In rats, a portion of Meckel's cartilage -that lying within the mandible but proximal to the rostral convergence of the bars -gives rise to no definitive structures. It offers especially favorable opportunity to study cartilage resorption. By the eighteenth fetal day it is established as a hyaline cartilage bar, and a thin perichondral bone shell starts to form on its lateral aspect, completing encirclement in the next two days. On day 19 cartilage within this bone shows chondrocyte hypertrophy, lacunar enlargement, and matrix calcification. Osteoclasts open a fenestra laterally in the bone and commence removal of calcified cartilage matrix. The erosion front expands rapidly, moving medially (preceded by cartilage hypertrophy and calcification) and extending proximally and distally along the segment. Chondroclasts (multinucleated cells identical with osteoclasts) dominate the erosion front. Capillaries and various mononucleated cells follow. Bone formation is much delayed except in the most rostral extremity, so that, contrary to the situation in endochondral osteogenesis, one is examining calcified cartilage resorption in uncomplicated form. This resorption, including the perichondral bone shell, is virtually complete by day 21, and intramembranous bony reorganization of the site is in progress at birth.Several features of chondroclasts, including some in dispute or not easily seen in vivo, are well displayed. These include ameboid form with pseudopodial extensions (sometimes filamentous), and fusion of some released chondrocytes with entering chondroclasts. Osteo/chondroclasts are often found in contact with perichondral bone at one extremity and calcified cartilage elsewhere on the same cell. There is evidence that matrix calcification is prerequisite to the chondroclastic activity.

The authors' previous report (Savostin-Asling and Asling, '73) demonstrated that Meckel's carilage is a favorable site for study of calcified cartilage resorption. In the present study the ultrastructural features at this resorption front have been examined by transmission and scanning electron microscopes (19-day rat retus). Multinucleated giant cells chondroclasts) dominated the erosion front. The many features which they showed in common with osteoclasts included abundant mitochondria, vacuolation, lysonsomes, sparsity of rough-sufaced endoplasmic reticulum, and deep infoldings at loci of contact with calcified matrix. Crumbling of matrix (with mineral crystals penetrating between these foldings) and fragmentation of collagen fibrils were also seen. The propensity of chondroclasts for spanning several opened lacunae provided special opportunity to demonstrate cell surface modifications in presence or absence of matrix contact. Amebiod processes extending into lacunae were seen by both transmission and scanning procedures; they were sometimes tipped with a veil of filamentous processes as small as 0.3 mum in diameter. Most hypertrophic chondrocytes. when released from lacunae, appeared to be disintegrating. However, in accord with previous evidence of their possible merger with chondroclasts (in light microscopic studies) there was also evidence for breakdown of cell walls between a chondroclast and a chondrocyte in intimate contact, with possibility of cytoplasmic continuity.

Mandibular bone from eight patients who had received therapeutic radiation (6,000-7,200 rads) for intra-oral cancer was obtained at surgery (1 month to 9 years after radiation) and compared histologically with non-irradiated mandibular bone from five subjects. Measurements made on the internal remodeling process of cortical bone included the extent of internal surface and the fraction indicating resorption, and the proportions of osteones which were incomplete (less than 3/4 filled with matrix), complete, and plugged. Appreciable differences were observed in all parameters except plugged osteones. The findings suggested early cessation of osteogenesis, and somewhat later cessation of resopriton, without subsequent resumption of either process. The histologic appearance of the osteoblasts, osteoclasts, and osteones was in accord. Microfractures found in the irradiated bone were not seen to have healed. Radiation damage to the osteoprogenitor cells is postulated.

No abstract

Experimental conditions simulating the induction of clinical pituitary gigantism and acromegaly were established by prolonged administration of growth hormone in high dosage to adult male rats starting at two different ages: 6 months (growth still active) and 14 1/2 months (growth virtually arrested). Treatment continued for 14 1/2 months, control receiving saline injections. Each group numbered eight at onset. Standardized x-rays of skull were made in ventro-dorsal and lateral planes, at onset, mid-period, and end of the study. Representative dimensions of cranial and facial segments were measured, including lengths, widths, palate dimensions, gnathic and interzygomatic angles, and incisor curvature. Some related indices were calculated. Means and standard errors were computed, usually on five to eight rats (oldest controls: three only). The response pattern of overall skull length was most illustrative. Younger adult controls grew actively until 14 months of age (5%) while injected rats grew still faster (8%); thereafter, controls grew negligibly (1%) and injected rats only slightly (2%). Older controls showed negligible skull elongation from 14 1/2 to 29 months of age, and growth hormone stimulated no gain. In the younger group, skull length gains were almost entirely in the facial region; cranium gained no length and widened only slightly. Cranial index increased slightly with the hormone. Facial (bizygomatic) width increased in both injected groups--proportionately in younger rats(to giganntism) and disproportionately in older rats. Palatal and dental growth followed facial patterns in both groups. Cranial vault bones thickened and, in older rats, developed surface irregularities, giving them a more massive, acromegaloid structure.