Autologous mesenchymal stem cells offer a new paradigm for salivary gland regeneration

Salivary gland(SG)dysfunction,due to radiotherapy,disease,or aging,is a clinical manifestation that has the potential to cause severe oral and/or systemic diseases and compromise quality of life.Currently,the standard-of-care for this condition remains palliative.A variety of approaches have been employed to restore saliva production,but they have largely failed due to damage to both secretory cells and the extracellular matrix(niche).

Management of the palato-radicular groove with a periodontal regenerative procedure and prosthodontic treatment:A case report

BACKGROUND Palato-radicular groove(PRG)is defined as an anomalous formation of teeth.The etiology of PRG remains unclear.The prognosis of a tooth with a PRG is unfavorable.The treatment of combined periodontal-endodontic lesions requires multidisciplinary management to control the progression of bone defects.Some researchers reported cases that had short-term observations.The management of teeth with PRGs is of great clinical significance.However,to date,no case reports have been documented on the use of bone regeneration and prosthodontic treatment for PRGs.CASE SUMMARY This case reported the management of a 40-year-old male patient with the chief complaint of slight mobility and abscess in the upper right anterior tooth for 15 d and was diagnosed with type II PRG of tooth 12 with combined endodonticperiodontal lesions.The accumulation of plaque and calculus caused primary periodontitis and a secondary endodontic infection.A multidisciplinary management approach was designed that included root canal therapy,groove sealing,a periodontal regenerative procedure,and prosthodontic treatment.During a 2-year follow-up period,a good prognosis was observed.CONCLUSION This report indicates that bone regeneration and prosthodontic treatment may contribute to the long-term favorable prognosis of teeth with PRGs.

Targeted Ptpn11 deletion in mice reveals the essential role of SHP2 in osteoblast differentiation and skeletal homeostasis

The maturation and function of osteoblasts(OBs)rely heavily on the reversible phosphorylation of signaling proteins.To date,most of the work in OBs has focused on phosphorylation by tyrosyl kinases,but little has been revealed about dephosphorylation by protein tyrosine phosphatases(PTPases).SHP2(encoded by PTPN11)is a ubiquitously expressed PTPase.PTPN11 mutations are associated with both bone and cartilage manifestations in patients with Noonan syndrome(NS)and metachondromatosis(MC),although the underlying mechanisms remain elusive.Here,we report that SHP2 deletion in bone gamma-carboxyglutamate protein-expressing(Bglap+)bone cells leads to massive osteopenia in both trabecular and cortical bones due to the failure of bone cell maturation and enhanced osteoclast activity,and its deletion in Bglap+chondrocytes results in the onset of enchondroma and osteochondroma in aged mice with increased tubular bone length.Mechanistically,SHP2 was found to be required for osteoblastic differentiation by promoting RUNX2/OSTERIX signaling and for the suppression of osteoclastogenesis by inhibiting STAT3-mediated RANKL production by osteoblasts and osteocytes.These findings are likely to explain the compromised skeletal system in NS and MC patients and to inform the development of novel therapeutics to combat skeletal disorders.

A Case Report of a Peripheral Giant Cell Granuloma in a Patient on Forteo

Peripheral giant cell granuloma (PGCG) is a common reactive gingival lesion that histologically resembles the central giant cell granuloma, and is a central lesion of the jaws. Occasionally, central giant cell granuloma-like lesions may be seen in association with hyperparathyroidism. Rarely, PGCG-like lesions have been described in a background of hyperparathyroidism. We describe the case of a 91-year-old woman taking teriparatide for the treatment of osteoporosis and presented with a peripheral giant cell granuloma of the mandibular posterior area.

Stem cell mechanisms during left ventricular remodeling post-myocardial infarction:Repair and regeneration

Post-myocardial infarction(MI),the left ventricle(LV)undergoes a series of events collectively referred to as remodeling.As a result,damaged myocardium is replaced with fibrotic tissue consequently leading to contractile dysfunction and ultimately heart failure.LV remodeling post-MI includes inflammatory,fibrotic,and neovascularization responses that involve regulated cell recruitment and function.Stem cells(SCs)have been transplanted post-MI for treatment of LV remodeling and shown to improve LV function by reduction in scar tissue formation in humans and animal models of MI.The promising results obtained from the application of SCs post-MI have sparked a massive effort to identify the optimal SC for regeneration of cardiomyocytes and the paradigm for clinical applications.Although SC transplantations are generally associated with new tissue formation,SCs also secrete cytokines,chemokines and growth factors that robustly regulate cell behavior in a paracrine fashion during the remodeling process.In this review,the different types of SCs used for cardiomyogenesis,markers of differentiation,paracrine factor secretion,and strategies for cell recruitment and delivery are addressed.