Blood and periodontal disease.

Bleeding-on-probing CAN be a useful
diagnostic tool, but only if you know how
to read the body’s cries for help.

by Larry Burnett, DDS
Springfield, VA

“Periodontal disease is a site-specific, episodic affliction.”

Periodontal bone destruction is rarely a linear process. More typically, the periodontal patient suffers rapid attachment loss in several pockets. This may be followed by a prolonged period of stability when nothing much seems to be happening. Then suddenly a flair-up may occur in a different pocket.

Our job at periodontal recall appointments is not to mindlessly scrape roots till they’re glassy smooth ... but to carefully scout the mouth looking for evidence of periodontal flair-ups, and then to intervene before the destruction becomes serious.

Why patients rarely die of periodontal disease.

The bugs that cause periodontitis are nasty fellows that theoretically should cause infections far more serious than bone loss.

Expose a cut to the filth in the typical perio pocket, and you could be looking at gangrene ... a raging bacteremia ... ... maybe death. Yet patients rarely show evidence that periodontal germs are spreading beyond the oral cavity.*

Why?

In my opinion, it’s because the body’s last line of defense against periodontal disease is very effective. Forget hygienists for a minute. Ignore home care. Just leave the body alone, and it will generally resolve matters on its own ... in its own way.

Don’t believe it? Read on.

In this series of articles I’ve tried to portray periodontal disease as an ongoing guerilla war between the forces of evil (bacteria and their by-products) and the forces of good (the patient’s immune system, good oral hygiene, and the professional dental team with our bag of tricks.)

The battle that rages in an infected pocket is extremely complicated. But here’s the nickel version ...

As the body’s T1 cells sense that the virulent pathogens have begun to multiply, the immune system marshals its forces. The first evidence of this is a classic inflammatory response. Blood circulation in the sulcular epithelium slows and the capillary walls become more permeable, so the pocket is bathed in antibodies, lymphocytes and leukocytes. At a recall appointment you may notice this battle as an increase in bleeding during probing.

If this first line of defense is effective (if those white cells do their stuff), the flare-up will calm down and enter a dormant phase. However if the pathogens have reached critical mass, the body’s measured response won’t be enough.

Several years ago I made a video that I’ve used repeatedly during patient education. I’d drawn a sample of crevicular fluid from a seriously diseased pocket and examined it under a phase-contrast microscope. You can see the undulating free-swimming pathogens everywhere. But one frame is particularly riveting. A large lymphocyte sits motionless as 10-15 rapidly vibrating spirochettes radiate out from its cell walls. Like a dying lion harassed by jackals, the body’s hunter cell has become victim of the hunted.

In the face of an overwhelming infections the body may activate a TISSUE DESTRUCTION STRATEGY.

The bacteria that cause periodontal disease require a hard non-sloughing surface surrounded by an anaerobic environment ... In other words, a tooth and a pocket. (Think about it. Have you ever seen a denture patient suffering gingivitis?) If its initial defense proves inadequate, the body may implement a scorched-earth policy. Since the forces of evil require a hard surface and pocket, the immune system begins to sacrifice teeth in order to save the patient.

It’s rather like tossing the cholera victim overboard in order to save the other passengers. At least that’s my interpretation of how teeth are lost to periodontal disease.

One thing is clear though: The enzymes that destroy the periodontal membrane (the prostaglandins and interleukin 1), aren’t produced by the pathogens ... they’re produced by the body’s own immune system. It’s the body itself that generates attachment loss ... that causes the bone level to drop and teeth to loosen and fall out.

Like I said, the body will resolve the infection in its own way. But the patient may not be happy with this cut-your-losses approach.

Your job as a diagnostician is to accurately read the body’s response to the disease ... and as a therapist, to intervene in the battle before the body implements its scorched-earth defense.

Bleeding scores as an early warning system.

Unfortunately, the most popular BOP scoring system is almost useless as a diagnostic tool. Bleeding is often indicated with a small red dot on the patient chart. This tells you that the patient bled, and it tells you where the patient bled, but it doesn’t tell you how much the patient bled.

Most studies have shown that these blood scores aren’t very helpful in predicting the activity of periodontal disease. In fact, in 70% of cases where blood is noted, the bleeding is not followed by bone loss. In other words, the BOP scores were not predictive of periodontal disease.

It’s true that the absence of blood during probing is almost always a good sign, because it suggests a lack of inflammation. But the converse isn’t true. The presence of blood doesn’t necessarily mean there IS inflammation. As you can see in the study described in the sidebar (“Blood as a red herring”) many perfectly healthy patients bleed.

And most perio patients (including my own) continue to bleed a bit, even though they are not suffering attachment or bone loss. If you use “lack of blood” as your criteria for success, you will begin to question your skills as a therapist because you’ll have very few “successes.”


Bleeding may mean nothing. Changes in bleeding may mean a lot.

A couple of years ago, I authored an article for Parkell Today (July 95) arguing that it’s virtually impossible to diagnose active periodontal disease using radiographs from a single appointment. That’s because a low bone level does not indicate active periodontal disease ... a dropping bone level indicates periodontal disease. And to detect a change in bone level you need to compare radiographs from at least two appointments.

Traditional 4-film mounts make it very difficult to compare radiographs. Put those same radiographs in serial mounts, however, and even small changes in bone level become obvious. It’s like looking at sequential frames of a motion picture. You actually SEE the bone level dropping.

In this article, I’m making the same argument for systematically tracking changes in bleeding.

First, use a system that records how much blood.

The BOP system I use has 4 classifications of increasing severity. It’s certainly not the only valid system, but it’s simple ... and it works for me.

Class 1 A small spot of blood localized at the probe site.
Class 2 A spot of blood that spreads along the gingiva.
Class 3 A spot of blood that spreads along the gingiva and up the proximal walls.
Class 4 A general “stuck pig” classification that applies to a major hemorrhagic response.

Keep impeccable records.

Bleeding at or below a pocket’s historical baseline is consistent with a state of health. Bleeding above the baseline should wave a red flag drawing your attention.

Suppose while probing the distal of #4, I discover Class 2 bleeding. I glance at my records and see that the pocket has a long bloody history, but without significant attachment loss. In fact, at the last appointment I’d recorded Class 3 bleeding. Since the BOP doesn’t seem to be getting worse (and may actually be getting better), there’s no cause for alarm.

However, if the pocket normally shows Blood & Periodontal Disease Class I bleeding, the change may signal a new flare-up.

So I’d spend some extra time ultrasonically debriding the pocket. I’d examine the tooth for overhangs, residual calculus or other contributing factors that might encourage the pathogens. I might supplement the cavitation with a shot of chlorhexidine or povidone iodine using my Periosonic irrigator.

As I mentioned, I consider changes in the bleeding scores much more significant than whether or not there’s blood.

The exception to this is Class 4 bleeding. When a touch of my probe elicits a red deluge, I don’t waste time studying my records or establishing baselines. I begin therapeutic intervention immediately. I don’t have any studies to support it, but it’s my strong clinical impression that serious bleeding indicates that the immune system has already initiated bone destruction. So I want to get in that pocket and give the immune system all the help I can.

Remember, we’re fighting an episodic and site-specific disease here. If you know how to read it, a change in bleeding pattern may serve as an early indicator that something is brewing. It not only suggests that a new episode is beginning ... it also identifies the specific sites that demand your attention.

I Lang NP, et al. Bleeding on probing asit relates,to probing pressure and gingival health. J Clin Perin. 18:257 261, 1991
2 Karayiannis A, et al. Bleeding on probing as it relates to probing pressure and gingival health in patients with a reduced but healthy periodontium. J Clin Perio. 19:471475, 1992

*Recent links between periodontal disease and systemic diseases suggest the body's defense isn't perfect

About the author ...

A graduate of the Medical College of Virginia School of Dentistry, Dr. Burnett has authored numerous articles and lectured extensively on conservative periodontal therapy throughout the US and Canada. A frequent speaker at both the ADA annual scienific session (1995, 1996, 1997, 1998) and AGD meetings (1994, 1995), he is featured in the video-based program “Advanced Ultrasonics in General Practice”

Dr. Burnett also conducts hands-on courses for dentist and hygienists.

He can be contacted at: Dr. Larry Burnett, 2221 SW First Ave #1224, Portland, OR 97201 Tel: 503-221-4237, lburnett2@comcast.net

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