Diabetes linked to higher risk of tooth and implant loss

A University of Gothenburg thesis by dentist Anna Trullenque Eriksson found that people with diabetes face greater risks for oral health problems, based on a large dataset from seven Swedish registers.

Key findings:

  • Periodontitis & tooth loss:
  • Type 1 diabetes: Risk increased only with poor blood sugar control. Over 10 years, 43.5% with poor control lost one or more teeth vs. 25.3% with good control and 29.0% of controls without diabetes.
  • Type 2 diabetes: Risk was elevated regardless of glycemic control, but strongest with poor control. 54.9% with poor control lost one or more teeth over 10 years vs. 44.0% with good control and 37.8% of controls.
  • Dental implants: Both type 1 and type 2 diabetes were associated with higher risk of peri-implantitis (inflammation/bone loss around implants) and implant loss. Poor blood sugar control was a key factor for worse outcomes.
  • Complications & social factors: Periodontitis was linked to higher risk of diabetes-related eye and kidney complications in both types. Complete tooth loss risk was especially high for people with diabetes who had lower income or less education. Data included Sweden and Denmark.

The study reinforces the link between diabetes and oral disease and suggests dental care should be part of diabetes prevention. It also provides new evidence that diabetes may affect long-term success of dental implants. Anna Trullenque Eriksson notes that collaboration between healthcare and dental providers is important.

Whole organ 3D imaging reveals remaining insulin producing cells in type 1 diabetes

Researchers at Umeå University used advanced 3D imaging to map entire human pancreases at microscopic resolution, comparing non-diabetic donors with a donor who had late-onset type 1 diabetes. Published as a peer-reviewed release.

While most insulin-producing β-cells in the islets of Langerhans were destroyed in the type 1 diabetic pancreas, hundreds of thousands of insulin-positive cells still remained.

Why it matters:

  • Unexpected location: These surviving β-cells were mostly found outside traditional islets — as individual cells or small clusters separated from other endocrine cell types. This is the inverse of non-diabetic pancreases, where β-cells are mainly islet-associated.
  • Challenges old assumptions: Traditional studies focus only on islets, so they likely underestimate how many β-cells actually survive in type 1 diabetes.
  • Therapeutic potential: The cells may be more resistant to autoimmune destruction, or new β-cells might still form. If certain pancreatic microenvironments promote β-cell survival, they could become targets for therapies aimed at stabilizing or expanding remaining β-cells.


Prof. Ulf Ahlgren says the pancreas can retain β-cells “in a way that has not previously been recognized.” Doctoral student Joakim Lehrstrand adds, “we must look beyond the islets when studying β‑cell biology in type 1 diabetes.”

The whole-organ 3D imaging method lets scientists study individual cells throughout the entire organ. The team believes this will be key for future research into type 1 diabetes, type 2 diabetes, and pancreatic cancer, by helping isolate specific regions for molecular analysis.

Study reveals strong link between type 2 diabetes and hearing loss

A recent study published in Otolaryngology–Head and Neck Surgery has found a significant link between type 2 diabetes and hearing loss. The study, which analyzed data from over 3,900 individuals with diabetes and 4,000 control subjects, revealed that people with type 2 diabetes are 4.19 times more likely to experience hearing loss.

The prevalence of hearing loss among patients with type 2 diabetes was found to range from 40.6% to 71.9%, with the risk increasing with the duration of diabetes. Those with diabetes for more than 10 years had a 2.07 times higher risk of hearing loss compared to those with shorter disease duration.

The study suggests that hearing loss in type 2 diabetes may be caused by microcirculatory alterations affecting the cochlea, leading to changes in the inner ear capillaries. Poor glucose control was also found to correlate with more severe hearing impairment.

Given the rising number of people with diabetes, this research highlights the importance of comprehensive diabetes care that includes hearing assessments. Hearing loss could serve as an early indicator of microvascular disease, allowing for earlier intervention to prevent further complications .

New discovery finds gene converts insulin-producing cells into blood-sugar boosters

A recent study by City of Hope has identified a gene called SMOC1 that plays a crucial role in the development of type 2 diabetes. The study found that SMOC1 can convert insulin-producing beta cells into cells that increase blood sugar levels, similar to alpha cells.

Key Findings

  • SMOC1 gene converts beta cells to alpha-like cells: The study found that SMOC1 expression in beta cells leads to a shift towards an alpha cell-like state, resulting in reduced insulin production and increased blood sugar levels.
  • Cell identity crisis in type 2 diabetes: The study suggests that beta cells in individuals with type 2 diabetes undergo an identity crisis, losing their unique traits and behaving more like alpha cells.
  • Potential therapeutic target: The discovery of SMOC1’s role in type 2 diabetes progression identifies a new therapeutic target for the treatment of the disease.

Implications

The study’s findings have implications for the treatment and management of type 2 diabetes. By understanding the role of SMOC1 in beta cell dysfunction, researchers may be able to develop new strategies to protect healthy beta-cell function and enhance insulin production.

Potential Applications

The study’s findings suggest several potential applications, including:

  • Diagnostic biomarker: SMOC1 could be used as a diagnostic biomarker for beta-cell malfunction in type 2 diabetes.
  • Therapeutic target: Blocking SMOC1 or reversing its effects may offer new strategies to protect healthy beta-cell function and enhance insulin production.
  • Cell-reprogramming therapies: Recognizing that some cells can switch types opens the door to cell-reprogramming therapies that could restore insulin production.

Conclusion

The study’s findings provide new insights into the complex mechanisms underlying type 2 diabetes and identify a new therapeutic target for the treatment of the disease. Further research is needed to explore the potential applications of these findings and to develop new treatments for type 2 diabetes.