Growth factors, especially TGF-β, are thought to initiate the production of reparative dentin by fibroblasts and mesenchymal cells of the pulp. Reparative dentin is produced at an average of 1.5 μm/day, but can be increased to 3.5 μm/day. The resulting dentin contains irregularly shaped dentinal tubules that may not line up with existing dentinal tubules. This diminishes the ability for dental caries to progress within the dentinal tubules. Cementum
The incidence of cemental caries increases in older adults as gingival recession occurs from either trauma or periodontal disease. It is a chronic condition that forms a large, shallow lesion and slowly invades first the roots cementum and then dentin to cause a chronic infection of the pulp (see further discussion under classification by affected hard tissue). Because dental pain is a late finding, many lesions are not detected early, resulting in restorative challenges and increased tooth loss. Diagnosis
The presentation of caries is highly variable. However, the risk factors and stages of development are similar. Initially, it may appear as a small chalky area (smooth surface caries), which may eventually develop into a large cavitation. Sometimes caries may be directly visible. However other methods of detection such as X-rays are used for less visible areas of teeth and to judge the extent of destruction. Lasers for detecting caries allow detection without ionizing radiation and are now used for detection of interproximal decay (between the teeth). Primary diagnosis involves inspection of all visible tooth surfaces using a good light source, dental mirror and explorer.
Hydrolases secreted into the blood stream cause little problem as they are inactivate at the near neutral pH of blood (7.4). It can be associated with N-acetylglucosamine-1-phosphate transferase (GNPTA). In a case report, I-cell disease was complicated by severe dilative cardiomyopathy (DCM).Though rare, a deficiency of phosphodiesterase which would cleave GlcNAc from the mannose-6-phosphate tag will also cause I-cell disease. The presence of lipids, glycosaminoglycans (GAGs) and carbohydrates in the blood provide for the distinguishing characteristic to separate I-cell from Hurler Syndrome. In Hurlers, only glycosaminoglycans would be present. Diagnosis
Diagnostic measures can include the following. Before birth:

Abnormally low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity in amniotic fluid cells or chorionic villiIn infants:

Elevated plasma lysosomal enzyme concentrations 
Decreased concentration of lysosomal enzymes in cultured fibroblasts and increased in the surrounding medium 
Presence of inclusion bodies in peripheral blood lymphocytes
Low concentrations of UDP-N-acetylglucosamine-1-phosphotransferase enzyme activity as measured in white blood cells

Treatment
There is no cure  for I-Cell disease/Mucolipidosis II disease; treatment is limited to controlling or reducing symptoms. Nutritional supplements, particularly iron and vitamin B12, are often recommended. Physical therapy to improve motor delays and speech therapy to improve language acquisition are treatment options. Surgery can remove the thin layer of corneal clouding to temporarily improve the complication. It is possible that bone marrow transplant may be helpful in delaying or correcting the neurological deterioration that occurs with I-Cell disease.