American Board of Endodontics (ABE) Oral Examination

Correct: In the natural periodontium, the connective tissue attachment is characterized by gingival fibers (Sharpey’s fibers) that insert perpendicularly into the cementum of the root surface. In contrast, dental implants lack cementum and a periodontal ligament; therefore, the collagen fibers in the peri-implant connective tissue zone are oriented parallel or circumferential to the implant surface and do not physically insert into the titanium or zirconia body.

Incorrect: Option B is incorrect because hemidesmosomes are responsible for the attachment of the junctional epithelium to the tooth or implant surface, not the connective tissue fibers, and these fibers do not insert into the titanium. Option C is incorrect because there is no histological evidence of transverse fiber groups providing mechanical interlock in the soft tissue zone; stability in the bone is achieved through osseointegration. Option D is incorrect because the peri-implant mucosa is actually less vascular and contains more collagen/fewer fibroblasts compared to the natural gingiva.

Takeaway: The fundamental histological difference in soft tissue attachment is that natural teeth possess perpendicular fiber insertion into cementum, while peri-implant fibers run parallel to the implant without insertion.

Correct: The success of periodontal surgery depends on the maintenance of the blood supply and the availability of progenitor cells for regeneration. The supraperiosteal vessels are the primary source of nutrition for the reflected flap, and their preservation prevents tissue necrosis. Additionally, the periodontal ligament (PDL) contains the necessary cellular components, such as fibroblasts and cementoblasts, that are essential for the formation of a new connective tissue attachment rather than a long junctional epithelium.

Incorrect: Removing all acellular cementum is an outdated concept that can impede the formation of a new connective tissue attachment by removing the biological scaffold needed for fiber insertion. Thinning the flap excessively can compromise the vascular plexus, leading to flap marginal necrosis or significant gingival recession. While bone curettage or decortication is used in specific guided tissue regeneration (GTR) contexts to increase blood flow from the marrow, it is not the primary requirement for general flap viability or standard periodontal reattachment compared to vascular and PDL preservation.

Takeaway: Periodontal surgical success relies on the preservation of the vascular supply and the biological integrity of the periodontal ligament and cementum to facilitate proper healing and attachment.

Correct: The semilunar coronally advanced flap, as described by Tarnow, is a technique where the apical blood supply to the flap is intentionally severed by the semilunar incision. Consequently, the survival of the coronally positioned tissue segment is entirely dependent on the collateral blood supply from the lateral papillary regions. To preserve these vascular channels, the incision must terminate within the attached gingiva. If the incision ends are too close to the sulcus or extend into mobile mucosa, the blood supply is compromised, and the risk of flap necrosis or recession recurrence increases.

Incorrect: Placing the incision at the mucogingival junction or within the alveolar mucosa is incorrect because the muscle pull and mobility of the mucosa lead to flap instability and significant scarring. Reflecting a full-thickness flap is not a requirement of the semilunar technique and does not address the primary physiological challenge of maintaining the lateral blood supply. Vertical releasing incisions are contraindicated in this specific technique as they would sever the very lateral blood vessels that the semilunar flap relies on for survival.

Takeaway: The success of a semilunar coronally advanced flap depends on preserving the lateral blood supply by ensuring the incision remains within the stable, attached gingiva.

Correct: The most widely accepted biological hypothesis for the link between periodontal disease and adverse pregnancy outcomes involves the hematogenous spread of oral pathogens (such as Fusobacterium nucleatum) or their inflammatory mediators (like PGE2 and TNF-alpha). When the sulcular and junctional epithelium is ulcerated due to chronic periodontitis, it serves as a portal of entry for bacteria into the bloodstream, eventually reaching the feto-placental unit and inducing labor-triggering inflammation.

Incorrect: The migration of gingival fibroblasts to the uterus is biologically impossible and not a recognized pathway for labor induction. Sharpey’s fibers are localized to the attachment of the tooth to the alveolar bone and cementum; their degradation is a local periodontal event and does not cause systemic collagen failure in the cervix. Cementum formation is a localized process on the root surface and does not act as a systemic mineral sink capable of affecting fetal bone development.

Takeaway: The primary link between periodontal disease and adverse pregnancy outcomes is the systemic dissemination of oral pathogens and inflammatory mediators through compromised sulcular and junctional epithelium.

Correct: In the peri-implant environment, the connective tissue attachment differs significantly from that of a natural tooth. While natural teeth have Sharpey’s fibers that insert perpendicularly into the cementum, the connective tissue fibers around an implant abutment (primarily Type I collagen) are oriented parallel to the long axis of the abutment and do not physically insert into the titanium or zirconia surface. This lack of perpendicular insertion makes the peri-implant seal more vulnerable to mechanical disruption compared to the natural periodontium.

Incorrect: The suggestion that fibers insert perpendicularly via cementum is incorrect because cementum does not form on dental implant abutments. Hemidesmosomes are responsible for the attachment of the junctional epithelium to the abutment surface, not the connective tissue fibers. Dentoperiosteal and transseptal fiber groups are specific to the anatomy of natural teeth and their relationship to the root and adjacent teeth; they do not exist in the same functional or anatomical capacity around an implant abutment.

Takeaway: Unlike natural teeth with perpendicular Sharpey’s fibers, peri-implant connective tissue fibers run parallel to the abutment surface and lack a physical insertion into the material.

Correct: Root concavities, particularly on the distal of mandibular molars and the mesial of maxillary premolars, represent significant anatomical challenges in periodontal therapy. These areas are often physically inaccessible to standard scaling and root planing instruments, as well as patient-performed oral hygiene aids. The resulting inability to effectively debride the area leads to persistent biofilm accumulation and continued periodontal destruction, which is a primary determinant in assigning a guarded or poor long-term prognosis.

Incorrect: The concentration of fibroblasts is a normal histological feature of the periodontal ligament and does not accelerate inflammation; rather, they are essential for tissue maintenance and repair. Bundle bone is the functional part of the alveolar bone where Sharpey’s fibers embed and is not a barrier to attachment. The rapid turnover of the junctional epithelium (approximately 4 to 6 days) is a normal physiological defense mechanism and is not the cause of progressive attachment loss in the presence of anatomical defects.

Takeaway: Anatomical root concavities are a critical factor in periodontal prognosis because they create niches that are inaccessible to mechanical debridement, leading to persistent disease.

Correct: In the natural periodontium, supracrestal connective tissue fibers (Sharpey’s fibers) insert perpendicularly into the cementum of the tooth, providing a strong mechanical barrier. Around implants, there is no cementum, and the collagen fibers in the connective tissue are oriented parallel or circumferential to the implant surface. This lack of physical attachment and the parallel orientation of the fibers make the peri-implant environment less resistant to the apical migration of plaque and the subsequent spread of inflammation into the alveolar bone.

Incorrect: The junctional epithelium around an implant does indeed form a hemidesmosomal attachment and basal lamina similar to that of a natural tooth, so claiming it lacks these is incorrect. Peri-implant connective tissue is actually more similar to scar tissue, meaning it is generally more collagenous and contains fewer fibroblasts and blood vessels than natural gingiva, not more. Finally, a biological width (or supracrestal tissue attachment) does exist around implants, consisting of a junctional epithelium and a connective tissue zone; it is not absent.

Takeaway: The lack of perpendicular fiber insertion and the parallel orientation of collagen fibers in the peri-implant mucosa significantly reduce the mechanical barrier against the apical progression of peri-implantitis.

Correct: Maxillary first premolars frequently possess a deep mesial developmental groove or root concavity. In mucogingival surgery, these anatomical features make it difficult to achieve close adaptation of the connective tissue graft and the overlying flap to the root surface. This lack of adaptation can lead to the formation of a dead space, preventing the stabilization of the fibrin clot and hindering the revascularization of the graft from the overlying flap and the lateral periodontal tissues, ultimately resulting in incomplete root coverage.

Incorrect: The lamina propria of the hard palate, the typical donor site for SCTG, is primarily composed of dense collagen fibers rather than elastic fibers; shrinkage is more related to graft thickness and surgical technique than elastic fiber content. While epithelial migration is a concern in periodontal healing, the primary challenge in this specific anatomical location (maxillary premolar) is the root morphology rather than the sulcular epithelium. Acellular extrinsic fiber cementum is the ideal substrate for new connective tissue attachment; removing it entirely to expose dentin is generally avoided as it may impair the biological potential for new attachment.

Takeaway: The presence of root concavities, particularly on maxillary premolars, is a critical anatomical risk factor that reduces the predictability of complete root coverage due to compromised graft adaptation.

Correct: Aggressive periodontitis, now classified under the 2017 World Workshop as Periodontitis Stage III/IV Grade C, is characterized by its rapid progression and strong familial aggregation. Because the disease often affects multiple family members due to genetic predispositions in host response, the first clinical step in addressing the pathogenesis and diagnostic confirmation is to evaluate the family history and screen siblings to identify other affected individuals who may be asymptomatic.

Incorrect: While PMN chemotactic defects are a significant part of the pathogenesis, functional leukocyte assays are generally reserved for research or refractory cases rather than initial clinical evaluation. Microbiological testing for Aggregatibacter actinomycetemcomitans provides supportive data but is not the primary diagnostic criterion for the localized phenotype. Evaluating transseptal fiber integrity through imaging is not a standard clinical method for assessing disease pathogenesis or progression in this context.

Takeaway: Familial aggregation is a primary diagnostic feature of aggressive periodontitis, necessitating the screening of family members as an initial step in clinical management and diagnosis confirmation.