Superior fixation and less periprosthetic stress-shielding of tibial components with a finned stem versus an I-beam block stem: a randomized RSA and DXA study with minimum 5 years’ follow-up

Background and purpose — The stem on the tibial component of total knee arthroplasty provides mechanical resistance to lift-off, shear forces, and torque. We compared tibial components with finned stems (FS) and I-beam block stems (IS) to assess differences in implant migration.

Patients and methods — In a patient-blinded RCT, 54 patients/knees (15 men) with knee osteoarthritis at a mean age of 77 years (70–90) were randomly allocated to receive tibial components with either a FS (n = 27) or an IS (n = 27). Through 5 to 7 years’ follow-up, implant migration was measured with RSA, periprosthetic bone mineral density (BMD) was measured with DXA, and surgeons reported American Knee Society Score (AKSS).

Results — At minimum 5 years’ follow-up, maximum total point motion (MTPM) was higher (p = 0.04) for IS (1.48?mm, 95% CI 0.81–2.16) than for FS (0.85?mm, CI 0.38–1.32) tibial components. Likewise, total rotation (TR) was higher (p = 0.03) for IS (1.51?, CI 0.78–2.24) than for FS (0.81?, CI 0.36–1.27). Tibial components with IS externally rotated 0.50° (CI –0.06 to 1.06) while FS internally rotated 0.09° (CI –0.20 to 0.38) (p = 0.03). Periprosthetic bone stress-shielding was higher (p < 0.01) up to 2 years’ follow-up for IS compared with FS in the regions medial to the stem (–13% vs. –2%) and posterior to the stem (–13% vs. –2%). Below the stem bone loss was also higher (p = 0.01) for IS compared with FS (–6% vs. +1%) up to 1-year follow-up. Knee score improved similarly in both groups up to 5 years’ follow-up.

Interpretation — Periprosthetic bone stress-shielding medial and posterior to the stem until 2 years, and tibial component migration at 5 years, was less for a finned compared with an I-shaped block stem design.

Trial registration: ClinicalTrials.gov identifier: NCT00175136.     

Clinical concepts for regenerative therapy in furcations

Furcation involvements present one of the greatest challenges in periodontal therapy because furcation‐involved molar teeth respond less favorably to conventional periodontal therapy compared with noninvolved molar or nonmolar teeth. Various regenerative procedures have been proposed and applied with the aim of eliminating the furcation defect or reducing the furcation depth. An abundance of studies and several systematic reviews have established the effectiveness of membrane therapy (guided tissue regeneration) for buccal Class II furcation involvement of mandibular and maxillary molars compared with open flap surgery. Bone grafts/substitutes may enhance the results of guided tissue regeneration. However, complete furcation closure is not a predictable outcome. Limited data and no meta‐analyses are available on the effects of enamel matrix proteins for furcation regeneration. Enamel matrix protein therapy has demonstrated clinical improvements in the treatment of buccal Class II furcation defects in mandibular molars; however, complete closure of the furcation lesion is achieved only in a minority of cases. Neither guided tissue regeneration nor enamel matrix protein therapy have demonstrated predictable results for approximal Class II and for Class III furcations. Promising preclinical data from furcation regeneration studies in experimental animals is available for growth factor‐ and differentiation factor‐based technologies, but very limited data are available from human clinical studies. Although cell‐based therapies have received considerable attention in regenerative medicine, their experimental evaluation in the treatment of periodontal furcation lesions is at a very early stage of development. In summary, the indications and the limitations for currently available treatment modalities for furcation defects are well established. New regenerative treatments are clearly needed to improve the predictability of a complete resolution of furcation defects.     

Response of MG63 osteoblasts on bacterial challenge is dependent on the state of differentiation

The present in vitro study examines molecular processes that are relevant during bone homeostasis after Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis infection with a focus on the differentiation level of osteoblasts. Regenerative processes are often hindered by the recurrence of bacterial infections, which can ultimately provoke a severe destruction of bone tissue. To obtain more detailed insights into such a complex scenario, we have used undifferentiated MG63 osteoblast‐like cells as an experimental paradigm to examine the impact of two oral pathogens, A. actinomycetemcomitans and P. gingivalis, on proliferation, cytotoxicity and osteogenic differentiation. Cell culture experiments were performed to analyze cellular behavior. The level of genes interfering with bone tissue integrity (matrix metalloproteinases and their tissue inhibitors) and osteogenic markers (alkaline phosphatase, Runx2, human β‐defensin‐2) was compared in undifferentiated versus differentiated MG63 cells using real‐time polymerase chain reaction. Functional activity of matrix metalloproteinases was quantified by zymography. Western blot analysis was used to verify the phosphorylation state of mitogen‐activated protein kinases p38 and extracellular‐signal‐regulated kinases 1/2. When co‐cultured with undifferentiated MG63 cells, oral pathogens provoked distinct cellular effects. Only A. actinomycetemcomitans reduced cell proliferation, increased cell death, and induced osteogenic differentiation. A comparison of matrix metalloproteinase network stability in the presence of oral pathogens revealed a partial sensitivity towards P. gingivalis but not A. actinomycetemcomitans. So, beside the proof of concept that MG63 cells co‐cultured with oral pathogens can serve as an in vitro model for mimicking destructive and regenerative events after bacterial infections, our data indicate that double infections might counterbalance otherwise positive effects.     

Hereditary Hemolytic Disease Secondary to Glucose-6-Phosphate Dehydrogenase Deficiency: Report of Three Cases with Special Emphasis on ATP Metabolism

1. Three cases of hereditary hemolytic disease secondary to G-6-PD deficiency are described. Two of the cases were first cousins of Scotch-Irish-English descent and the mode of inheritance was believed to be sex-linked.The third case was of Turkish origin; no family studies were availale.

2. The mothers, who were heterozygous for G-6-PD deficiency, showed onlyminimal expression of the defect, which was manifested by a slightly decreasedred cell survival in both mothers and an abnormal methemoglobin reductiontest in one of them.

3. All three cases showed a more pronounced fall in erythrocyte ATP afterincubation with phenylhydrazine than that observed in primaquine-sensitiveNegroes whose red cells were less deficient in G-6-PD.

4. It is suggested that the inability of the G-6-PD-deficient erythrocyte tomaintain adequate levels of ATP may be an important factor in the pathogenesis of the hemolytic process.

Submitted on August 26, 1963 Accepted on October 24, 1963