Endodontic Periodontic Lesions

By Ronald Ordinola-Zapata¹, DDS, MS, PhD; JT Crepps^1,2, DDS, MS; Blake Clarke¹ , DDS

The relationship between the dental pulp and periodontium is complex and dynamic, exemplified by the occurrence of endodontic-periodontal lesions. These lesions can develop through various anatomical and iatrogenic pathways, including furcation canals, dentinal cracks, vertical root fractures, and cemental tears (1, 2).

Microbial biofilms, a multicellular population encased in an extracellular matrix (3), play a crucial role in all endodontic infections. These biofilms characteristically adhere to organic and inorganic substrates such as enamel, dentin or cementum (3-5). The root canal microbiome primarily consists of a mixed infection of anaerobic bacteria, many with highly proteolytic capabilities (6-10). See Figure 1.

Biofilm-associated infections are caused by a complex interplay of microbial and enzymatic activity (11). Hemolysins, the most common microbial toxin in root canals (9), break down inflammatory tissue, allowing anaerobic bacteria to utilize reduced ferrous iron essential for microbial activity (9). Oral bacteria can produce harmful substances that trigger immune responses and promote further bacterial proliferation, establishing a cycle of infection and inflammation (12, 13). Importantly, bacterial byproducts can infiltrate various anatomical routes, facilitating the spread of infection and bone resorption between endodontic and periodontal tissues. This interconnection is key to understanding the development and progression of endodontic-periodontal lesions.

Communication pathways between a contaminated pulp canal space and the periodontium can be either physiological or iatrogenic. While the apical foramen is the most common pathway, accessory canals, furcation canals, and exposed dentinal tubules also provide routes for microbial toxins to diffuse into the periapical tissues and furcation area. These pathways are considered physiological (14). Another source of communication is caused by root damage. See Figure 2.  Dentinal cracks, perforations, and vertical root fractures are usually contaminated which can also produce bone resorption (15-17). Furthermore, anatomical anomalies (i.e., palatogingival groove) can also influence the route bacterial byproducts take to reach the attachment apparatus or the pulp canal space.

Simon, Glick, and Frank (2), classified endodontic-periodontic lesions into primary endodontic lesions, primary endodontic lesions with secondary periodontal involvement, primary periodontal lesions, primary periodontal lesions with secondary endodontic involvement, and “true” combined lesions (18). Primary endodontic infections are characterized by pulp necrosis or untreated endodontic disease, which can lead to drainage adjacent to the gingival sulcus. This could create a tissue-destructive process which proceeds from the apical region towards the gingival margin (19). Radiolucencies in the furcation area of non-vital posterior teeth may indicate the presence of furcation canals or a crack located on the floor of the pulp chamber. Resorption at the furcation can also be the result of apical inflammation. Walton (15) found in animal experiments that the primary “movement” of apical lesions was towards the furcation in 53% of the cases. Jansson & Ehnevid (20) revealed that teeth that exhibited periapical pathology at both roots had significantly greater periodontal probing depths than teeth without periapical pathology.  Also, furcation depths of higher than 3 mm were significantly more frequent in molars with periapical pathology (20). See Figures 3 and 4.

It is important to note that primary endodontic lesions occur exclusively in the presence of pulpal disease (2). Diagnostic measures such as sensibility testing, identification of mechanical allodynia, transillumination, and periodontal probing are critical for differentiating between primary endodontic lesions and primary periodontal lesions. Untreated primary endodontic lesions may also become secondarily involved with periodontal breakdown if plaque or calculus form at the gingival margin resulting in marginal periodontitis (2). Overall, healing of the endodontically induced areas could be anticipated but the prognosis also depends on periodontal treatment to remove the additional sources of inflammation.

While the impact of pulpal disease on the periodontium is well-established, the reverse relationship – the effect of periodontal disease on the pulp – has been the subject of considerable debate by numerous researchers. In the 1970s, Bergenholtz & Lindhe (21) performed a study on monkeys in which periodontal disease was induced in 92 permanent teeth. After six months, 30-40% of horizontal bone loss was observed. Histological analysis showed that 57% of the dental pulps presented secondary dentin formation, calcifications, and mild localized inflammation. However, only one case developed pulp necrosis (21). Overall, the chances for pulpal damage when periodontal disease is present are low, unless the periodontal pocket and subgingival plaque reaches the apical third and cementum damage is present (22).

Teeth with root damage can also produce endodontic periodontic lesions. A cracked tooth is defined as a thin surface disruption of enamel and dentin, and possible cementum of unknown depth of extension (23). In these cases, the coronal crack can establish a communication pathway between the oral environment, the pulp chamber and the periodontal ligament. See Figure 5. Bacterial colonization along the crack line is linked to pulpal inflammation and necrosis (24). Posterior teeth are subject to the same principles of materials science. In particular, they are subject to cyclic loading or fatigue failure, which is the most common form of mechanical failure (25-27). It is important to note that the force or stress required to initiate and propagate a crack decrease as the number of loading cycles increases. According to Arola & Reprogel (28) the flexural strength of coronal dentin decreases almost 20 MPa per decade of life due to the repetitive nature of masticatory forces, chances for crack formation and propagation increases progressively with aging. Eventually, the contaminated crack will extend to the pulp chamber (24) and, ultimately could face the crestal bone causing bone resorption changes.

Vertical root fractures are defined as a fracture in the root whereby the fractured segments are incompletely separated. See Figure 6. It may occur buccal-lingually or mesial-distally and often leads to an isolated periodontal defect or sinus tract (23). Potential irritants previously identified in these fractures are bacteria, necrotic tissue, and food debris (29). Mandibular molars (34%) and maxillary premolars (22%) are most frequently affected (30). Vertical root fractures appear to be more correlated with previously treated teeth than teeth with necrotic pulps (31). The communication pathway created by these fractures can lead to periodontal destruction adjacent to the root fracture. See Figure 7. Practitioners should be aware of the overlap in clinical presentation of vertical root fractures and other causes of endodontic-periodontal lesions. In previously treated teeth, clinicians typically suspect vertical root fractures, but they must consider the possibility of a chronic apical abscesses presenting as narrow, deep probing depths as a pathway of drainage through the sulcus. Although vertical root fractures may not be completely evident on CBCT scans, three-dimensional imaging allows the clinician to obtain other information that may be related to root canal treatment failure like missed canals, resorptive defects, strip perforations among others. Accurate diagnosis is crucial and prevents unnecessary treatment to the patient.

Another factor associated with periodontal bone loss are cemental tears (32). This is a surface root fracture involving the cementum and sometimes the root dentin that occurs at the cemental dentinal interface (33). If the cemental tear is located at the apical level it could resemble an endodontic failure, at the middle level it will create a periodontal pocket or mimic periodontal disease (32-37). Cemental tears are more prevalent in incisors (74%) and are located on the interproximal surface (79%) (35). Seventy-one percent of patients with cemental tears are over 60 years old (34, 35). Overall, the prognosis of these cases is questionable. The surgical approach is more successful compared to the non-surgical one (57 vs 28%). Cases located at the cervical and middle third have better prognosis compared to cemental tears located at the apical third (60 vs 11%), (34). See Figure 8.

Treatment Approaches

Treatment approaches for endodontic-periodontal lesions vary based upon etiology. Primary endodontic lesions arise exclusively from an endodontic source and can be treated with endodontic treatment alone (1). Primary periodontal lesions with secondary endodontic involvement or true combined lesions require endodontic treatment first followed by appropriate periodontal treatment 1-2 months later after a periodontal re-evaluation (38). However, Gupta et al. (39) found in a randomized clinical trial that nonsurgical periodontal treatment may be performed simultaneously with endodontic treatment in the management of concurrent endodontic-periodontal lesions without communication. Therefore, the observation period after endodontic treatment may not be required. Treatment options for cracked teeth include placing glass-ionomer intraorifice barrier apical to the crack line (40), while those with vertical root fractures may undergo root amputation or extraction. Those with complex anatomical variations, such as a palatogingival grooves, may be best treated with intentional replantation or other surgical approaches (41).

Endodontic-periodontal lesions, regardless of cause, present a complex clinical scenario that can challenge even experienced practitioners. The dynamic between pulpal and periodontal tissues is influenced by microbial biofilms, anatomical variations and iatrogenic factors. Recognition of these various etiologies allows clinicians to develop targeted and evidence-based treatment plans that lead to better outcomes for patients, including multidisciplinary care with periodontists when indicated.

References

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Affiliations:

¹ Division of Endodontics, Department of Restorative Sciences, School of Dentistry, University of Minnesota, Minneapolis.

² Private Practice, Missoula, Montana.