what is the cause of gum disease?” he or she would probably answer “plaque.” All people who leave plaque on their teeth for a significant length of time will eventually get gingivitis, but not all will develop periodontitis. Some reasons for this discrepancy include genetics, stress, systemic diseases, smoking status, and type of pathogens present in the oral microflora.  

A recently published paper in the Journal of Periodontology, “A Re-Evaluation of Scaling and Root Planing,” reviews the peer-reviewed literature on calculus, biofilm, scaling and root planing, and periodontitis.1 The paper, which includes original scanning electron photomicrographs of surface and cross-sectional views of diseased roots magnified more than a 1,000 times, can be accessed here: through the end of September 2021. 

Although scaling and root planing is extremely effective at reducing clinical inflammation and probing depths, some residual calculus will remain depending on the pocket depth, root anatomy, mode of attachment, time spent, and operator skill and experience.2 The beneficial effects of complete subgingival calculus removal on the resolution of inflammation are well known. Nevertheless, for a variety of reasons, over the past several decades clinicians, educators, and state board examiners have diminished the significance of complete calculus removal in favor of establishing a “biocompatible root surface” as a necessary requirement to the eradication of the periodontal disease process. The critical question is: Can a root surface with retained calculus be compatible with health? 

High-powered microscopes reveal calculus to be a porous mineralized structure, like a dry sponge, allowing viable periodontal pathogens to live within its framework.3 Multiple studies show a relationship between calculus and inflammation in the adjacent soft tissue wall of the periodontal pocket. The reservoirs of bacteria living within calculus may function over time to release toxins into the periodontal pocket, causing the disease to progress. 


Dental hygienists are charged with a difficult task when treating patients with moderate to advanced periodontitis. Many factors are at play: pocket depth and location; proximity of adjacent teeth; presence of furcation involvement; patient cooperation; time allowed; length, shape, and sharpness of the hand instrument; and design and power of the ultrasonic insert/tip.

One of the most important factors is the type of attachment of the calculus to the subgingival root surface. Calculus attaches to the root surface in three main ways. First, when pockets deepen, the exposed cemental surface has a rough texture due to a series of tiny mounds, only seen with a powerful microscope, each a former insertion site for the periodontal ligament fibers. Glycoproteins, coming from the crevicular fluid, form a sticky pellicle layer on the pebble-like surface of the cementum. Free-floating subgingival microbes become initial colonizers of the root surface and are rapidly joined by additional bacteria to initiate the early stages of a biofilm. Eventually the biofilm thickens and becomes partially calcified and surrounds bacteria-filled channels and spaces. When accessible, these deposits may be easily removed with overlapping strokes of hand and ultrasonic scalers as the retentive properties of the cemental mounds provide minimal adhesion.

Second, many root surfaces contain resorption defects, known as surface cavitations or lacunae, which may penetrate through the cementum to the dentin and, in turn, may lock the calculus into undercuts, making removal very difficult, even in pockets of moderate depth. 

Third, calculus can bind directly to the hydroxyapatite crystalline structure of cementum.4 Studies show that this attachment may be stronger than the cohesive strength within the calculus itself. Thus, when a dental instrument is used to remove the calculus, a portion of the basal layer remains firmly attached to the tooth. The oral health professional usually cannot tell this has happened and “fractured calculus” remains. When only partially removed, residual calculus becomes burnished, or smooth, and is often undetectable by a periodontal probe or scaler insert/tip, blending with the surrounding root surface, resulting in an inflammatory lesion in the adjacent soft tissues. This, ultimately, fuels future pocket increases. If this process persists unabated, eventually the tooth will be lost. Burnished calculus is a prime reason periodontal diseases continue to progress after scaling and root planing.


Bacteria can invade root cementum and dentin through porosities, root fissures, and micro-channels found on the root surface. The presence of bacteria in root cementum and dentin has been observed in numerous studies using light, scanning electron microscopy, and culture studies.1,5 It is difficult to tell when bacteria exist in these spots, so unless the oral health professional is using a periodontal endoscope or videoscope, a hard, smooth surface is the ultimate goal.

Dental hygienists are often taught that removal of subgingival endotoxin—toxic substances contained inside the cell that are released when the cell disintegrates—is important, but that it is only loosely attached to the root surface, and can easily be removed with ultrasonic instrumentation during subgingival scaling. To some extent this is true, but what is not as well known is that endotoxin can penetrate the outer surface of cementum6 and invade surface cracks and the depths of root resorption defects, making its removal very difficult. Residual endotoxin in these defects after scaling and root planing will prevent healing. 


Due to a variety of factors, dental hygienists may not be able to remove all of the calculus, biofilm, and endotoxins during scaling and root planing. The possibility of pocket re-infection means a thorough assessment of the results of periodontal therapy should be done 4 weeks to 6 weeks after scaling and root planing has been completed. This period is optimal because the trauma caused by the instrumentation will have resolved and any repopulation of residual bacteria will have reached sufficient numbers that inflammation from microbial sources, if present, will be evident.

The re-evaluation appointment should be of sufficient length, allowing time for assessing pocket depth, root smoothness, clinical attachment levels, and inflammatory indicators such as exudate or bleeding on probing. Although bleeding on probing may give a false positive for the presence of disease, its absence is evidence of health. If it is determined the inflammation has been resolved and the pocket depths have been reduced, the patient is ready for maintenance, or supportive periodontal therapy. If not, retreatment, or referral, may be indicated.

As periodontitis is a chronic disease, with periods of quiescence and exacerbation, it requires constant monitoring, excellent patient self-care, and frequent maintenance scalings. The frequency of the supportive periodontal therapy visits should be determined by the extent of the bone loss, presence of systemic and local risk factors, and potential for future tooth loss. Every 3 months to 4 months is a common interval for supportive periodontal therapy, but an even shorter interval may be appropriate for some patients.


Dental hygienists may be placed in a difficult situation when they believe they have done all they can and the patient should be referred to a specialist, but the general dentist disagrees. This is unfortunate. A prompt referral can be critical in situations where the patient is rapidly losing bone. Periodontists receive extensive training in the treatment of advanced and refractory periodontitis cases and may possess sophisticated equipment to enhance the therapeutic results of scaling and root planing. In addition, some calculus deposits can only be accessed and removed by surgery. Hard and soft tissue augmentation and regenerative procedures can often be utilized to change a periodontal prognosis of a tooth from “poor” to “good.”

Periodontal patients should have annual examinations consisting of a complete pocket charting, mobility changes, and vertical bitewing radiographs that show the interdental osseous crests. Apical movement of bone levels over time is indicative of serious clinical attachment loss and is more important than a stable pocket depth.


Dental hygienists are strategic players in a drama that affects the well-being of millions of patients. The challenge is to continually develop the knowledge and clinical skills to deliver the quality of care so needed today by an expansive population of patients that trust and depend on them. 


  1. Cobb CM, Sottosanti JS. A re-evaluation of scaling and root planing. J Periodontol. March 4, 2021. Epub ahead of print.
  2. Heitz-Mayfield LJ, Trombelli L, Heitz F, Needleman I, Moles D. A systematic review of the effect of surgical debridement vs. non-surgical debridement for the treatment of chronic periodontitis. J Clin Periodontol. 2002;29(Suppl 3):92–102.
  3. Calabrese N, Galgut P, Mordan N. Identification of Actinobacillus actinomycetemcomitans, Treponema denticola and Porphyromonas gingivalis within human dental calculus: a pilot investigation. J Inter Acad Periodontol. 2007;9:118–128.
  4. Rohanizadeh R, Legeros RZ. Ultrastructural study of calculus-enamel and calculus-root interfaces. Arch Oral Biol. 2005;50:89–96.
  5. Giuliana G, Ammatuna P, Pizzo G, Capone F, D’Angelo M. Occurrence of invading bacteria in  radicular dentin of periodontally diseased teeth: microbiological findings. J Clin Periodontol. 1997;24:478–485.
  6. Hughes FJ, Smales FC. The distribution and quantitation of cementum-bound  lipopolysaccharide on periodontally diseased root surfaces of human teeth. Arch Oral Biol. 1990;35:295–299.

From Dimensions of Dental Hygiene. June 2021;19(6):14-15.

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