Introduction
Periodontitis develops rather insidiously, and due in large part to modifiable risk factors. In the dentist's office, early identification of those at risk for developing this disease can be difficult, since by far the largest proportion of patients will not develop it. Roughly 5% to 10% of the population will have periodontitis, and only 1% of that group will experience refractory disease.
Constant monitoring and reevaluation of the periodontal patient is required to prevent disease progression. Today, we also recognize that periodontitis is an inflammatory condition, and as such must be treated using a medical model of care.
Understanding when to use pharmacological and other nonsurgical approaches, and in which patients, will improve the dental professional's ability to prevent bone loss in this population, and to avoid the morbidity and potential side-effects of surgery when possible.
1. What risk factors make an individual more susceptible to developing periodontitis, and how can they be managed?
Dr. Lai: Several longitudinal studies have identified smoking as the most significant modifiable risk factor for developing periodontitis. Immune diseases such as HIV/AIDs, diabetes and a genetic predisposition to developing periodontitis are also risk factors. There is a weaker association in the literature that suggests patients with a high degree of psychological stress are prone to the disease, as well, although the mechanism is not yet clear. Risk indicators for periodontitis include older age, lower socio-economic strata and a lack of access to regular dental care.
Dr. Tenenbaum: Prevention and management involves good oral home care with a focus on the basics to remove the bacterial challenge – brushing teeth twice a day, preferably with an electric toothbrush, cleaning between teeth with floss and stimulators, and supplementing with an oral rinse containing chlorhexidine, essential oils or cetylpyridinium chloride. Regular cleanings at the dental office two to four times per year, depending on the severity of disease, are also important.
Smoking is one of the most difficult addictions to treat, but patients should be encouraged to quit and referred to appropriate resources that can increase their chances. Patients with poorly controlled type 2 diabetes are at greater risk for developing periodontitis, while the risk is almost the same for well-controlled diabetes as it is for non-diabetics. There is a bidirectional relationship between both conditions – so adequately controlling one will positively influence the other. Attention to blood sugar control therefore needs to be excellent.
Finally, immunocompromised patients must maintain meticulous oral hygiene and use an antibacterial rinse to keep bacterial loads down in order to prevent periodontal problems from developing.
2. What daily oral care regimens are effective in preventing or mitigating periodontitis?
Dr. Lai: There has been a shift in the literature from the idea that perfect oral hygiene is absolutely critical to avoid the development of periodontitis to the recognition that the long-term outcome of the disease is actually based on how the host reacts to the presence of bacteria. That said, it's important to teach patients the proper ways to brush and to use interdental aids – as Dr. Tenenbaum says, a focus on the basics. Good oral care is a habit, and since poor habits are hard to break, constant monitoring and re-education is necessary to ensure patients comply.
3. What is the role of biofilm, and how is it prevented or removed?
Dr. Tenenbaum: A biofilm is a very complex biologic entity. It's a bacterial society in which the bacteria actually exchange genes – and in particular resistance genes. Bacteria within biofilms are several- fold more resistant to antibiotics and antimicrobial rinses than are planktonic bacteria in the periodontal pocket, and therapeutic agents have a hard time penetrating the biofilm to kill bacteria. It can be disrupted by brushing, flossing and other mechanical means such as scaling and root planing (SRP), rendering the bacteria more susceptible to kill with antibacterial rinses or antibiotics.
4. What therapies can be done concomitantly, and when is intensive periodontal treatment indicated?
Dr. Tenenbaum: Certainly with scaling and root planing it is important to include antibacterial rinses, flossing and brushing as part of the treatment protocol. In some cases, where patients don't respond to scaling and root planing and despite improved oral hygiene still have deep periodontal pockets with bleeding, surgery is necessary to gain access to root surfaces covered by a biofilm or calculus deposits that contain pathogenic biofilm byproducts. The other pillar of intensive periodontal therapy is recall treatment every three months for scaling and root planing and oral hygiene instruction. This has been shown to not only have positive microbiological outcomes but behavioural ones as well (that is, patients' good habits can be reinforced while their bad hygiene habits can be reduced).
Dr. Lai: The evidence tells us that nothing is as effective at physical removal of biofilm as scaling and root planing, and so that is always the first line of defense. Concomitant therapies can also include the use of antibiotics to interfere with the formation of biofilm once periodontitis is present.
5. What factors determine the use of a systemic or locally administered antibiotic (LAA), such as Arestin®?
Dr. Lai: Before opting for periodontal surgery, dentists need to assess the effectiveness of scaling and root planing and oral hygiene instruction. If these approaches have not been successful, the next step is to consider whether the patient would benefit from additional, non-surgical options.
Dr. Tenenbaum: If there is still evidence of deep periodontal pockets, bleeding, pain on probing or pus emanating from several pockets one to two months following the completion of the debridement stage of therapy, then consideration of an antibiotic is warranted. Systemic antibiotics are used when there are several disease sites. LAAs are useful when, following the debridement phase, the patient still has isolated pockets with active disease.
I regularly use LAAs in my practice to treat periodontitis under three common scenarios. First, if the patient has one or two involved areas upon presentation or after scaling, I will use an LAA along with rescaling at those sites. Second, if after a patient has been scaled and one to two sites still require surgical intervention, I will first try an LAA to get them under control. Third, if after scaling they improve but still have several areas of disease, and if after subsequent treatment with a systemic antimicrobial they still have one to five dispersed pockets, those can be treated effectively with an LAA.
When I see a patient whose disease has responded well to SRP and/or systemic antibiotics, but in whom a few problematic pockets remain, there is no question that I will use an LAA.
Dr. Lai: LAAs are a regular part of the armamentarium in my practice, as well – typically in patients who have had treatment for periodontitis but are now in the maintenance phase of therapy, but also in patients with localized disease sites.
6. Does the LAA take the place of SRP, or is it used adjunctively?
Dr. Tenenbaum: LAAs are always used as an adjunct to SRP – I would never recommend using them alone. While some evidence has suggested that patients treated with an LAA alone did as well as those receiving SRP alone, there is no long-term data available. When you consider long-term patient care, I can't conceive of a situation where you can use an antimicrobial to treat periodontal disease when there are still local etiological problems present.
7. At what pocket depth would you start considering the use of an LAA?
Dr. Tenenbaum: From my perspective, approximately 5mm would be the point where I consider using an LAA, because that's also the point where one has to consider surgery. But there has to be other signs of active disease, such as bleeding on probing and inflammation – pocket depth alone is not the only indicator. Certainly, if a pocket is 3mm with bleeding, I will try an LAA to gain control.
Dr. Lai: The best results, in my experience, are seen in what I consider moderately deep pocket depths, usually around the 4mm to 6mm mark. And I agree – overall periodontal risk assessment is more important in determining when to use any treatment than pocket depth in isolation.
8. What is the clinical relevance of LAAs for reduction of bleeding on probing and pocket depth, as well as infection control?
Dr. Lai: Combining both SRP and an LAA has been shown to produce incrementally better clinical outcomes than either approach alone.
There are a variety of studies that demonstrate in 30%-40% of cases greater than 2mm probing depth reduction when using LAAs. That's clinically significant. It makes the difference between maintaining the patient or moving on to surgery. Bleeding on probing has typically been a secondary outcome measure in published trials. We know that SRP is very effective for reducing bleeding; evidence suggests that the beneficial effects of LAAs are more pronounced in terms of the reduction of inflammation in deeper pockets.
The evidence also strongly supports that LAAs deliver the antibiotic at a concentration that is 1,000 times higher than that needed to kill bacteria. So, as an added benefit, even if the patient has a developed a certain level of resistance it won't be a major negative factor.
Dr. Tenenbaum: LAAs are clinically relevant in each scenario. There are papers by Paquette et al, which, for example, looked at Arestin in chronic periodontal disease, that show statistically significant reductions in mean probing depth using an LAA alone, and an increased effect using an LAA plus SRP.
There has been some misunderstanding about the clinical significance of a 2mm to 2.5mm mean reduction in pocket depth as reported in some published trials, which does seem unimpressive until you consider that they are mean values. This statistical approach washes the effects of LAA treatment on deeper sites out of the results – but the fact is, the effects on pocket depth reduction are similar for LAAs as for SRP. No one would argue that SRP, the cornerstone of treating periodontal disease, is not clinically relevant because it produces 'only' a 1.5mm to 2mm reduction.
Remembering that local antibiotics should only be used adjunctively with SRP, LAAs have nonetheless been shown do just as well as SRP on bleeding on probing and in controlling the microbial flora in periodontal pockets. There are log reductions of periodontal pathogenic bacteria in pockets treated with LAA.
Certainly there are cases where, after standard therapy, patients still have areas that need attention, and here is where LAAs are most useful. These areas seem to respond very well to the use of LAAs and debridement.
9. Are there other benefits of using an LAA over a systemic antibiotic?
Dr. Lai: LAAs are also useful in terms of patient compliance, since there aren't several pills to take each day over the course of many weeks. Since they are delivered locally, patients experience virtually none of the side effects associated with systemic antibiotics, and there is minimal risk of developing multidrug resistant bacteria.
10. What is your clinical experience using Arestin or other LAAs in management of chronic periodontitis?
Dr. Lai: In my experience, patients with chronic periodontitis respond well to SRP and oral hygiene instruction, since by far their biggest challenge is compliance with oral care regimes. However, in patients for whom conventional treatment on localized areas is not effective, I use LAA as part of their management. I see more significant responses upon a subsequent round of SRP and reapplication of the LAA, perhaps three months after the first treatment. I am sometimes very surprised at the response and at the improvement I see in probing depth reduction and elimination of inflammation.
Dr. Tenenbaum: There are many periodontal diseases, but the most common forms that present can be managed very well via infection control using the three treatment pillars: SRP, systemic antimicrobials and LAAs. This also holds for chronic periodontitis, one of the most common forms of periodontal disease.
The evidence tells us that LAAs can play a role in treating chronic disease. In my experience – and I have discussed this with colleagues who agree – antibiotics have allowed us to do noticeably fewer surgeries. With the advent of LAAs, surgery is no longer the only option in patients with a few pockets. When I try an LAA in these cases, greater than 50% of the time an area that would have required
surgery in the past does not require it. And they are quick and simple to administer, so LAA treatment can be done immediately. Surgery will always be an important part of our treatment armamentarium, but now we know that when the sequence of treatment moves from SRP to systemic antimicrobial and then to an LAA, we can markedly reduce the need for surgical intervention.
