Resident’s Name: Michael Hatton Date: 12/13/2017
Article Title: An Overview of Chronic Oral Graft-Vs-Host Disease Following Pediatric Hematopoietic Stem Cell Transplantation
Authors: Da Fonseca, M; Hong CA
Journal: Pediatric Dentistry
Date: Mar/Apr 2008
Major Topic: Medically compromised patients
Type of Article: Review article
Review of the pathogenesis, prevention, and treatment of pediatric chronic GVHD, focusing on its oral manifestation and dental management in children.
1) Mouth can be major or ONLY site of cGVHD presentation – pediatric dentists must be able to recognize conditions.
2) Patients who survive HSCT at least 10 years at 8.3x risk of new solid cancer, mainly squamous cell carcinomas of skin and oral cavity.
3) Research on management of pediatric oral cGVHD almost non-existent.
Hematopoetic stem cell transplantation (HSCT) is the treatment of choice for many hematologic, genetic, oncologic, and immunological diseases. It is also one of the most aggressive treatments among the different cancer therapies, and is associated with severe conditioning-related toxicity, which include profound neutropenia, a high level of prophylatic immunosuppression and graft vs host disease (GVHD). GVHD remains a significant complication of HSCT and is a frequent reason for nonrelapse morbidity and mortality following allogenic HSCT.
GVHD is thought to be due to improper recovery of the immune system leading to recognition of T cells as foreign, impaired T and B cell production, impaired antibody production, and functional asplenia; thus clinical manifestations of cGVHD closely resemble that of autoimmune diseases.
Acute Graft-Vs-Host Disease (aGVHD) – distinctive syndrome of dermatitis, hepatitis, and enteritis developing within 100 days of allogeneic HSCT
Chronic Graft-Vs-Host Disease (cGVHD) – tends to be a more pleiotropic (diverse effects) syndrome generally developing after 100 days. 20% of patients receiving matched sibling transplants develop disease, 40% of patients receiving matched unrelated donor recipients develop disease. cGVHD can be categorized as: de novo, quiescent (following acute), or progressive (following acute).
Most significant risk-factors for developing cGVHD:
· Patient age 10 years or older
· Donor age 5 years or older
· Female donor to male recipient
· Use of total body irradiation as part of transplant conditioning regimen
· Diagnosis of hematologic malignancy
· Previous aGVHD
cGVHD course and prognosis:
· infectious complications, leading to death
· progressive organ failure from GVHD involvement, leading to death
· risk of new solid cancers – mainly Squamous Cell Carcinomas of skin and oral cavity
cGVHD prevention and treatment: Best approach to reduce GVHD-related mortality is prevention
· Interference with T cell activation and function, ie. cyclosporine and tacrolimus
· Interference with T cell proliferation, ie. methotrexate and mycophenolate mofetil (MMF)
· Reduction of T cell numbers, ie. Alemtuzumab and antithymocyte globulin
· Interference with cytokine function, ie. corticosteroids
· Supportive care: local measures, ie physical therapy, deep tissue massage, optimal oral care, antibiotic prophylaxis, dietary concerns, sunblock
Oral and Dental Aspects:
· Mouth can be major or ONLY site of cGVHD presentation
· Oral cGVHD often starts with xerostomia and/or oral sensitivity
· Risk of development of Oral Squamous Cell Carcinomas
· Atrophy and erythema or lichenoid lesions of buccal and labial mucosa
· Oral pain not limited to ulcerations
· Erosive lesions
· Jaundice of oral mucosa