The Cracked Tooth: Histopathologic and Histobacteriologic Aspects

In the 1970’s in North America, dentists were faced with a huge onslaught of patients with periodontal disease and caries. The large cohort baby boomers grew up in the 25 cent coke and a chocolate bar era and their dental health reflected it. Organized dentistry responded to this challenge with massive public education programs for both dentists and the public. Dentists developed programs for their patients that involved regular visits for preventative cleanings, fluoride, and examinations. Forty-five years on, the vast majority of the Canadian public has neither periodontal disease nor caries. The golden age is over!

Now, I believe, we are in the early stages-of recognition-of a new public dental health crisis. Cracked teeth! Cracked teeth maybe one of the most challenging situations that we are presented with in dentistry today from a diagnostic, treatment planning, and patient acceptance perspective.

A cracked tooth can be defined as an incomplete fracture of the tooth structure that can progress to affect the pulp and periodontal ligament. Possible causes for this include repetitive heavy mastication, occlusal interferences, trauma, caries, parafunctional habits, as well as iatrogenic dental treatment.

Cracks are so prevalent that they have become “normal”. A recent study (Imura JOE 2013:38) found 60% of virgin molar teeth had cracks. As dentists we see them but rarely take any action until symptoms force our hand. A part of the problem, I think, is that we in dentistry don’t fully understand the significance of cracks.

E Inflammatory cell (lymphocytes) infiltrate subjacent to crack x400
G Bacteria (purple) invading dentinal tubules

Ricucci et al, JOE 41:3, 343-357, set out to fill this gap in our understanding. The authors set out to evaluate the effect of cracks and attrition on the supporting dentin and pulp. Twenty human teeth (12 posterior, 8 anterior) were collected with a pulpal diagnosis of reversible pulpitis, irreversible pulpitis, or pulpal necrosis. These teeth were restorable and were extracted at the patient’s request or for prosthetic reasons.

The teeth were fixed, demineralized, serial sectioned at 4 microns and mounted on slides. The sections were stained for visualization of inflammatory cells (Hematoxylin &Eosin) or bacteria (Brown and Brenn). Stained sections were evaluated under light microscopy at x100, x400, and x1000.

The authors found that all the teeth evaluated contained cracks and all cracks were colonized by bacterial biofilms. When the crack reached the dentin, bacteria was found to have invaded the dentinal tubules bisected by the crack. Severe accumulations of inflammatory cells were found in the pulp zone subjacent to these cracks. In many cases, the crack extended to the pulp, leading to pulpal reactions with intensities ranging from acute inflammation to total pupal necrosis.

The question for us now is what, if anything, do we do when we see patients with cracked teeth. Firstly, we must inform our patients. With the results of Ricucci’s study we can tell them that their teeth have cracks, the cracks contain bacteria, and that at some point their pulps may become inflamed and infected, requiring endodontic intervention and prosthetic protection. This sows the seed for definitive treatment in the future.

Secondly, if there are symptomatic teeth, i.e. teeth which are temperature or bite sensitive, then appropriate endodontic treatment followed by cuspal protection is warranted. Do not be reticent to remove inflamed and infected pulps. Ricucci’s work shows us that these pulps are not normal and histologically show signs of degeneration and bacterial ingress. Our highest endodontic success rates occur when root canal therapy is initiated prior to the pulps becoming fully necrotic. It is in our patient’s best interests to intervene before there is periapical pathology present.

Thirdly, if the teeth are asymptomatic (following pulp tests to confirm vitality), then it becomes incumbent upon us to recommend a crack prevention program. This program, not unlike the caries and periodontal disease preventions programs of the 70’s and 80’s, should first confirm there are no caries or periodontal disease present then move on to a thorough occlusal evaluation. This evaluation needs to address TMJ position and stability as well as CR, CO, and any working or non-working interferences which may be present. While this may not eliminate all future cracks, and certainly will not eliminate parafunctional habits, it can, through occlusal analysis, splint therapy, and appropriate occlusal, orthodontic, or prosthetic rehabilitation mitigate future problems. Maybe the golden age is not over, just different!

Dr. Bittner was in private practice in general dentistry for 11 years in Langley prior to his Endodontic specialty training. He has been practicing the Dental Specialty of Endodontics since 1995.

In his free time, Dr. Bittner loves to participate in a variety of sports including most recent, golfing! He also enjoys being a new grandfather, which if you ask him is just the best!

On June 1, 2015, posted in: News for Doctors by