AATD, alpha-1 antitrypsin deficient; AUG, augmentation therapy; PFTnorm, pulmonary function testing normal; AAT, alpha-1 antitrypsin; COPD, chronic obstructive pulmonary disease; FVC, forced vital capacity; FEV1, forced expiratory volume at 1 sec; VO2peak, peak oxygen consumption during exercise.
In the situation of a deficient patella, patelloplasty, augmentation procedures and very rarely patellectomy are other viable options.
In the present report, we present a series of 9 patients with a total of 10 lateral augmentation of deficient alveolar ridges using graft material applied through the subperiosteal tunneling approach.
All patients received alveolar bone augmentation in the deficient ridge areas.
In this research article, we evaluate the use of sub-periosteal tunneling (tunnel technique) combined with alloplastic in situ hardening biphasic calcium phosphate (BCP, a compound of β-tricalcium phosphate and hydroxyapatite) bone graft for lateral augmentation of a deficient alveolar ridge.
It was shown that when AtSPX3 was repressed by RNAi it resulted in augmentation of P-deficient symptoms and altered allocation of internal P, leading to the conclusion that AtSPX3 plays an important role in plant adaptation to P deficiency (Duan et al., 2008).
A variety of implant-driven bone augmentation techniques for the deficient alveolar bone have been proposed.
In 1989, the American Thoracic Society ATSS) recommended 31 AAT augmentation therapy for severely deficient patients with significant airflow obstruction, if they had quit smoking and were receiving optimal medical therapy.
Furthermore, in apolipoprotein-E-deficient mice, HDM challenge results in augmentation of AHR and mucous cell metaplasia (Yao et al., 2010).
(Figs. 4, 5, 6, 7, 8, 9, and 10) Fig. 4 Female patient with severe peri-implantitis in regions 35, 36, 37. PPD ≥7 mm and BOP with suppuration and fistula 36, deficient keratinized mucosa due to hard tissue augmentation 5.5 years ago Fig. 5 Crater-shaped peri-implant defects.
Nevertheless, lung disease due to AAT deficiency can be prevented by protein augmentation therapy (American Thoracic/European Respiratory Society, 2003; Wewers et al, 1987) or replenishment of the deficient gene product via AAV-mediated muscle-directed gene therapy (Brantly et al, 2009; Flotte et al, 2004).
