Vitamin D deficiency in both rickets and osteomalacia results in an excess of unmineralized matrix. The following sequence insues in rickets: Overgrowth of epiphyseal cartilage due to inadequate provi sional calcification and fallure of the cartilage cells to mature and disintegrate Persistence of distorted, irregular masses of cartilage, which project into the marrow cavity Deposition of ostegid matrix on inadequately mineralized car- Maginous remnants Dauction of the orderly replacement of cartilage by osteoid Matrix, with enlargement and lateral expansion of the osteo- Chondral junction (Fig. 9-278) Nutritional diseases 441 Abnormal overgrowth of capillaries and fibroblasts in the disorganized zone resulting from microfractures and stresses on the inadequately mineralized, weak, poony formed bon0 Deformation of the skeleton due to the loss of structural rigidity of the developing bones The gross skeletal changes in rickets depend on the severity and duration of the process and, in particular, the stresses to which individual bones are subjected. During the nonambula tory stage of intancy, the head and chest sustain the greatest stresses. The softened occipital bones may become flattened. and the panetal bones can be buckled inward by pressure: with the release of the pressure, elastic recoil snaps the bones back into their original positions (craniotabes). An excess of osteoid produces frontal bossing and a squared appearance to the head. Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, pro- ducing the "rachitic rosary." The weakened metaphyseal areas of the nibs are subject to the pull of the respiratory muscles and thus bend inward, creating anterior protrusion of the sternum (pigeon breast deformity). When an ambulating child develops rickets, deformities are likely to affect the spine. pelvis, and tibia, causing lumbar lordosis and bowing of the legs (Fig. 9-27C). In adults with osteomalacia, the lack of vitamin D deranges the normal bone remodeling that occurs throughout life. The newly formed osteoid matrix laid down by osteoblasts is inad- equately mineralized, thus producing the excess of persistent osteoid that is characteristic of osteomalacia. Although the contours of the bone are not affected, the bone is weak and vulnerable to gross fractures or microfractures, which are most likely to affect vertebral bodies and femoral necks. The unmin- eralized osteoid appears as a thickened layer of matrix (which stains pink in hematoxylin and eosin preparations) arranged about the more basophilic, normally mineralized trabeculae.