Conservative Management of Chronic Internal Resorption With Concomitant Periapical Pathology Using Injectable Platelet-Rich Fibrin: A Review of Literature

Pathophysiology of internal resorption

Internal resorption results from chronic pulpal inflammation, often due to trauma, caries, or restorative procedures, causing damage to the protective predentin layer. This leads to the recruitment of multinucleated clastic cells, which resorb dentinal walls.^[4] Once the pulpal infection spreads beyond the apex, periapical periodontitis may ensue, characterized by periapical bone loss and chronic inflammation. After an infection, persistent chronic inflammation encourages a type of internal resorption that happens gradually. After root canal treatment or metaplastic resorption, a mineralized tissue resembling cementum or bone is formed, but it is not dentin. Reichart et al. referred to this metaplastic tissue as “reparative cementum” or “osteodentin-like material.”^[5] Internal root resorption is initiated along the root canal wall and may result in the progressive destruction of the adjacent radicular dentine.^[6] IRR may consist of granulation tissue only (inflammatory internal root resorption) or a combination of granulation and bone-like tissue (replacement internal root resorption).^[7]

Internal resorption typically results from a persistent, ongoing inflammatory process. The progression of internal resorption is contingent upon the existence of both necrotic pulp, either coronal to the point of resorption or partially so, which permits a continuous influx of bacteria and their antigens into the root canal, and vital pulp tissue at or below the resorption area. Microbial stimulation is essential for the continuation of resorption.

Diagnostic tools and considerations

Clinical signs may be absent until late stages, where symptoms like discoloration, swelling, or sinus tract may appear. Radiographically, internal resorption presents as a well-demarcated, symmetrical radiolucency within the root canal. CBCT imaging offers superior resolution for assessing lesion extent and periapical involvement.^[3] About 2% of internal resorption cases show clinical symptoms, while most are asymptomatic. It is more likely to be observed in males than in females. Usually, internal resorption occurs in the apical or midsection of the root. A “pink spot” on the crown may be a clinical symptom, or it may be discovered accidentally on routine radiography. Necrosis in the pulp may be partial or total.^[8,9]

Radicular cyst formation in chronic internal resorption

A pathologic cavity that is entirely or partially bordered by epithelium in a region of apical periodontitis and results from a tooth’s root canal infection is called a radicular cyst. The inflammatory proliferation of the periapical tissues, particularly involving Malassez’s epithelial cell rests, is likely the primary factor contributing to the development of radicular cysts. While some suggestions have been put up as potential reasons for cyst formation, the precise mechanism is still unknown.^[10]

Root canal infections are the source of radicular cysts. While pocket-type radicular cysts may be treated with traditional root canal therapy, true-type radicular cysts may require surgical management. Radicular cysts are not self-sustaining lesions like those resulting from development or neoplasia; therefore, recurrence is rare unless the infection in the tooth’s root canal persists. Radicular cysts have a good prognosis following endodontic therapy.^[11]

Conventional management strategies

The primary objectives in managing internal resorption with periapical pathology include arresting the resorptive process, disinfecting the root canal, regenerating periapical tissues, and sealing the canal to prevent reinfection.

I-PRF: A regenerative adjunct

I-PRF is a second-generation platelet concentrate prepared through low-speed centrifugation without anticoagulants. It is rich in platelets, leukocytes, and growth factors like platelet-derived growth factor (PDGF), transforming growth factor (TGF-β), and VEGF, which support angiogenesis, fibroblast migration, and extracellular matrix remodelling.^[12] I-PRF can be injected directly into root canals or periapical areas and solidifies into a fibrin matrix, providing a scaffold for cell migration and tissue regeneration. Unlike PRP, I-PRF offers a slower release of growth factors and better integration with surrounding tissues.

Studies have demonstrated that I-PRF enhances the proliferation of dental pulp stem cells and fibroblasts, promoting faster and more complete periapical healing.^[13] Animal and human case series reports improved clinical and radiographic outcomes in cases of periapical lesions treated with I-PRF in comparison to conventional therapy alone.^[14,15] In vitro studies also confirm that I-PRF modulates inflammation and supports the differentiation of odontoblastic cells, making it particularly suitable for cases involving internal resorption where dentin regeneration is desirable.^[16]

Operative Procedures

Following the administration of local anaesthesia, crevicular and interdental incisions were given spanning from 11–13, and a full-thickness periodontal flap was reflected. After debridement, a sample of autologous venous blood obtained from the patient using a sterile syringe without the use of an anticoagulant was used to prepare I-PRF. The complete blood was transferred to a 5 mL plain tube and subjected to centrifugation for a duration of 3 min at a speed of 700 rpm under clean conditions. This process led to the formation of a liquid I-PRF layer on the top of the tube while the red blood cells settled at the bottom. Following this, the liquid form of I-PRF was extracted from the upper yellow fluid layer using a plastic syringe, mixed with the bone graft, and placed with respect to tooth 11. Single interrupted sutures were placed. The patient was recalled after 7, 14, and 21 days. After six months post-treatment, due to the inadequate width of attached gingiva, a gingivectomy was performed with respect to tooth 11 to give a proper contour [Figure 3]. Since there was the presence of a radicular cyst with respect to tooth 12, cyst enucleation was performed [Figure 4]. MTA was placed with respect to tooth 11 as illustrated in Figure 5, and the patient was recalled after 2 weeks, 1 month, and 3 months post-treatment [Figure 6].

Close

Figure 3: Gingivectomy done with respect to tooth 11 to give a proper contour (yellow arrow).

Export to PPT

Close

Figure 4: Cyst enucleation (yellow arrow).

Export to PPT

Close

Figure 5: Placement of mineral trioxide aggregate (yellow arrow).

Export to PPT

Close

Figure 6: Three months postoperative photograph showing satisfactory healing with respect to tooth 11 (yellow arrow).

Export to PPT

This case emphasizes the importance of a proper multidisciplinary approach for achieving successful treatment outcomes. In our management of the pink tooth, the patient benefited from the treatment and expressed satisfaction with the outcome.

Despite the promising regenerative potential of I-PRF, certain limitations must be acknowledged. The lack of standardized preparation protocols, variability in centrifugation parameters, and limited long-term clinical evidence restrict its widespread clinical adoption. Additionally, most available studies are in vitro, animal-based, or case series, with relatively few randomized controlled trials. Compared to established materials such as calcium hydroxide and MTA, which have well-documented success rates and long-term outcomes, I-PRF remains an adjunct rather than a replacement. While conventional endodontic therapy focuses primarily on disinfection and sealing, I-PRF aims to enhance biological healing; however, its superiority over traditional approaches has not yet been conclusively established.

Continued research on standardized I-PRF protocols, especially with CBCT monitoring and histological confirmation of healing, is required. Combining I-PRF with bioceramic materials may further enhance outcomes in complex resorption cases.